Strona 44 z 46 PierwszyPierwszy ... 344243444546 OstatniOstatni
Pokaż wyniki od 646 do 660 z 678

Wątek: NATURALNE sposoby optymalizacji CIAŁA i DUSZY.

  1. #646
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    FEBRUARY 20, 2019
    Exercise in morning or afternoon to shift your body clock forward



    Exercise can shift the human body clock, with the direction and amount of this effect depending on the time of day or night in which people exercise. That's according to new research in published in The Journal of Physiology. These findings suggest exercise could counter the effects of jet lag, shift work, and other disruptions to the body's internal clock (e.g. military deployments) helping individuals adjust to shifted schedules.

    The circadian "body"' clock is the 24 hour cycle that regulates many physiological processes including sleeping and eating. Many factors affect this internal body clock including light and time cues. Exercise has been known to cause shifts in the circadian clock however very little is known about this effect.

    This study found that exercising at 7 am or between 1 and 4 pm advanced the body clock to an earlier time, and exercising between 7 and10 pm delayed the body clock to a later time. Exercising between 1 and 4 am and at 10 am, however, had little effect on the body clock, and the phase-shifting effects of exercise did not differ based on age nor gender.

    The researchers at University of California, San Diego and Arizona State University examined body clocks following exercise in 101 participants for up to five and a half days. The baseline timing of each participant's body clock was determined from urine samples collected every 90 minutes to measure the time of the evening rise in melatonin and the peak of melatonin several hours later. Participants then walked or ran on a treadmill at a moderate intensity for one hour per day for three consecutive days. They exercised at one of eight different times of day or night, but each individual exercised at the same time on all three days or nights. The timing of the body clock was re-assessed following the third exercise session.

    Given that the subjects tested were more physically active than average, the results might not translate to the average person. Further research will look at combining exercise with bright lights and melatonin to see what impact this has on body clocks, as well as examining the effect of changes in exercise duration and intensity on the body clock.

    Shawn Youngstedt, first author on the paper, said:

    "Exercise has been known to cause changes to our body clock. We were able to clearly show in this study when exercise delays the body clock and when it advances it. This is the first study to compare exercise's effects on the body clock, and could open up the possibility of using exercise to help counter the negative effects of jet lag and shift work."
    bez neuroprzekaźników, bez chemii, bez kabli czysta fizyka
    pora wyciągnąć ajfona z pod poduszki:

    19.02.2019
    W mózgu odkryto nowy rodzaj komunikacji między neuronami

    W najistotniejszej dla uczenia się i pamięci części mózgu działa na odległość komunikacja niewymagająca żadnego styku neuronów i żadnego typu synapsy. Działa dzięki polu elektrycznemu. Czysta fizyka, żadnej zaangażowanej chemii. Można na tę nowo odkrytą aktywność wpływać. Choć jeszcze nie wiadomo, do czego ona tak naprawdę służy.

    Grupa badawcza neurofizjologów pod kierunkiem Dominique’a Duranda z Uniwersytetu Case Western Reserve (prywatny uniwersytet badawczy w Cleveland w stanie Ohio, w USA, słynący z rozwoju nowych technologii oraz nauk ścisłych i inżynierii) dokonała przełomu w badaniach nad mózgiem. Na łamach „The Journal of Physiology” opublikowała właśnie dowód na istnienie wcześniej nieznanej formy komunikacji neuronalnej w części mózgu zwanej hipokampem.

    Rozprzestrzenia się ona samoistnie w tkance mózgowej i może „przeskakiwać bezprzewodowo” z neuronów w jednej części tkanki mózgowej do drugiej. Nawet jeśli wziąć skalpel i te części po prostu chirurgicznie całkowicie oddzielić. Uzyskane wyniki były tak szokujące, że recenzenci pracy domagali się ponownego powtórzenia całego cyklu doświadczeń, zanim zezwolili na publikację. Choć swe doświadczenia uczeni z Cleveland wykonali na myszach, jest oczywistym, że ich odkrycie ma także zastosowanie do mózgu ludzkiego.

    Integracja to nieustanna komunikacja

    Mózg, jako część układu nerwowego, zbudowany jest głownie z komórek nerwowych – neuronów. To najbardziej wyspecjalizowane i bardzo trudne do regeneracji komórki naszego ciała. W mózgu człowieka – w samej korze mózgowej – doliczono się od kilkunastu do 30 miliardów neuronów. Każdy neuron ma swe komórkowe ciało oraz liczne stosunkowo krótkie wypustki zwane dendrytami.

    Najdłuższe wypustki (na ogół występuje jedna) noszą miano aksonów. Każdy z neuronów dzięki swym wypustkom połączony jest tak anatomicznie, jak funkcjonalnie, z kilkoma tysiącami swoich kolegów. I zasadniczo bez przerwy z nimi rozmawia. To oznacza, że tych połączeń w mózgu Jana Kowalskiego może być mniej więcej tyle, co ciał niebieskich we Wszechświecie. I to one zapewniają mózgowi centralną rolę integratora i kontrolera zarządzającego naszym organizmem.

    Komunikacja pomiędzy neuronami odbywa się na trzy podstawowe dotąd znane nauce sposoby. Po pierwsze w mikroprzestrzeniach pomiędzy zakończeniami pojedynczych neuronów, w tzw. synapsach. Tam na drodze chemicznej przekazywany jest sygnał o wzbudzeniu. Pobudzenie to zaś rozprzestrzenia się wzdłuż neuronu bardzo szybko jako sygnał elektryczny – miejscowa depolaryzacja błony komórkowej. Czyli potencjał czynnościowy. Wszystko zaś trwa milisekundę. Bo jak nauczyliśmy się jako dzieci z wierszyka Tuwima, prąd elektryczny jest „bystry”.

    Co to oznacza? Neuron jest komórką pobudliwą, czyli jego błona komórkowa jest spolaryzowana (wewnątrz minus, na zewnątrz plus). Aktywność synaptyczna to zamiana na sygnał chemiczny chwilowej i przemieszczającej się wzdłuż błony aksonu depolaryzacji elektrycznej (plusy w konkretnym miejscu wchodzą do środka i taka „iskra” biegnie dalej). Sygnał chemiczny to uwolnienie na zewnątrz, do synapsy, tzw. neurotransmiterów zamkniętych dotąd w podbłonowych pęcherzykach.

    Uwolnione neurotransmitery są w stanie wywołać depolaryzację w kolejnym neuronie, który ma swoje zakończenie w tej samej synapsie (czyli zmienić jego potencjał spoczynkowy na czynnościowy). On to przekaże wzdłuż swego aksonu, do kolejnej synapsy. I tak dalej, i tak dalej, aż do spolaryzowanej błony komórki efektorowej (np. mięśnia), która wykona pożądaną od niej pracę – np. skurczy się. Zaś na samym początku tego funkcjonalnego nerwowego połączenia znajduje się receptor, np. komórki pręcików i czopków w siatkówce oka, które „zobaczą” przeszkodę, jaką noga musi ominąć.
    Po drugie, komunikacja pomiędzy neuronami może odbywać się bezpośrednio, w ścisłych dość połączeniach błon komórkowych, zwanych neksusami czy synapsami elektrycznymi. Są to szczelinowe połączenia jonowo-metaboliczne. Przez nie, już bez pośrednictwa pęcherzyków, pewne substancje potrafią się przemieszczać pomiędzy tak ściśle połączonymi komórkami dzięki nagromadzeniu w neksusie specjalnych kanałów białkowych. Komunikacja ta jest gwałtowniejsza niż w synapsie chemicznej.

    Po trzecie, znana jest również, już od XIX wieku, komunikacja, czy raczej sprzężenie sąsiednich neuronów. Przemieszczanie się potencjału czynnościowego w aktywnym aksonie powoduje bowiem zmiany pobudliwości w sąsiednim aksonie nieaktywnym. Zmiany te przypisuje się lokalnym prądom potencjału czynnościowego. Na przykład prądy, które powodują depolaryzację (pobudzenie) aktywnego nerwu, wywołują odpowiednią hiperpolaryzację sąsiedniego włókna spoczynkowego. Tak to włókno spoczynkowe staje się chwilowo jeszcze mniej pobudliwe.
    Czwarty element

    Dla neurofizjologów było jasne, że ta lista nie wyczerpuje sposobów na komunikację w układzie nerwowym. Na przykład obserwowano od dekad, że mózg wykazuje powolne fale oscylacji nerwowych, pojawiających się w korze mózgowej i hipokampie, kiedy śpimy. Hipotetycznie zatem miałyby one odgrywać rolę w konsolidacji pamięci. Profesor Durand ze swoją grupą badawczą od lat badał naturę owych wolnych oscylacji w hipokampie.

    To parzysta struktura niczym otwarte obręcze czy strzemiona obejmuje półkule wzgórza (centralna struktura mózgu okryta korą mózgową). To w hipokampie zagnieżdża się pamięć operacyjna. Tu znajdujemy (lub nie!) odpowiedź na pytania: „Jak ja tu trafiłem?” albo „Gdzie ja to położyłem?”, zanim rozpoczniemy gorliwą modlitwę do św. Antoniego Padewskiego.
    Prof. Durand i jego zespół obserwowali owe oscylacje in vitro, badając fale mózgowe w plastrach hipokampa wyoperowanych z mózgu myszy. Odkryli oni, że powolne oscylacje mogą generować pola elektryczne, które z kolei aktywują komórki sąsiednie, stanowiące formę komunikacji neuronowej bez chemicznej transmisji synaptycznej czy innych bezpośrednich połączeń. Pamiętajmy bowiem, że wzdłuż neuronów sygnał rozprzestrzenia się już elektrycznie. Że jest dokładnie tak, jak to opisał Morfeusz Noemu w „Matrixie”: „Prawdziwe to są tylko sygnały elektryczne interpretowane przez twój mózg”.

    Najbardziej szokującym odkryciem prof. Duranda było to, że te powstające pod wpływem – jak się dotąd uważa – spontanicznych oscylacji pola elektryczne mogą aktywować neurony nawet wtedy, gdy je całkowicie chirurgicznie odciąć. O ile zapewnić im następnie pozostawanie w fizycznej bliskości. To znaczy, że w mózgu można przekazać sygnał nerwowy bez żadnego realnego kontaktu. Wystarczy w miarę wspólna lokalizacja komunikujących części.
    Jeszcze nie wiadomo, czemu służy w mózgu to wszystko, co właśnie odkryli Amerykanie. Wiadomo jednak, że można tę komunikację modulować za pomocą przykładania słabych pól elektrycznych. Niewątpliwy przełom w neurobiologii autorstwa prof. Duranda wymaga zatem prowadzenia dalszych badań i nad jego naturą, i poszukiwań odpowiedzi na pytanie o rolę tej nowo odkrytej metody komunikacji dla funkcjonowania naszego mózgu. A tym samym funkcjonowania nas jako istot myślących.
    https://www.tvp.info/41375915/w-mozg...edzy-neuronami

    Gdy brakuje witaminy D, rusztowanie otaczające neurony jest łatwiej rozkładane przez enzymy

    Witamina D jest niezbędna do prawidłowego działania sieci perineuronalnej, która stabilizuje połączenia między neuronami. To może wyjaśniać, czemu jej niedobory prowadzą do takich zaburzeń, jak depresja.

    Ponad miliard ludzi na świecie ma niedobór witaminy D. Związek między niedoborami tej witaminy i problemami poznawczymi jest zaś badaczom dobrze znany - opowiada prof. Thomas Burne z Uniwersytetu Queensland. Niestety, nie wiadomo, jak dokładnie witamina D wpływa na budowę i działanie mózgu.

