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Wątek: NATURALNE sposoby optymalizacji CIAŁA i DUSZY.

  1. #916
    Sztywny Pal Azji
    May 2014
    2 552
    w skrócie:
    w metabolicznych przyczynach problemów sercowych, problemem okazuje się podniesiony cukier, który wywraca (wycisza) zegar śródbłonka, który staje się bardziej podatny na "przyklejanie się" nieszczęsnych elementów lipidowo cholesterolowych. Problem czasu - ciąg dalszy.

    Glucose wears down circadian clocks in obesity, may drive cardiovascular risk

    High glucose in obesity appears to gum up the works of the circadian clocks inside our cells that help regulate the timing of many body functions across the 24-hour day and drive the risk of cardiovascular disease, scientists say.

    "We have demonstrated that glucose and cardiovascular problems are intrinsically linked in obesity," says Dr. David Stepp, vascular biologist in the Vascular Biology Center and Leon Henri Charbonnier Endowed Chair in Physiology at the Medical College of Georgia at Augusta University.
    "We have also demonstrated that high glucose impairs circadian clock function. Now we want to know if we fix the clock, do we fix the cardiovascular problems," says Stepp.

    He and Dr. David Fulton, director of the Vascular Biology Center and Regents professor in the MCG Department of Pharmacology and Toxicology, are principal investigators on a $2.7 million grant from the National Institutes of Health that is enabling the use of intermittent fasting and a developing category of clock repair drugs to find the answer.

    Circadian clocks set the rhythm of our bodies so that we eat, sleep and wake at the right time. What is less well recognized is the important role of circadian clocks in anticipating these events and preparing our organs and cells so they function optimally at the right time as well as anticipating when to rest and rejuvenate, says Fulton.

    "Every cell in your body has