    Australijski zespół odkrył, że poziom witaminy D oddziałuje na sieć perineuronalną. Gdy jest jej tyle, co trzeba, silna, wspierająca sieć wokół neuronów [...] stabilizuje połączenia między komórkami.

    Gdy podczas eksperymentów z diety zdrowych dorosłych myszy wyeliminowano witaminę D, po 20 tygodniach okazało się, że w porównaniu do grupy kontrolnej, znacząco gorzej przebiegało u nich uczenie i zapamiętywanie. Naukowcy stwierdzili, że w hipokampie, rejonie mózgu kluczowym dla uczenia, doszło do silnie zaznaczonego zaniku sieci perinneuronalnych. Zaobserwowaliśmy także spadek liczby i siły połączeń między neuronami w tym obszarze. Wiele wskazuje więc na to, że deficyty uczenia przestrzennego można przypisać zaburzeniu właściwej łączności strukturalnej hipokampa.

    Australijczycy uważają, że witamina D odgrywa ważną rolę w stabilizowaniu sieci. Kiedy jej poziom spada, rusztowanie jest łatwiej rozkładane przez enzymy.

    Kiedy neurony w hipokampie tracą swoje wspierające sieci perineuronalne, mają problem z zachowaniem połączeń, co ostatecznie prowadzi do utraty funkcji poznawczych.

    Burne uważa, że niedobór witaminy D może silniej oddziaływać na hipokamp, bo jest on bardziej aktywną strukturą. Można go porównać do kanarka w kopalni - szwankuje w pierwszej kolejności, bo wyższe zapotrzebowanie energetyczne uwrażliwia go na niedobór niezbędnych składników odżywczych [...]. Intrygujące jest to, że niedobór witaminy D silniej wpływa na prawy niż na lewy hipokamp.

    Burne podkreśla, że utrata funkcji tego obszaru może się w istotny sposób przyczyniać do flagowych objawów schizofrenii: dużych deficytów pamięciowych oraz zaburzonego postrzegania rzeczywistości.

    Akademicy cieszą się, że zmiany dot. sieci perineuronalnych wykryto u dorosłych myszy. Mam nadzieję, że skoro są one dynamiczne, istnieje szansa na ich odbudowanie, co pozwala myśleć o nowych metodach terapii.
    correlation doesn't imply causation

  2. #647
    Czyli jak będę ćwiczył rano to stanę się rannym ptaszkiem, tak?

  3. #648
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    elementów układanki jest dużo więcej. Aktywność fizyczna jest jednym z wielu "dawców czasu".
    Białko zegarowe BMAL1 wbija się do mięśni, wyrównując wzorzec (można to sobie tak tłumaczyć)

    chodzi o przesunięcie(to przykład):



    Czyli jak będę ćwiczył rano to stanę się rannym ptaszkiem, tak?
    odpowiadając na pytanie: nie koniecznie, ale może pomóc.
    Osoby, które ćwiczą rano mogę empirycznie potwierdzić, że lepiej im się wieczorem zasypia (o ile nie ma większego spierdolenia w tle).
    Ostatnio edytowane przez htw ; 21-02-19 o 15:36
    correlation doesn't imply causation

  4. #649
    U mnie basen o 7 kończył się zazwyczaj drzemką po 9

  5. #650
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Może za dużo w jacuzzi siedziałeś
    correlation doesn't imply causation

  6. #651
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    2019 Feb 20
    The Effect of Light on Sleep and Sleep-Related Physiological Factors Among Patients in Healthcare Facilities: A Systematic Review.

    OBJECTIVES:
    Lighting is one of the environmental factors which can improve patient sleep in healthcare environments. Due to the high degree of variation in study designs and results on this topic, the implications have been difficult to interpret. This review consolidates studies on the impact of bright light exposure on sleep to identify lighting conditions that can be applied and researched in future healthcare environments.

    METHODS:
    We searched for peer-reviewed articles on the impact of light on sleep or sleep-related outcomes in healthcare settings. We provided detailed analysis of the direct links between light and sleep, and a more cursory analysis of links between light and sleep-related factors, from 34 articles which met our inclusion criteria.

    RESULTS:
    The current state of the literature includes evidence on how various durations and intensities of morning, midday, and evening bright light exposure, as well as whole-day light exposure interventions can improve specific aspects of sleep. Lighting interventions differed in all attributes (illuminance levels, exposure time, exposure duration, and spectral qualities) but showed promising results in improving patients' sleep.

    CONCLUSIONS:
    Short-term bright light exposure in the morning, up to 2 hr of moderate (3,000-10,000 lux) morning exposures, up to 4 hr of moderate evening exposure, and whole-day exposures to lower illuminance levels (<3,000 lux) can improve patient sleep outcomes. Based on new findings on the mechanism through which light impacts sleep, future studies should be more specific about the spectral qualities of light sources.
    ćwiczenia stymulują wychwyt glukozy niezależnie od insy:

    https://www.jci.org/articles/view/108050
    https://www.ncbi.nlm.nih.gov/pubmed/6391198
    https://www.ncbi.nlm.nih.gov/pubmed/6389452
    https://www.ncbi.nlm.nih.gov/pubmed/7015876
    https://www.ncbi.nlm.nih.gov/pubmed/3102297
    https://www.ncbi.nlm.nih.gov/pubmed/7573437
    https://www.ncbi.nlm.nih.gov/pubmed/10331428
    https://www.ncbi.nlm.nih.gov/pubmed/10545524
    https://www.ncbi.nlm.nih.gov/pubmed/16803855
    https://www.ncbi.nlm.nih.gov/pubmed/17327455

    Scientists from the National Institute of Environmental Health Sciences (NIEHS), part of NIH, speculate that biologic age may be tied to environmental exposures.
    ups.

    FEBRUARY 22, 2019
    Older biologic age linked to elevated breast cancer risk

    Biologic age, a DNA-based estimate of a person's age, is associated with future development of breast cancer, according to scientists at the National Institutes of Health. Biologic age was determined by measuring DNA methylation, a chemical modification to DNA that is part of the normal aging process. The study showed for every five years a woman's biologic age was older than her chronologic or actual age, known as age acceleration, she had a 15 percent increase in her chance of developing breast cancer. The study was published online Feb. 22 in the Journal of the National Cancer Institute.
    https://medicalxpress.com/news/2019-...-elevated.html

    FEBRUARY 22, 2019
    Researchers report successful measurement of vitamin D in human hair

    A new study by researchers from Trinity College Dublin and St James's Hospital has reported for the first time that vitamin D can be measured in human hair. The paper has been published in the international, peer-reviewed journal of human nutrition, Nutrients.
    https://medicalxpress.com/news/2019-...uman-hair.html

    Smartphones help researchers better understand the nature of depression and anxiety

    Decades of research into anxiety and depression have resulted in the development of models that help explain the causes and dimensions of the two disorders.
    https://medicalxpress.com/news/2019-...n-anxiety.html

    ciekawe czy naukowcy/psychiatrzy wpadną na pomysł wysyłania notyfikacji pod tytułem:

    Hej, wydaje się, że jesteś tu za długo. Odłóż już telefon, jest 22, czas do spania.
    Jutro weekend, może rozważysz, spędzenie wolnego czasu na zewnątrz, może pograsz w kosza?
    może odwiedzić babcie, pojedziesz na pyszny obiad żeby porozmawiać o życiu i przemijaniu
    jak już pisałem ciało zaczyna wyostrzać się na inse, UV coraz wyższe, niebieskiego coraz więcej dzień coraz dłuższy.




    https://www.sciencedirect.com/scienc...16648017303507

    metabolizm się zmienia.

    Przy okazji jutro mamy piękny dzień i można robić witaminę D:

    Kidy i ile ?



    Developed with world authority on Vitamin D, Dr. Michael Holick.
    Michael F. Holick (born 1946) is an American adult endocrinologist, specializing in the field of vitamin D, such as the identification of both calcidiol, the major circulating form of vitamin D, and calcitriol, the active form of vitamin D. His work has been the basis for diagnostic tests and therapies for vitamin D-related diseases. He is a professor of medicine at the Boston University Medical Center and editor-in-chief of the journal Clinical Laboratory.
    https://en.wikipedia.org/wiki/Michael_F._Holick

    Ostatnio edytowane przez htw ; 22-02-19 o 19:11
    correlation doesn't imply causation

  7. #652
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    pisałem, że noc nie jest nudna:

    Dodano: 22 luty 2019r.
    Nauka przez sen jest możliwa? Naukowcy: śpiący mózg może kodować nowe informacje

    Naucz się nowego języka w czasie snu! – to może brzmieć jak kiepska reklama, jednak nowe badania dostarczają dowodów na to, że podczas snu także można się czegoś nauczyć. Oczywiście puszczanie sobie w trakcie snu nagrań w innym języku nie sprawi, że po kilku nocach będziemy go dokładnie znali. Może jednak zwiększyć naszą zdolności w przyswajaniu nowych słów – wynika z badań opublikowanych w „Current Biology”.

    Naukowcy od dawna wiedzieli, że sen odgrywa istotną rolę w procesie zapamiętywania i uczenia się. W jednej z faz snu nasze mózgi zajmują się porządkowaniem i konsolidowaniem informacji z minionego dnia. Rzeczy ważne są zapamiętywane, zaś nieistotne usuwane.

    Jak dotąd naukowcy uważali, że podczas snu nie możemy nauczyć się niczego nowego. Jednak badania naukowców z Uniwersytetu w Bernie w Szwajcarii pokazują, że zdolność mózgu do uczenia się jest aktywna także podczas snu.

    Wyniki badań zostały opublikowane na łamach pisma „Current Biology”.



    - Odkryliśmy, że śpiący mózg może kodować nowe informacje oraz zachowywać je na dłuższy czas – mówi Marc Zust, współautor badań. - Co więcej, śpiący mózg jest w stanie tworzyć nowe skojarzenia – dodaje.

    Badania polegały na tym, że osobom śpiącym, w fazie snu wolnofalowego, puszczano pary nagranych słów. Pierwsze było wymyślonym wyrazem nieistniejącego języka, drugie jego tłumaczeniem. Celem badania było odkrycie, czy nowoutworzone „pseudosłowa” będą się jakoś kojarzyć uczestnikom eksperymentu.

    Warto w tym miejscu dodać, że ludzie biorący udział w badaniu nie wiedzieli, że nocą odtwarzano im jakieś dźwięki. Po przebudzeniu uczestnikom prezentowano nieistniejące słowa, jednak tym razem bez ich tłumaczeń. Następnie proszono ich, by wyobrazili sobie obiekt, który to słowo miałoby reprezentować i określili, czy jest on większy, czy mniejszy od pudełka po butach. Dzięki temu naukowcy mieli nadzieję dotrzeć do podświadomości badanych.

    Badacze stwierdzili, że uczestnicy eksperymentu potrafili poprawnie klasyfikować obce słowa z dokładnością o 10 proc. wyższą, niż gdyby zgadywali. Rezultat ten sugeruje, że w czasie snu mózg może zapamiętywać.

    - Jeśli śpiącym ludziom przedstawimy słowo „bitkum”, a następnie połączymy je w parę ze słowem „ptak”, mózg może wytworzyć nowe połączenia, które powiążą kompletnie nowe słowo z już istniejącą koncepcją ptaka w naszym mózgu – mówi Zust. – Taki ślad w pamięci sprawia, że gdy po przebudzeniu usłyszysz słowo „bitkum” skojarzy ci się ono. Będziesz miał podświadome przeczucie dotyczące tego słowa, nawet jeśli będziesz pewny, że słyszysz je pierwszy raz w życiu - dodaje.

    Zapamiętywanie podczas snu wychodzi lepiej przy fazach większej aktywności mózgu. U części osób biorących udział w badaniu przeprowadzono funkcjonalne obrazowanie metodą rezonansu magnetycznego (fMRI) w trakcie snu. Gdy śpiącemu człowiekowi odtwarzano nowe słowa, w mózgu aktywowały się obszary odpowiedzialne za język oraz hipokamp – struktury w mózgu odpowiedzialnej głównie z pamięć i zdolność do uczenia się.

    - Oznacza to, że struktury odpowiadające za pamięć pozwalają na zapamiętywanie niezależnie od tego czy jesteśmy świadomi, czy śpimy – uważa Zust.

    Naukowcy mają nadzieję, ze dalsze badania pomogą osobom mającym trudności z nauką lub osobom starszym, z ograniczonymi zdolnościami poznawczymi. – To niesamowite, że jesteśmy zdolni do przeprowadzania tak wyrafinowanych operacji w mózgu nawet podczas snu – mówi Zust.
    https://dzienniknaukowy.pl/czlowiek/...owe-informacje

    Split and continuous sleep in teens impact cognition and glucose levels differently

    Many adolescent students sleep less than the recommended duration of 8-10 hours a night. It is unclear; however, whether short night sleep combined with an afternoon nap is as good as having the same amount of sleep continuously during the night without a nap. Researchers at Duke-NUS Medical School have demonstrated for the first time that different sleep schedules with the same total sleep opportunity over 24 hours may have dissimilar effects on cognition and glucose levels. This is the first study to gather experimental evidence on the notion that 'what may be appropriate sleep for one health goal may not be for another'.

    The handful of studies that examined split sleep schedules with normal total sleep duration in working-age adults found that both schedules yield comparable brain performance. However, no study has looked at the impact of such schedules on brain function and glucose levels together, especially when total sleep is shorter than optimal. The latter is important because of links between short sleep and risk for diabetes.

    The researchers measured cognitive performance and glucose levels following a standardized load in students, aged 15-19 years, during two simulated school weeks with short sleep on school days and recovery sleep on weekends. On school days, these students received either continuous sleep of 6.5 hours at night or split sleep (night sleep of 5 hours plus a 1.5-hour afternoon nap).

    "We undertook this study after students who were advised on good sleep habits asked if they could split up their sleep across the day and night, instead of having a main sleep period at night," said Prof. Michael Chee, Director of the Centre for Cognitive Neuroscience, Professor of Neuroscience and Behavioral Disorders Programme, Duke-NUS Medical School and one of the study's senior authors. "We found that compared to being able to sleep 9 hours a night, having only 6.5 hours to sleep in 24 hours degrades performance and mood. Interestingly, under conditions of sleep restriction, students in the split sleep group exhibited better alertness, vigilance, working memory and mood than their counterparts who slept 6.5 hours continuously. This finding is remarkable as the measured total sleep duration over 24 hours was actually less in the former group," Prof. Chee added.

    However, for glucose tolerance, the continuous schedule appeared to be better. "While 6.5 hours of night sleep did not affect glucose levels, the split sleep group demonstrated a greater increase in blood glucose levels to the standardized glucose load in both simulated school weeks," noted Dr. Joshua Gooley, Associate Professor of Neuroscience and Behavioral Disorders Programme, Principal Investigator at the Centre for Cognitive Neuroscience, Duke-NUS Medical School and the senior co-author of this study.

    Although further studies are necessary to see if this finding translates to a higher risk of diabetes later in life, the current findings indicate that beyond sleep duration, different sleep schedules can affect different facets of health and function in directions that are not immediately clear.

    Professor Patrick Casey, Senior Vice Dean of Research, Duke-NUS Medical School, commented, "Recent sleep surveys show that Singaporeans are among the world's most sleep deprived people. This is the latest in a series of studies from a team of researchers from the Neuroscience and Behavioural Disorders Programme and Centre for Cognitive Neuroscience that have provided valuable insights into the importance of good sleep."
    https://www.sciencedaily.com/release...0222101312.htm

    How diabetes causes muscle loss

    Diabetes mellitus is associated with various health problems including decline in skeletal muscle mass. A research group led by Professor Wataru Ogawa at the Kobe University Graduate School of Medicine revealed that elevation of blood sugar levels leads to muscle atrophy and that two proteins, WWP1 and KLF15, play key roles in this phenomenon. These findings were published on February 21 in the online edition of JCI Insight.


    Muscle mass decline associated with ageing impairs our physical activity, making us susceptible to a variety of health problems and thus leading to shortened lifespans. Age-dependent muscle mass decline and the consequent impairment of physical activity is known as "sarcopenia," a serious health burden in aging societies.

    We already knew that patients with diabetes mellitus are prone to muscle loss as they age, but an underlining mechanism for this phenomenon remains unclear. Diabetes mellitus is a disease caused by insufficient action of the hormone insulin. Insulin not only lowers blood sugar levels, but promotes the growth and proliferation of cells; insufficient action of insulin has been thought to result in the suppression of growth and proliferation of muscle cells, which in turn contribute to the decline in skeletal muscle mass.

    Professor Ogawa's research team made the surprising discovery that a rise in blood sugar levels triggers the decline in muscle mass, and uncovered the important roles of two proteins in this phenomenon. They found that the abundance of transcription factor KLF15 increased in skeletal muscle of diabetic mice, and mice that lack KLF15 specifically in muscle were resistant to diabetes-induced skeletal muscle mass decline. These results indicate that diabetes-induced muscle loss is attributable to increased amounts of KLF15.

    The team investigated the mechanism for how the abundance of KLF15 is increased in skeletal muscle of diabetic mice. They found that elevation of blood sugar levels slows down the degradation of KLF15 protein, which leads to an increased amount of this protein. Professor Ogawa's team also discovered that a protein called WWP1 plays a key role in regulating the degradation of KLF15 protein.

    WWP1 is a member of proteins called ubiquitin ligase. When a small protein called "ubiquitin" binds to other proteins, the degradation of the ubiquitin-bound proteins is accelerated. Under normal conditions, WWP1 promotes the degradation of KLF15 protein by binding ubiquitins to KLF15, keeping cellular KLF15 abundance low. When blood sugar levels rise, the amount of WWP1 decreases, which in turn decelerates the degradation of KLF15 and thus the increase in the cellular abundance of KLF15.

    This study uncovered for the first time that elevation of blood sugar levels triggers muscle mass decline, and that the two proteins WWP1 and KLF15 contribute to diabetes-induced muscle mass decline.

    As well as diabetes mellitus, other conditions such as physical inactivity or ageing result in muscle mass loss. The proteins KLF15 and WWP, which have been shown to contribute to diabetes-induced muscle mass loss, may also be related to other causes of muscle loss. Currently, no drug is available for the treatment of muscle loss. Professor Ogawa comments: "If we develop a drug that strengthens the function of WWP1 or weakens the function of KLF15, it would lead to a groundbreaking new treatment."
    https://www.sciencedaily.com/release...0222101309.htm
    correlation doesn't imply causation

  8. #653
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Frazzer, ja się pytam - gdzie jest kurwa FOTA ?


    Autophagy as a Therapeutic Target to Enhance Aged Muscle Regeneration.

    Skeletal muscle has remarkable regenerative capacity, relying on precise coordination between resident muscle stem cells (satellite cells) and the immune system. The age-related decline in skeletal muscle regenerative capacity contributes to the onset of sarcopenia, prolonged hospitalization, and loss of autonomy. Although several age-sensitive pathways have been identified, further investigation is needed to define targets of cellular dysfunction. Autophagy, a process of cellular catabolism, is emerging as a key regulator of muscle regeneration affecting stem cell, immune cell, and myofiber function. Muscle stem cell senescence is associated with a suppression of autophagy during key phases of the regenerative program. Macrophages, a key immune cell involved in muscle repair, also rely on autophagy to aid in tissue repair. This review will focus on the role of autophagy in various aspects of the regenerative program, including adult skeletal muscle stem cells, monocytes/macrophages, and corresponding age-associated dysfunction. Furthermore, we will highlight rejuvenation strategies that alter autophagy to improve muscle regenerative function.
    https://www.ncbi.nlm.nih.gov/pubmed/30791569


    Ultraviolet Irradiation of Skin Alters the Faecal Microbiome Independently of Vitamin D in Mice.

    Reduced sunlight exposure has been associated with an increased incidence of Crohn's disease and ulcerative colitis. The effect of ultraviolet radiation (UVR) on the faecal microbiome and susceptibility to colitis has not been explored. C57Bl/6 female mice were fed three different vitamin D-containing diets for 24 days before half of the mice in each group were UV-irradiated (1 kJ/m²) for each of four days, followed by twice-weekly irradiation of shaved dorsal skin for 35 days. Faecal DNA was extracted and high-throughput sequencing of the 16S RNA gene performed. UV irradiation of skin was associated with a significant change in the beta-diversity of faeces compared to nonirradiated mice, independently of vitamin D. Specifically, members of phylum Firmicutes, including Coprococcus, were enriched, whereas members of phylum Bacteroidetes, such as Bacteroidales, were depleted. Expression of colonic CYP27B1 increased by four-fold and IL1β decreased by five-fold, suggesting a UVR-induced anti-inflammatory effect. UV-irradiated mice, however, were not protected against colitis induced by dextran sodium sulfate (DSS), although distinct faecal microbiome differences were documented post-DSS between UV-irradiated and nonirradiated mice. Thus, skin exposure to UVR alters the faecal microbiome, and further investigations to explore the implications of this in health and disease are warranted.
    https://www.ncbi.nlm.nih.gov/pubmed/...WSy_aga_BL7hmQ

    Close social relationships correlate with human gut microbiota composition

    Social relationships shape human health and mortality via behavioral, psychosocial, and physiological mechanisms, including inflammatory and immune responses. Though not tested in human studies, recent primate studies indicate that the gut microbiome may also be a biological mechanism linking relationships to health. Integrating microbiota data into the 60-year-old Wisconsin Longitudinal Study, we found that socialness with family and friends is associated with differences in the human fecal microbiota. Analysis of spouse (N = 94) and sibling pairs (N = 83) further revealed that spouses have more similar microbiota and more bacterial taxa in common than siblings, with no observed differences between sibling and unrelated pairs. These differences held even after accounting for dietary factors. The differences between unrelated individuals and married couples was driven entirely by couples who reported close relationships; there were no differences in similarity between couples reporting somewhat close relationships and unrelated individuals. Moreover, married individuals harbor microbial communities of greater diversity and richness relative to those living alone, with the greatest diversity among couples reporting close relationships, which is notable given decades of research documenting the health benefits of marriage. These results suggest that human interactions, especially sustained, close marital relationships, influence the gut microbiota.
    https://www.nature.com/articles/s415...dR8pAr9_RUDPXE

    nieźle pokazane:

    correlation doesn't imply causation

  9. #654
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Review: The role of zinc in the endocrine system.

    Zinc is essential in the regulation of a variety of physiological and biochemical events in the organism. It plays a critical role in maintaining the cell membrane integrity, protein-carbohydrate-lipid metabolism, immune system, wound injury and in the regulation of a number of other biological processes associated with normal growth and development. Physiological and biochemical levels of many hormones are affected by zinc metabolism. Therefore, growth impairment, hypogonadism, and some endocrine diseases are associated with the deficiency of zinc. These effects of zinc are considered versatile. Zinc increases the synthesis of the growth hormone and its number of receptors; thus, it is an important mediator in the binding of this hormone to its receptor. Found in a large quantity in the pancreas tissue, zinc has a part in the regulation of the effect of insulin. Zinc is involved to much more thyroid hormone metabolism such as hormone synthesis, receptor activity, conversion of T4 to T3, and production of carrier proteins. The low levels of zinc and high levels of leptin in obese individuals point to a critical relationship between zinc and leptin. Zinc is related to enzyme activity to melatonin synthesis. Melatonin has regulatory activity for zinc absorption from gastrointestinal system. Zinc particularly affects the conversion of testosterone to dihydrotestosterone, as 5α-reductase that is involved in this conversion is a zinc-dependent enzyme. In consideration of these relations, zinc is accepted to play critical roles in the endocrine system. The aim of the current review is to draw attention to the effects of zinc on the endocrine system.
    https://www.ncbi.nlm.nih.gov/pubmed/30772815


    Bright light therapy for depression in Parkinson disease: A randomized controlled trial.

    METHODS:
    In this double-blind controlled trial, we randomized patients with PD and MDD to treatment with BLT (±10,000 lux) or a control light (±200 lux). Participants were treated for 3 months, followed by a 6-month naturalistic follow-up. The primary outcome of the study was the Hamilton Depression Rating Scale (HDRS) score. Secondary outcomes were objective and subjective sleep measures and salivary melatonin and cortisol concentrations. Assessments were repeated halfway, at the end of treatment, and 1, 3, and 6 months after treatment. Data were analyzed with a linear mixed-model analysis.

    RESULTS:
    We enrolled 83 participants. HDRS scores decreased in both groups without a significant between-group difference at the end of treatment. Subjective sleep quality improved in both groups, with a larger improvement in the BLT group (B [SE] = 0.32 [0.16], p = 0.04). Total salivary cortisol secretion decreased in the BLT group, while it increased in the control group (B [SE] = -8.11 [3.93], p = 0.04).

    CONCLUSION:
    BLT was not more effective in reducing depressive symptoms than a control light. Mood and subjective sleep improved in both groups. BLT was more effective in improving subjective sleep quality than control light, possibly through a BLT-induced decrease in cortisol levels.
    https://www.ncbi.nlm.nih.gov/pubmed/30770426

    Gut microbiota requires vagus nerve integrity to promote depression

    Chronic stress constitutes one of the strongest risk factors for depression and can disrupt various aspects of homeostasis, including gut microbiota composition. We found that stress-induced changes in gut microbiota promote depression and decrease adult hippocampal neurogenesis upon transfer to antibiotic-treated recipient mice. Subdiaphragmatic vagotomy abrogated the microbiota-induced effects on behavior and neurogenesis, suggesting that gut microbiota can influence brain plasticity and behavior through vagal afferents.

    Effects of Light Therapy on Mood and Insulin Sensitivity in Patients With Type 2 Diabetes and Depression: Results From a Randomized Placebo-Controlled Trial

    OBJECTIVE Depression is common in patients with type 2 diabetes, and adversely affects quality of life and diabetes outcomes. We assessed whether light therapy, an antidepressant, improves mood and insulin sensitivity in patients with depression and type 2 diabetes.

    RESEARCH DESIGN AND METHODS This randomized, double-blind, placebo-controlled trial included 83 patients with depression and type 2 diabetes. The intervention comprised 4 weeks of light therapy (10,000 lux) or placebo light therapy daily at home. Primary outcomes included depressive symptoms (Inventory of Depressive Symptomatology [IDS]) and insulin sensitivity (M-value derived from the results of a hyperinsulinemic-euglycemic clamp). Secondary outcomes were related psychological and glucometabolic measures.

    RESULTS Intention-to-treat analysis showed that light therapy was not superior to placebo in reducing depressive symptoms (−3.9 IDS points [95% CI −9.0 to 1.2]; P = 0.248) and had no effect on insulin sensitivity (0.15 mg/kg*min [95% CI −0.41 to 0.70]; P = 0.608). Analyses incorporating only those participants who accurately adhered to the light therapy protocol (n = 51) provided similar results, but did suggest positive effects of light therapy on depression response rates (≥50% reduction in IDS points) (26% more response; P = 0.031). Prespecified analysis showed effect moderation by baseline insulin sensitivity (P = 0.009) and use of glucose-lowering medication (P = 0.023). Light therapy did not affect depressive symptoms in participants with higher insulin sensitivity or those who use only oral glucose lowering medication or none at all, but it did produce a relevant effect in participants with lower insulin sensitivity (−12.9 IDS points [95% CI −21.6 to −4.2]; P = 0.017) and a trend toward effectiveness in those using insulin (−12.2 IDS points [95% CI −21.3 to −3.1]; P = 0.094). Light therapy was well tolerated.

    CONCLUSIONS Although this trial is essentially inconclusive, secondary analyses indicate that light therapy might be a promising treatment for depression among a subgroup of highly insulin-resistant individuals with type 2 diabetes.
    http://care.diabetesjournals.org/con...lR_jsfBbmnfoIk

    aktywność jest ogromnym zegarem z ogromnym potencjałem ! GRUBO

    Two years supervised resistance training prevented diabetes incidence in people with prediabetes: a randomized control trial


    Aim
    To explore the long‐term effects of aerobic training (AT), resistance training (RT) and combined training (AT+RT) on the prevention of T2D incidence in patients with prediabetes.

    Materials and methods
    In this randomized controlled trial, people with prediabetes (fasting glucose ≥5.6 mmol/L and <7.0 mmol/L and/or 2‐hour glucose ≥7.8 mmol/L and <11.1 mmol/L on the 75‐g oral glucose‐tolerance test and/or haemoglobin A1c ≥5.7% and <6.4%) were randomly assigned to the control group, AT group, RT group or AT+RT group. Supervised exercise programmes, including AT, RT and AT+RT, were completed for 60 minutes per day, three non‐consecutive days per week for 24 months. The primary outcome was the incidence of T2D; secondary outcomes were blood glucose and lipid levels, for example, total cholesterol (TC) and standard 2‐hour oral glucose tolerance (2hPG).

    Results
    A total of 137 (80%) subjects with a mean age of 59 years (45 men, 92 women) entered the final analysis. After 24 months of intervention, the incidences of T2D adjusted by sex and age were significantly decreased by 74% (95% CI 38‐89%), 65% (95% CI 21‐85%) and 72% (95% CI 36‐87%) in the AT+RT, RT and AT groups compared with the control group (HR: AT+RT 0.26(95% CI 0.11−0.62), RT 0.35(0.15‐0.79) and AT 0.28(95% CI 0.13‐0.64)). The cumulative T2D incidences were significantly lower in the AT+RT, RT, and AT groups than in the control group (21%, 26% and 22% VS 69%). The blood glucose and lipid profiles improved more in the AT, RT and AT+RT groups than in the control group.

    Conclusion
    RT and RT plus AT were as effective as isolated AT in preventing progression to T2D.

    dla przypomnienia:

    Clock + Bmal1 działają na zmianę (współpracują) z Per + Cry (cryptochrome). Clock i Bmal podnosi się w ciągu dnia (podczas łączenia w parę) i po osiągnięciu odpowiedniego pułapu (objętości) zaczyna się wygaszanie. Wygaszanie powoduje ekspresję (aktywowanie) kolejnego białka nazwanego Per (periodyczny) - tym razem nocny Per aktywuje odpowiednie nocne instrukcje komórki(np naprawdę DNA, regeneracja itd).



    +



    teraz z samego serca

    Circadian rhythms and the molecular clock in cardiovascular biology and disease

    Key points
    Molecular clocks are found in all cardiovascular cell types.

    Various cardiovascular functions, including endothelial function, thrombus formation, blood pressure and heart rate, are regulated by the circadian clock.

    Disruption of 24-h rhythms leads to cardiovascular disease, including heart failure, myocardial infarction and arrhythmias.

    24-h rhythms are present in the development, risk factors, incidence and outcome of cardiovascular disease.

    Cardiovascular disease leads to disrupted circadian rhythm and sleep problems.
    The Earth turns on its axis every 24 h; almost all life on the planet has a mechanism — circadian rhythmicity — to anticipate the daily changes caused by this rotation. The molecular clocks that control circadian rhythms are being revealed as important regulators of physiology and disease. In humans, circadian rhythms have been studied extensively in the cardiovascular system. Many cardiovascular functions, such as endothelial function, thrombus formation, blood pressure and heart rate, are now known to be regulated by the circadian clock. Additionally, the onset of acute myocardial infarction, stroke, arrhythmias and other adverse cardiovascular events show circadian rhythmicity. In this Review, we summarize the role of the circadian clock in all major cardiovascular cell types and organs. Second, we discuss the role of circadian rhythms in cardiovascular physiology and disease. Finally, we postulate how circadian rhythms can serve as a therapeutic target by exploiting or altering molecular time to improve existing therapies and develop novel ones.


    https://www.nature.com/articles/s41569-019-0167-4


    było juz ale znowu, komórki tłuszczowe mają swój zegar:

    Fat cells work different 'shifts' throughout the day

    Fat cells in the human body have their own internal clocks and exhibit circadian rhythms affecting critical metabolic functions, new research in the journal Scientific Reports, finds.

    Researchers led by Dr. Jonathan Johnston from the University of Surrey conducted the first ever analysis of circadian rhythms in human fat taken from people isolated from daily environmental changes. Circadian rhythms are approximately 24-hour changes governed by the body's internal clocks. Misalignment of 'human clocks' with each other and the environment is believed to be a major contributor to obesity and poor health.

    During this unique study seven participants underwent regulated sleep-wake cycles and meal times before entering the laboratory, where they maintained this routine for a further three days.

    Participants then experienced a 37- hour 'constant routine' during which time they did not experience daily changes in light-dark, feed-fast and sleep-wake cycles. Biopsies of fat tissue were taken at six hourly intervals and then followed by an analysis of gene expression.

    Researchers identified 727 genes in the fat tissue that express their own circadian rhythm, many carrying out key metabolic functions. A clear separation in gene rhythms was identified with approximately a third peaking in the morning and two thirds in the evening.

    Morning-peaking transcripts were associated with regulation of gene expression and nucleic acid biology (vital for cell functioning), while evening-peaking transcripts associated with redox activity and organic acid metabolism.


    These rhythms, which are independent of external factors such as light and feeding, demonstrate that genes within fat cells naturally complete their functions at different times during the day which could impact on metabolic processes.

    Fat cells play an important role in our body, acting as energy stores and controlling metabolism and appetite via hormone secretion.

    Lead author Dr. Jonathan Johnston, Reader in Chronobiology and Integrative Physiology, at the University of Surrey, said: "Tissues made up of fat cells don't just store excess energy, they are active metabolic tissues, full of their own rhythms.

    "This is the first time that we have been able to identify such rhythms in human fat. This provides us with more information about how human metabolism changes across the day and possibly why the body processes foods differently during day and night."
    Conclusions
    Molecular analysis of serial adipose tissue biopsies, taken under highly controlled conditions and coupled with in-depth bioinformatic analysis, has revealed the importance of circadian biology on a key human metabolic tissue. The most common rhythmic processes in human subcutaneous white adipose are those linked to fatty acid metabolism. However, rhythmicity was also observed in other fundamental cell processes, e.g. transcription and translation, nucleic acid metabolism and the citric acid cycle. The circadian timing system thus has an intimate relationship with many core aspects of human physiology and pathways relevant to therapeutics.
    https://www.nature.com/articles/s41598-019-39668-3

    https://medicalxpress.com/news/2019-...VR_iONfJ8vlrd4


    We've long known there's a link between insomnia and chronic disease. Now our findings suggest that depression and heart disease are actually a result of persistent insomnia."
    Insomnia-associated gene regions suggest underlying mechanisms, treatment targets
    https://medicalxpress.com/news/2019-...98-019-39668-3
    correlation doesn't imply causation

  10. #655
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    FEBRUARY 25, 2019
    Being surrounded by green space in childhood may improve mental health of adults



    Children who grow up with greener surroundings have up to 55% less risk of developing various mental disorders later in life. This is shown by a new study from Aarhus University, Denmark, emphasizing the need for designing green and healthy cities for the future.

    A larger and larger share of the world's population now lives in cities and WHO estimates that more than 450 million of the global human population suffer from a mental disorder, a number that is expected to increase.

    Now, based on satellite data from 1985 to 2013, researchers from Aarhus University have mapped the presence of green space around the childhood homes of almost one million Danes and compared this data with the risk of developing one of 16 different mental disorders later in life.

    The study, which is published today in the prestigious American Journal PNAS, shows that children surrounded by the high amounts of green space in childhood have up to a 55% lower risk of developing a mental disorder—even after adjusting for other known risk factors such as socio-economic status, urbanization, and the family history of mental disorders.

    The entire childhood must be green

    Postdoc Kristine Engemann from Department of Bioscience and the National Centre for Register-based Research at Aarhus University, who spearheaded the study, says: "Our data is unique. We have had the opportunity to use a massive amount of data from Danish registers of, among other things, residential location and disease diagnoses and compare it with satellite images revealing the extent of green space surrounding each individual when growing up."

    Researchers know that, for example, noise, air pollution, infections and poor socio-economic conditions increase the risk of developing a mental disorder. Conversely, other studies have shown that more green space in the local area creates greater social cohesion and increases people's physical activity level and that it can improve children's cognitive development. These are all factors that may have an impact on people's mental health.

    "With our dataset, we show that the risk of developing a mental disorder decreases incrementally the longer you have been surrounded by green space from birth and up to the age of 10. Green space throughout childhood is therefore extremely important," Kristine Engemann explains.

    Green and healthy cities

    As the researchers adjusted for other known risk factors of developing a mental disorder, they see their findings as a robust indication of a close relationship between green space, urban life, and mental disorders.

    Kristine Engemann says: "There is increasing evidence that the natural environment plays a larger role for mental health than previously thought. Our study is important in giving us a better understanding of its importance across the broader population."

    This knowledge has important implications for sustainable urban planning. Not least because a larger and larger proportion of the world's population lives in cities.

    "The coupling between mental health and access to green space in your local area is something that should be considered even more in urban planning to ensure greener and healthier cities and improve mental health of urban residents in the future," adds co-author Professor Jens-Christian Svenning from the Department of Bioscience, Aarhus University.
    Kontakt wzrokowy przygotowuje mózg do konktaktów społecznych

    Kontakt wzrokowy między dwiema osobami symultanicznie aktywuje te same obszary mózgu. Zjawisko to stanowi podstawę skutecznej interakcji społecznej.

    Norihiro Sadato z Narodowego Instytutu Nauk Psychologicznych badał pary dorosłych osób. Ochotników badano za pomocą hiperskanowania funkcjonalnym rezonansem magnetycznym. W każdym skanerze umieszczano kamerę i wyświetlacz. Aktywność mózgu monitorowano w 2 sytuacjach: 1) przy relacji on-line na żywo i 2) w warunkach przekazywania obrazu z 20-s opóźnieniem.

    Okazało się, że w 1. scenariuszu obserwowano wzajemny wpływ na mruganie, a także podwyższoną aktywację móżdżku i wzmożoną łączność w obrębie limbicznego układu lustrzanego.

    Autorzy artykułu z pisma eNeuro uważają, że kontakt wzrokowy w czasie rzeczywistym przygotowuje mózg do dzielenia stanów mentalnych z innymi.


    wstajesz do budzika? w zasadzie spierdoliłeś już przed wstaniem z łózka

    2019 Feb 26
    Timing modulates the effect of sleep loss on glucose homeostasis.

    CONTEXT:
    Chronobiological factors may modulate the impact of sleep loss on glucose homeostasis. However, these interactions have not been systematically assessed in humans.

    OBJECTIVE:
    To assess effect of sleep loss during the late vs. early night on glucose homeostasis.

    DESIGN:
    Fifteen normal-weight men participated in three conditions of a randomized, balanced cross-over study comprising two conditions with shortened sleep (4 h of sleep during the first or the second night-half, respectively) and a control condition with 8 h of sleep. Glucose, insulin, cortisol, and glucagon were measured. Insulin sensitivity and secretion were assessed by a botnia clamp.

    RESULTS:
    Sleep loss compared to regular sleep duration reduced insulin sensitivity (M-Value; P=0.031) irrespective of early- or late-night timing (p=0.691). The Disposition Index, i.e., the ß-cell response adjusted for insulin sensitivity, also tended to be impaired by short sleep (p=0.056), but not by sleep timing (p=0.543). In contrast, sleep loss in the second, but not the first night-half induced reductions in morning glucagon and cortisol (p<0.031) followed by a transient increase in cortisol (p<0.044).

    CONCLUSIONS:
    While sleep deprivation acutely reduces insulin sensitivity irrespective of its nocturnal timing, sleep loss in the early morning compromises α-cell and HPA axis activity to a greater extent than sleep loss in the first night-half. This pattern suggests that the timing of sleep restriction can partly potentiate its deleterious metabolic effects.
    https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract


    Okazuje się, tylko ~ 40% z kontrolowanych przez zegar genów są rytmiczne zarówno dla mężczyzn i kobiety. Jesteśmy różni również w odmierzaniu czasu:

    We found 90 (43%) rhythmic genes in both male and female flies (Figure 4A and Supplemental Table S8), which were enriched in genes involved in circadian rhythms, metabolism, signaling transmission, and light response (Supplemental Figure S6A and Supplemental Table S9).
    https://journals.sagepub.com/eprint/...ShareContainer

    Changes in Redox Signaling in the Skeletal Muscle with Aging.

    Abstract
    Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy.
    https://www.ncbi.nlm.nih.gov/m/pubme...20regeneration


    February 25, 2019
    Working long hours linked to depression in women

    The study of over 20,000 adults, published today in the BMJ's Journal of Epidemiology & Community Health, found that after taking age, income, health and job characteristics into account, women who worked extra-long hours had 7.3% more depressive symptoms than women working a standard 35-40 week. Weekend working was linked to a higher risk of depression among both sexes.
    https://www.sciencedaily.com/release...0225192140.htm
    Ostatnio edytowane przez htw ; 27-02-19 o 15:29
    correlation doesn't imply causation

  11. #656
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    nie spłacisz długu, odsypiając w weekend:

    FEBRUARY 28, 2019
    Sleeping in on the weekend won't repay your sleep debt



    Think sleeping in on the weekend can repair the damage from a week of sleepless nights?

    Not so, according to University of Colorado Boulder research published today in Current Biology.


    In fact, on some health measures, trying to play catch-up for a few days and then returning to poor sleep habits makes things worse.

    "Our findings suggest that the common behavior of burning the candle during the week and trying to make up for it on the weekend is not an effective health strategy," said senior author Kenneth Wright, director of the Sleep and Chronobiology Lab.

    Previous research has shown that insufficient sleep can boost risk of obesity and diabetes, in part by boosting the urge to snack at night and decreasing insulin sensitivity—or the ability to regulate blood sugar. Some adverse health impacts kick in after just one night of lost sleep, recent CU Boulder research has shown.

    Sleeping in on the weekend can help the body recover mildly during those two days, studies suggest. But the effects don't last.

    Wright and lead author Chris Depner, an assistant research professor of Integrative Physiology, wanted to determine what happens when people cycle back and forth between a sleep-deprived work week and a few days of catch-up.

    They enlisted 36 healthy adults age 18 to 39 to stay for two weeks in a laboratory, where their food intake, light exposure and sleep were monitored.

    After baseline testing, the volunteers were divided into groups. One was allowed plenty of time to sleep—9 hours each night for 9 nights. The second was allowed 5 hours per night over that same period. The third slept no more than 5 hours nightly for 5 days followed by a weekend when they could sleep as much as they liked before returning to 2 days of restricted sleep.

    Both sleep-restricted groups snacked more at night, gained weight and saw declines in insulin sensitivity during the study period. While those in the weekend recovery group saw mild improvements (including reduced nighttime snacking) during the weekend, those benefits went away when the sleep-restricted work week resumed.

    "In the end, we didn't see any benefit in any metabolic outcome in the people who got to sleep in on the weekend," said Depner.

    On some measures, the weekend recovery group showed worse outcomes. For instance, in the group which had their sleep restricted the whole time, whole body insulin sensitivity declined by 13 percent. In the weekend recovery group it worsened by 9 to 27 percent, with sensitivity in the muscles and liver scoring worse than the other groups.

    "It could be that the yo-yoing back and forth—changing the time we eat, changing our circadian clock and then going back to insufficient sleep is uniquely disruptive," said Wright.

    Even when given the chance, people found it difficult to recover lost sleep. While they gained some ground Friday and Saturday, their body clocks shifted later Sunday night making it hard to fall asleep even though they had to get up early Monday.

    In the end, the recovery group got just 66 minutes more sleep on average. Men made up more lost sleep than women.

    Wright says it's possible that weekend recovery sleep could be an effective health countermeasure for people who get too little sleep a night or two per week. They hope to explore this in future studies.

    For now, the takeaway is this: Consistency matters.

    "This study demonstrates the importance of getting sufficient sleep on a regular schedule," said Michael Twery, Ph.D., director of the National Center on Sleep Disorders Research (NCSDR) at the National Heart, Lung, and Blood Institute, part of the National Institutes of Health. "Frequently changing sleep schedules is a form of stress associated with metabolic abnormalities."

    So try to get 7 hours of sleep as many nights as possible.
    https://medicalxpress.com/news/2019-...epay-debt.html

    February 27, 2019
    Not all sleep is equal when it comes to cleaning the brain

    New research shows how the depth of sleep can impact our brain's ability to efficiently wash away waste and toxic proteins. Because sleep often becomes increasingly lighter and more disrupted as we become older, the study reinforces and potentially explains the links between aging, sleep deprivation, and heightened risk for Alzheimer's disease.

    "Sleep is critical to the function of the brain's waste removal system and this study shows that the deeper the sleep the better," said Maiken Nedergaard, M.D., D.M.Sc., co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center (URMC) and lead author of the study. "These findings also add to the increasingly clear evidence that quality of sleep or sleep deprivation can predict the onset of Alzheimer's and dementia."

    The study, which appears in the journal Science Advances, indicates that the slow and steady brain and cardiopulmonary activity associated with deep non-REM sleep are optimal for the function of the glymphatic system, the brain's unique process of removing waste. The findings may also explain why some forms of anesthesia can lead to cognitive impairment in older adults.

    The previously unknown glymphatic system was first described by Nedergaard and her colleagues in 2012. Prior to that point, scientists did not fully understand how the brain, which maintains its own closed ecosystem, removed waste. The study revealed a system of plumbing which piggybacks on blood vessels and pumps cerebral spinal fluid (CSF) through brain tissue to wash away waste. A subsequent study showed that this system primarily works while we sleep.

    Because the accumulation of toxic proteins such as beta amyloid and tau in the brain are associated with Alzheimer's disease, researchers have speculated that impairment of the glymphatic system due to disrupted sleep could be a driver of the disease. This squares with clinical observations which show an association between sleep deprivation and heightened risk for Alzheimer's.

    In the current study, researchers conducted experiments with mice that were anesthetized with six different anesthetic regimens. While the animals were under anesthesia, the researchers tracked brain electrical activity, cardiovascular activity, and the cleansing flow of CSF through the brain. The team observed that a combination of the drugs ketamine and xylazine (K/X) most closely replicated the slow and steady electrical activity in the brain and slow heart rate associated with deep non-REM sleep. Furthermore, the electrical activity in the brains of mice administered K/X appeared to be optimal for function of the glymphatic system.

    "The synchronized waves of neural activity during deep slow-wave sleep, specifically firing patterns that move from front of the brain to the back, coincide with what we know about the flow of CSF in the glymphatic system," said Lauren Hablitz, Ph.D., a postdoctoral associate in Nedergaard's lab and first author of the study. "It appears that the chemicals involved in the firing of neurons, namely ions, drive a process of osmosis which helps pull the fluid through brain tissue."

    The study raises several important clinical questions. It further bolsters the link between sleep, aging, and Alzheimer's disease. It is known that as we age it becomes more difficult to consistently achieve deep non-REM sleep, and the study reinforces the importance of deep sleep to the proper function of the glymphatic system. The study also demonstrates that the glymphatic system can be manipulated by enhancing sleep, a finding that may point to potential clinical approaches, such as sleep therapy or other methods to boost the quality of sleep, for at-risk populations.

    Furthermore, because several of the compounds used in the study were analogous to anesthetics used in clinical settings, the study also sheds light on the cognitive difficulties that older patients often experience after surgery and suggests classes of drugs that could be used to avoid this phenomenon. Mice in the study that were exposed to anesthetics that did not induce slow brain activity saw diminished glymphatic activity.

    "Cognitive impairment after anesthesia and surgery is a major problem," said Tuomas Lilius, M.D., Ph.D., with the Center for Translational Neuromedicine at the University of Copenhagen in Denmark and co-author of the study. "A significant percentage of elderly patients that undergo surgery experience a postoperative period of delirium or have a new or worsened cognitive impairment at discharge."
    https://www.sciencedaily.com/release...0227173111.htm

    Co się dzieje po usunięciu hipokampu?


    sposobów na upośledzanie jest sporo:

    Smoking and alcohol: Double trouble for the brain?

    Along with many other harmful health consequences, smoking tobacco causes chemical changes, oxidative stress and inflammation in the brain. Excessive alcohol use can have similar effects. Surprisingly, however, very few studies have examined the combined impact of smoking and alcohol on the brain. Now, researchers reporting in ACS Chemical Neuroscience have shown that in rats, the joint use of tobacco and alcohol could increase neural damage in particular brain regions.

    According to the National Institute on Alcohol Abuse and Alcoholism, many people who smoke tobacco also drink alcohol excessively, and vice versa. Therefore, studying the combined effects of the two drugs on the central nervous system could yield valuable insights. But most previous studies have examined the consequences of one or the other in isolation. That's why Alana Hansen and colleagues wanted to find out how drinking and smoking together affect regions of the rat brain involved in drug addiction.

    The researchers treated rats with alcohol, tobacco smoke or both twice a day for 28 days and then compared their brains with control animals that didn't receive either substance. They found that the combined alcohol and smoking treatment increased the level of reactive oxygen species in the hippocampus compared with control animals or rats given tobacco smoke alone. In all of the brain areas studied, combined alcohol and smoking increased the levels of specific pro-inflammatory cytokines more than either treatment alone. And in the striatum and frontal cortex, rats with both treatments showed lower levels of brain-derived neurotrophic factor, a growth factor that helps existing neurons survive and stimulates the growth of new ones. These results suggest that alcoholics who smoke could be at additional risk for neural damage, the researchers say.
    https://www.sciencedaily.com/release...0227140020.htm

    ale nie trzeba palić i pić jednocześnie można np. olewać spanie:

    Nocturnal mnemonics: sleep and hippocampal memory processing
    https://www.frontiersin.org/articles...012.00059/full

    28 February 2019
    Transcriptional Basis for Rhythmic Control of Hunger and Metabolism within the AgRP Neuron

    Highlights
    •The hypothalamic clock network aligns hunger and metabolism with sleep and wakefulness

    •The AgRP neuron clock remodels transcription in response to energy state

    •AgRP RiboTag profiling uncovers post-transcriptional control of bioenergetics

    •The transcriptional response to leptin requires an intact molecular clock


    The alignment of fasting and feeding with the sleep/wake cycle is coordinated by hypothalamic neurons, though the underlying molecular programs remain incompletely understood. Here, we demonstrate that the clock transcription pathway maximizes eating during wakefulness and glucose production during sleep through autonomous circadian regulation of NPY/AgRP neurons. Tandem profiling of whole-cell and ribosome-bound mRNAs in morning and evening under dynamic fasting and fed conditions identified temporal control of activity-dependent gene repertoires in AgRP neurons central to synaptogenesis, bioenergetics, and neurotransmitter and peptidergic signaling. Synaptic and circadian pathways were specific to whole-cell RNA analyses, while bioenergetic pathways were selectively enriched in the ribosome-bound transcriptome. Finally, we demonstrate that the AgRP clock mediates the transcriptional response to leptin. Our results reveal that time-of-day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and food acquisition with the sleep/wake state.
    https://www.sciencedirect.com/scienc...300634#undfig1

    a na dole:
    Atomic models of the Bacillus PS3 ATP synthase in three rotational states.

    o kurwa piękne

    https://static-movie-usa.glencoesoft...128-video1.mp4

    i statycznie:



    (tak tak własnie dlatego kupujemy magnez)
    https://www.sciencedirect.com/scienc...50413119300634
    correlation doesn't imply causation

  12. #657
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Matthew Walker, Ph.D., is a professor of neuroscience and psychology at the University of California, Berkeley, and serves as the Director of the Center for Human Sleep Science. Formerly, Dr. Walker served as a professor of psychiatry at the Harvard Medical School.

    Walker's research examines the impact of sleep on human health and disease. One area of interest focuses on identifying "vulnerability windows" during a person's life that make them more susceptible to amyloid-beta deposition from loss of slow wave sleep and, subsequently, Alzheimer's disease later in life.

    Dr. Walker earned his undergraduate degree in neuroscience from the University of Nottingham, UK, and his Ph.D. in neurophysiology from the Medical Research Council, London, UK. He is the author of the New York Times best-selling book Why We Sleep: Unlocking the Power of Sleep and Dreams.


    co się dzieje z fotonami po zachodzi słońca jest kluczowe:

    27 February 2019
    Down‐regulation of AKT and MDM2, Melatonin induces apoptosis in AGS and MGC803 cells

    Melatonin, a neurohormone secreted by the pineal gland, has a variety of biological functions, such as circadian rhythms regulation, anti-oxidative activity, immunomodulatory effects, and anit-tumor etc.. At present, its anti-tumor effect has attracted people's attention due to its extensive tissue distribution, good tissue compatibility, and low toxic and side effects. In the gastrointestinal tract, there is high level of melatonin and many studies showed melatonin has effects of anti-gastric cancer. In this experiment, human gastric cancer cell lines AGS and MGC803 were used to investigate the intracellular molecular mechanism of melatonin against gastric cancer. After AGS and MGC803 have been treated with melatonin, the changes of cell morphology and cellular structure were observed under electron microscope. Flow cytometer and apoptosis detection kits were used to analyze the effect of apoptosis on AGS and MGC803. The alterations of apoptosis-related proteins Caspase 9, Caspase 3 and up-stream regulators AKT, MDM2 including expression, phosphorylation and activation were detected to analyze the intracellular molecular mechanism of melatonin inhibiting gastric cancer. In AGS and MGC803 cells with melatonin exposure, cleaved Caspase 9 was up-regulated and Caspase 3 was activated, moreover, MDM2 and AKT expression and phosphorylation were down-regulated. Melatonin promoted apoptosis of AGS and MGC803 cells by the down-regulation of AKT and MDM2. This article is protected by copyright. All rights reserved.
    +

    dane które znamy:



    The multiple means that have been proposed by which melatonin may interfere with the growth of experimental tumors are listed. The blue boxes identify the process that are impacted by melatonin while the green boxes list the potential mechanisms involved. The information in red mentions the synergistic actions of melatonin with radio- or chemotherapies (left) and on the right it is noted that some cancers resistant to therapy can be made sensitive by treatment with melatonin.


    This figure illustrates the likely role of melatonin in influencing L1 expression and DNA damage. During the day (left) which circulating melatonin levels are at their nadir, L1 mRNA causes L1-mediated DNA damage. At night in darkness (center), the elevation of melatonin in the blood acts on the MT1 melatonin receptor to suppress L1 mRNA and ORF1 (open reading frame) protein. By this means, melatonin reduces L1-associated genomic stability thereby reducing the risk of cancer. Contaminating the night with light reduces melatonin levels leading to high L1 mRNA and protein expression causing L1-mediated DNA damage (right).
    Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412427/

    i to wszystko ZA DARMO ! bez większego wysiłku.

    ciekawe badanie:

    Insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift

    Conclusion
    The part played by Jerry Reaven in linking the dots between the various components of the MetS and the relevance of MetS to ASCVD, NAFLD, PCOS and T2D has been enormously important. The search for the unifying mechanism has been contentious. Here, we make a case for putting ‘insulin hypersecretion’ into this role, while considering insulin resistance as a protective downstream response. This necessitates a complete revision of the conceptual framework within which we view insulin resistance and the pathophysiology of the MetS and obesity-associated T2D, which if confirmed, has major implications for the prevention and management of these metabolic conditions.
    https://journals.sagepub.com/doi/ful...r_pub%3Dpubmed

    Ostatnio edytowane przez htw ; 01-03-19 o 17:54
    correlation doesn't imply causation

  13. #658
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    nudne kości:

    było ale dla przypomnienia:

    How broken sleep promotes cardiovascular disease



    Figure 1 | Sleep fragmentation accelerates atherosclerosis. McAlpine et al.3 induced long-term sleep fragmentation in mice by moving a bar across the bottom of their cages during their sleep period. Such treatment reduces the levels of the protein hypocretin, which is produced in the brain’s hypothalamus. Hypocretin receptors are present on cells in the bone marrow (pre-neutrophils) that will develop into a type of white blood cell called a neutrophil. Pre-neutrophils sense the lack of hypocretin and produce increased amounts of a protein known as colony-stimulating factor-1 (CSF-1). Uninhibited CSF-1 production stimulates stem cells that give rise to all types of white blood cell (haematopoietic stem cells; HSCs) to produce increased numbers of pre-neutrophils and pre-monocytes (white blood cells that will develop into monocytes). Mature neutrophils and monocytes migrate to arterial walls, where the monocytes develop into macrophage cells. Macrophages and, to a lesser extent, neutrophils promote the formation of plaques, a hallmark of atherosclerosis — a condition that can have harmful cardiovascular effects.
    https://www.nature.com/articles/d41586-019-00393-6

    Przeszczep szpiku kostnego chroni i odmładza mózgi myszy

    Ustalenia naukowców wydają się potwierdzać model, który przynajmniej częściowo przypisuje spadek zdolności poznawczych starzeniu się komórek krwi, które są wytwarzane w szpiku kostnym. Wyniki badań wskazują, że przeszczep szpiku kostnego pobranego z młodego organizmu może zahamować związane z wiekiem pogorszenie funkcji poznawczych u starszych osób.

    Jeśli dalsze badania potwierdzą podobne procesy u ludzi, odkrycia mogą stanowić ścieżkę do projektowania nowych terapii spowalniających progresję chorób neurodegeneracyjnych, w tym choroby Alzheimera, które dotykają milionów ludzi na całym świecie.
    Ustalenia naukowców zostały opublikowane w czasopiśmie „Communications Biology”.
    - Już wcześniejsze badania wykazały, że wprowadzanie krwi od młodych myszy może odwrócić pogorszenie funkcji poznawczych u starszych myszy, jednak mechanizmy za tym stojące nie są dobrze zrozumiałe. Nasze badania sugerują, że odpowiedź leży w konkretnych właściwościach młodych komórek krwi – powiedziała dr Helen Goodridge z Cedars-Sinai Medical Center w USA, autorka badania.
    W badaniach uczeni przeszczepili szpik kostny pobrany od 4-miesięcznych myszy do starszych, 18-miesięcznych osobników. Część starszych gryzoni otrzymała przeszczep od swoich rówieśników. Sześć miesięcy później obie grupy gryzoni przeszły standardowe testy laboratoryjne mierzące poziom ich aktywności i zdolności uczenia się, a także pamięci przestrzennej i roboczej.
    Myszy, które otrzymały młody szpik kostny, osiągnęły lepsze wyniki, niż myszy, które otrzymały szpik kostny od gryzoni w ich wieku. Miały w testach także lepsze wyniki od grupy kontrolnej starych myszy, które nie otrzymały żadnych przeszczepów.
    Zespół badawczy zbadał następnie hipokamp zwierząt - ​​region mózgu związany z pamięcią. Okazało się, że stare myszy z młodym szpikiem kostnym posiadały więcej połączeń między neuronami w hipokampie, niż myszy, którym przeszczepiono szpik kostny od ich rówieśników, mimo że obie grupy gryzoni miały mniej więcej taką samą liczbę neuronów. Połączenia między neuronami, tzw. synapsy, mają kluczowe znaczenie dla wydajności mózgu.
    Dalsze testy wykazały możliwy powód brakujących synaps. Komórki krwi wytworzone przez młody szpik kostny zmniejszyły aktywację mikrogleju – komórek odpornościowych w mózgu. Mikroglej wspiera zdrowie neuronów, ale może stać się nadmiernie aktywny i uczestniczyć w odłączaniu synaps. Badacze przyznali, że przy słabej aktywności komórek mikrogleju neurony pozostałyby zdrowe i więcej synaps przetrwałoby.

    - Wkraczamy w erę, w której nasza populacja będzie liczyć coraz więcej starszych osób. Równocześnie zauważamy coraz więcej przypadków choroby Alzheimera, co stanowi ogromne obciążenie dla systemu opieki zdrowotnej - powiedział dr Clive Svendsen, współautor nowego badania. - Nasza praca wskazuje, że spadek zdolności poznawczych u myszy można znacznie zmniejszyć poprzez dostarczenie młodych komórek krwi, które przeciwdziałają utracie synaps związanych ze starzeniem – dodał.
    ciekawe mięśnie i ważne rybki:

    The impact of exercise and nutrition on the regulation of skeletal muscle mass



    The maintenance of skeletal muscle mass and strength throughout life is a key
    determinant of human health and well-being. There is a gradual loss of both skeletal muscle
    mass and strength with ageing (a process termed sarcopenia) that increases the risk of functional
    dependence, morbidity and mortality. Understanding the factors that regulate the size of human
    muscle mass, particularly during the later years of life, has therefore become an area of intense
    scientific inquiry. The amount of muscle mass is determined by coordinated changes in muscle
    protein synthesis (MPS) and muscle protein breakdown (MPB). In this review, we assess both
    classicalandcontemporaryworkthathasexaminedhowresi stanceexerciseandnutritionimpact
    onMPSandMPB.Specialconsiderationisgiventotheroleof differentsourcesofdietaryprotein
    (foodvs.supplements)andnon-proteinnutrientssuchasomega-3fattyacidsinregulatingMPS.
    We also critically evaluate recent studies that have employed novel ‘omic’ technologies such as
    dynamicproteinprofilingtoprobeforchangesinratesofM PSandMPBattheindividualprotein
    levelfollowingexercise.Finally,weprovidesuggestion sforfutureresearchthatwehopewillyield
    important information for the development of exercise and nutritional strategies to counteract
    muscle loss in a variety of clinical settings.

    https://physoc.onlinelibrary.wiley.c....1113/JP275443

    Elevated resting heart rate, physical fitness and all-cause mortality: a 16-year follow-up in the Copenhagen Male Study

    Methods This was a prospective cohort study: the Copenhagen Male Study, a longitudinal study of healthy middle-aged employed men. Subjects with sinus rhythm and without known cardiovascular disease or diabetes were included. RHR was assessed from a resting ECG at study visit in 1985–1986. VO2Max was determined by the Åstrand bicycle ergometer test in 1970–1971. Subjects were classified into categories according to level of RHR. Associations with mortality were studied in multivariate Cox models adjusted for physical fitness, leisure-time physical activity and conventional cardiovascular risk factors.

    Results 2798 subjects were followed for 16 years. 1082 deaths occurred. RHR was inversely related to physical fitness (p<0.001). Overall, increasing RHR was highly associated with mortality in a graded manner after adjusting for physical fitness, leisure-time physical activity and other cardiovascular risk factors. Compared to men with RHR ≤50, those with RHR >90 had an HR (95% CI) of 3.06 (1.97 to 4.75). With RHR as a continuous variable, risk of mortality increased with 16% (10–22) per 10 beats per minute (bpm). There was a borderline interaction with smoking (p=0.07); risk per 10 bpm increase in RHR was 20% (12–27) in smokers, and 14% (4–24) in non-smokers.

    Conclusions Elevated RHR is a risk factor for mortality independent of physical fitness, leisure-time physical activity and other major cardiovascular risk factors.
    https://heart.bmj.com/content/99/12/...rhU0j6z8uFm8eo


    2019 Mar 1
    The leptin sensitizer celastrol reduces age-associated obesity and modulates behavioral rhythms.

    The prevalence of obesity increases with age in humans and in rodents. Age-related obesity is characterized by leptin resistance and associated with heightened risk of metabolic disorders. However, the effect of leptin resistance per se has been difficult to disentangle from other effects of aging. Here we demonstrate that celastrol, a natural phytochemical that was previously shown to act as a leptin sensitizer, induces weight loss in aged animals, but not in young controls. Celastrol reduces food intake and lowers fasting glucose without affecting energy expenditure. Unexpectedly, administration of celastrol just before the dark period disrupted circadian rhythms of sleep and activity. This regimen was also associated with loss of lean mass an outcome that would not be desirable in elderly patients. Adjusting the timing of celastrol administration by 12 hr, to the beginning of the light period, avoided interference with circadian rhythms while retaining the reductions in body weight and adiposity. Thus, targeting leptin signaling is an effective strategy to ameliorate age-associated weight gain, and can profoundly impact circadian rhythms.
    correlation doesn't imply causation

  14. #659
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Modyfikacja wyborów żywieniowych (Instagram zastąpił leptynę) ):



    New University of Liverpool research, published in Pediatrics, highlights the negative influence that social media has on children's food intake.

    Current research shows celebrity endorsement and television advertising of unhealthy foods increases children's intake of these foods. However, children are increasingly exposed to marketing through digital avenues, such as on social media, and the impact of marketing by YouTube video bloggers (vloggers) on these outcomes has, until now, not been known.

    According to a recent report by Ofcom children in the UK now access social media more than ever before. Approximately 93% of 8-11-year-olds go online, 77% use YouTube and 18% have a social media account. In older children (12-15-year-olds), 99% go online, 89% use YouTube and 69% have a social media account. Both age groups watch YouTube vloggers.

    Vloggers' influence

    Ph.D. student Anna Coates, from the University's Appetite and Obesity research group, conducted a study to examine the effect of social media marketing of snack foods (healthy and unhealthy), via vloggers' Instagram pages, on children's snack intake.

    During the study 176 children, aged between 9 and 11 years, were randomly split into three equal groups and were shown artificially created, but realistic, Instagram pages of popular vloggers (each has millions of followers). One group was shown images of the vlogger with unhealthy snacks, the second group was shown images of the vlogger with healthy snacks and the third group was shown images of the vlogger with non-food products. The participants' subsequent intake of snacks (healthy and unhealthy options) were measured.

    Children in the group that viewed the unhealthy snack images consumed 32% more kcals from unhealthy snacks specifically and 26% more kcals in total (from healthy and unhealthy snacks) compared with children who saw the non-food images. There was no significant difference in total kcal intake, or healthy snack kcal intake, between children who saw the Instagram profile with healthy images and those who saw the non-food images.

    Impactful and exploitative

    Of the study Anna Coates, said: "These findings suggest that the marketing of unhealthy foods, via vloggers' Instagram pages, increases children's immediate energy intake. The results are supported by celebrity endorsement data, which show unhealthy food endorsements increase children's unhealthy food intake, but healthy food endorsements have little or no effect on healthy food intake.

    "Young people trust vloggers more than celebrities so their endorsements may be even more impactful and exploitative. Tighter restrictions are needed around the digital marketing of unhealthy foods that children are exposed to, and vloggers should not be permitted to promote unhealthy foods to vulnerable young people on social media."
    z cyklu endocrine disruptors:

    Chemical pollutants in the home degrade fertility in both men and dogs, study finds

    New research by scientists at the University of Nottingham suggests that environmental contaminants found in the home and diet have the same adverse effects on male fertility in both humans and in domestic dogs.

    There has been increasing concern over declining human male fertility in recent decades with studies showing a 50% global reduction in sperm quality in the past 80 years. A previous study by the Nottingham experts showed that sperm quality in domestic dogs has also sharply declined, raising the question of whether modern day chemicals in the home environment could be at least partly to blame.
    https://medicalxpress.com/news/2019-...fertility.html

    dla przypomnienia:



    Association between Sleep Disturbances and Liver Status in Obese Subjects with Nonalcoholic Fatty Liver Disease: A Comparison with Healthy Controls

    The relevance of sleep patterns in the onset or evolution of nonalcoholic fatty liver disease (NAFLD) is still poorly understood. Our aim was to investigate the association between sleep characteristics and hepatic status indicators in obese people with NAFLD compared to normal weight non-NAFLD controls. Ninety-four overweight or obese patients with NAFLD and 40 non-NAFLD normal weight controls assessed by abdominal ultrasonography were enrolled. Hepatic status evaluation considered liver stiffness determined by Acoustic Radiation Force Impulse elastography (ARFI) and transaminases. Additionally, anthropometric measurements, clinical characteristics, and biochemical profiles were determined. Sleep features were evaluated using the Pittsburgh Sleep Quality Index (PSQI). Hepatic status parameters, anthropometric measurements, and clinical and biochemical markers differed significantly in NAFLD subjects compared to controls, as well as sleep efficiency, sleep disturbance score, and sleep quality score. In the NAFLD group, a higher prevalence of short sleep duration (p = 0.005) and poor sleep quality (p = 0.041) were found. Multivariate-adjusted odds ratio (95% confidence interval) for NAFLD considering sleep disturbance was 1.59 (1.11–2.28). Regression models that included either sleep disturbance or sleep quality predicted up to 20.3% and 20.4% of the variability of liver stiffness, respectively, and after adjusting for potential confounders. Current findings suggest that sleep disruption may be contributing to the pathogenesis of NAFLD as well as the alteration of the liver may be affecting sleep patterns. Consequently, sleep characteristics may be added to the list of modifiable behaviors to consider in health promotion strategies and in the prevention and management of NAFLD.
    https://www.mdpi.com/2072-6643/11/2/322


    correlation doesn't imply causation

  15. #660
    Sztywny Pal Azji
    Dołączył
    May 2014
    Postów
    1 392
    Aerobic exercise for adult patients with major depressive disorder in mental health services: A systematic review and meta‐analysis

    Abstract
    Although exercise is associated with depression relief, the effects of aerobic exercise (AE) interventions on clinically depressed adult patients have not been clearly supported. The purpose of this meta‐analysis was to examine the antidepressant effects of AE versus nonexercise comparators exclusively for depressed adults (18–65 years) recruited through mental health services with a referral or clinical diagnosis of major depression. Eleven e‐databases and bibliographies of 19 systematic reviews were searched for relevant randomized controlled clinical trials. A random effects meta‐analysis (Hedges’ g criterion) was employed for pooling postintervention scores of depression. Heterogeneity and publication bias were examined. Studies were coded considering characteristics of participants and interventions, outcomes and comparisons made, and study design; accordingly, sensitivity and subgroup analyses were calculated. Across 11 eligible trials (13 comparisons) involving 455 patients, AE was delivered on average for 45 min, at moderate intensity, three times/week, for 9.2 weeks and showed a significantly large overall antidepressant effect (g = –0.79, 95% confidence interval = –1.01, –0.57, P < 0.00) with low and nonstatistically significant heterogeneity (I2 = 21%). No publication bias was found. Sensitivity analyses revealed large or moderate to large antidepressant effects for AE (I2 ≤ 30%) among trials with lower risk of bias, trials with short‐term interventions (up to 4 weeks), and trials involving individual preferences for exercise. Subgroup analyses revealed comparable effects for AE across various settings and delivery formats, and in both outpatients and inpatients regardless symptom severity. Notwithstanding the small number of trials reviewed, AE emerged as an effective antidepressant intervention.

    https://onlinelibrary.wiley.com/doi/....1002/da.22842

    Daily Stressors, Past Depression, and Metabolic Responses to High-Fat Meals: A Novel Path to Obesity

    Background
    Depression and stress promote obesity. This study addressed the impact of daily stressors and a history of major depressive disorder (MDD) on obesity-related metabolic responses to high-fat meals.

    Methods
    This double-blind, randomized, crossover study included serial assessments of resting energy expenditure (REE), fat and carbohydrate oxidation, triglycerides, cortisol, insulin, and glucose before and after two high-fat meals. During two separate 9.5-hour admissions, 58 healthy women (38 breast cancer survivors and 20 demographically similar control subjects), mean age 53.1 years, received either a high saturated fat meal or a high oleic sunflower oil meal. Prior day stressors were assessed by the Daily Inventory of Stressful Events.

    Results
    Greater numbers of stressors were associated with lower postmeal REE (p = .008), lower fat oxidation (p = .04), and higher insulin (p = .01), with nonsignificant effects for cortisol and glucose. Women with prior MDD had higher cortisol (p = .008) and higher fat oxidation (p = .004), without significant effects for REE, insulin, and glucose. Women with a depression history who also had more stressors had a higher peak triglyceride response than other participants (p = .01). The only difference between meals was higher postprandial glucose following sunflower oil compared with saturated fat (p = .03).

    Conclusions
    The cumulative 6-hour difference between one prior day stressor and no stressors translates into 435 kJ, a difference that could add almost 11 pounds per year. These findings illustrate how stress and depression alter metabolic responses to high-fat meals in ways that promote obesity.
    04 March 2019
    Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state

    Purpose
    This review provides a current perspective on the mechanism of vitamin D on skeletal muscle function with the emphasis on oxidative stress, muscle anabolic state and muscle energy metabolism. It focuses on several aspects related to cellular and molecular physiology such as VDR as the trigger point of vitamin D action, oxidative stress as a consequence of vitamin D deficiency.

    Method
    The interaction between vitamin D deficiency and mitochondrial function as well as skeletal muscle atrophy signalling pathways have been studied and clarified in the last years. To the best of our knowledge, we summarize key knowledge and knowledge gaps regarding the mechanism(s) of action of vitamin D in skeletal muscle.

    Result
    Vitamin D deficiency is associated with oxidative stress in skeletal muscle that influences the mitochondrial function and affects the development of skeletal muscle atrophy. Namely, vitamin D deficiency decreases oxygen consumption rate and induces disruption of mitochondrial function. These deleterious consequences on muscle may be associated through the vitamin D receptor (VDR) action. Moreover, vitamin D deficiency may contribute to the development of muscle atrophy. The possible signalling pathway triggering the expression of Atrogin-1 involves Src-ERK1/2-Akt- FOXO causing protein degradation.

    Conclusion
    Based on the current knowledge we propose that vitamin D deficiency results from the loss of VDR function and it could be partly responsible for the development of neurodegenerative diseases in human beings.


    i coś miękkiego na koniec:

    Jak brak snu uszkadza mózg

    Szkoda ci czasu na sen? Lepiej tak nie myśl. Brak snu zniechęca do seksu i dosłownie niszczy mózg, co właśnie wykazali uczeni.

    On zjada sam siebie! – wykrzyknął dr Michele Bellesi z Universita Politecnica delle Marche we włoskiej Ankonie, kiedy zobaczył, jak zmienia się mózg u niewyspanych myszy. Komórki nerwowe znikały u nich jedna za drugą. Sprawcą tego były nadaktywne komórki glejowe, które odpowiadają za utrzymanie porządku w mózgu i pełnią rolę odkurzacza. U niewyspanych myszy wymiatały one jednak nie tylko uszkodzone komórki i zbędne białka, ale zjadały wszystko, co napotkały na swej drodze.

    Wyjątkowo niszczycielskie okazały się przede wszystkim największe z nich, zwane astrocytami. Pomagają one w przenoszeniu sygnałów między komórkami nerwowymi, a gdy trzeba, usuwają niepotrzebne synapsy, czyli połączenia pomiędzy komórkami, za pośrednictwem których neurony komunikują się ze sobą. Dzięki takiemu odświeżeniu sieci połączeń mózg może dokonywać selekcji wiedzy zdobytej w ciągu dnia – porządkować ją i uaktualniać.

    U myszy, które się wysypiają, astrocyty niszczą nie więcej niż 6 proc. synaps. Natomiast u niewyspanych zwierząt tempo ich usuwania jest dużo większe. Dr Bellesi obliczył, że u myszy, które były za wcześnie budzone w ciągu pięciu dni eksperymentu, zniknęło ok. 8 proc. synaps, a u zwierząt, którym przez ten czas w ogóle nie pozwolono spać, zginęło prawie 14 proc. – Po raz pierwszy wykazaliśmy, że z powodu braku snu część synaps jest dosłownie zjadana przez astrocyty – powiedział dr Bellesi w rozmowie z popularnonaukowym tygodnikiem „New Scientist”.

    Nie jest to jednak aż tak zła wiadomość. Niewielki niedobór snu sprawia, że mózg intensywnie oczyszcza się ze źle działających komórek nerwowych i synaps. Dzięki temu przebudowana sieć połączeń między neuronami staje się bardziej wydajna, przypuszcza uczony. Dopiero brak snu przez dłuższy czas staje się niebezpieczny. Wtedy przemęczony umysł nie potrafi odróżnić śmieci od potrzebnych elementów i pedantycznie usuwa wszystko, co uzna za zbędne.

    Dlaczego jednak mózg myszy na te porządki potrzebuje aż 12 godzin na dobę? Czy regularny, relaksujący sen go rozleniwia, czy rzeczywiście ma tyle do zrobienia po każdym aktywnym dniu, że szybciej pracować się nie da? Nie zważa nawet na to, że w czasie wielu godzin snu mysz, podobnie jak każde inne zwierzę, staje się świetnym łupem dla drapieżników. Nie może też wtedy wypełniać najważniejszych funkcji życiowych, jak zdobywanie pokarmu i rozmnażanie. Po co zatem ewolucja wymyśliła sen? Może pojawił się on przez przypadek i tylko organizm, a zwłaszcza mózg chętnie korzystają z tych chwil relaksu? Na te pytania nauka nie znalazła jeszcze odpowiedzi. Na razie wiadomo, że mózg niewyspany zachowuje się zupełnie inaczej niż wyspany.

    Pozbawione snu laboratoryjne szczury giną w ciągu miesiąca. U ludzi po kilku nieprzespanych nocach pojawiają się omamy i halucynacje, a osoby z rzadką genetyczną chorobą zwaną śmiertelną bezsennością rodzinną żyją co najwyżej trzy lata od momentu jej ujawnienia się. Schorzenie jest wywołane mutacją w genie, który wpływa na białka w rejonie mózgu odpowiedzialnym m.in. za regulowanie snu. I mimo najróżniejszych leków na bezsenność i wyszukanych terapii ludzie ci nie są w stanie zasnąć.

    Są jednak osoby, które nie śpią wiele lat i żyją. – Dostawałam telefony od ludzi, którzy przez dziesięć lat nie mogli zmrużyć oka – opowiada Anna Falkiewicz, dziennikarka, która prowadziła nocną audycję „Radiowy telefon zaufania”. – A to jeszcze nie są rekordziści – mówi dr Michał Skalski, specjalista zaburzeń snu. Miał pacjentów, którzy trafili do niego po 15 latach bezsennych nocy. Natomiast światowy rekordzista podobno nie zmrużył oka przez 33 lata i nieźle funkcjonował. Być może miał jakąś mutację w genie DEC2, zwanym też genem krótkiego snu. Prof. Ying-Hui Fu z University of California w San Francisco, która go odkryła, uważa, że nosiciele zmiany w tym genie mogą żyć komfortowo, śpiąc dużo mniej, niż się powszechnie zaleca. A może i w ogóle obywając się bez snu.

    Jednak większość ludzi takiej mutacji nie ma i musi przesypiać siedem-osiem godzin na dobę. A gdy na sen przeznacza mniej czasu, pojawiają się kłopoty. Dopadają one nie tylko ludzi zapracowanych, ale także osoby w podeszłym wieku. – Bo wbrew powszechnej opinii ludzie starsi potrzebują tyle samo snu co młodzi. A jeśli śpią krócej, to może być pierwszą oznaką, że w rejonach mózgu odpowiedzialnych za sen ulegają degradacji komórki nerwowe – twierdzi dr Matthew Walker z University of California w Berkeley.
    https://www.newsweek.pl/wiedza/nauka...-mozgu/g9eyvbm

    jak nie szanujesz zachodu słońca, nie wyłączysz trzustki, oczekuj kolejnego dnia, że z automatu wpadnie więcej niż powinno i chuja ma się to do Twojej silnej woli

    Melatonin Absence Leads to Long-Term Leptin Resistance and Overweight in Rats
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881424/

    Melatonin Treatment Improves Insulin Resistance and Pigmentation in Obese Patients with Acanthosis Nigricans
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867607/
    correlation doesn't imply causation

Uprawnienia umieszczania postów

  • Nie możesz zakładać nowych tematów
  • Nie możesz pisać wiadomości
  • Nie możesz dodawać załączników
  • Nie możesz edytować swoich postów
  •  

Dołącz do nas na FB

Partnerzy

MMA odzywki sklep plany treningowe spalacz tłuszczu legginsy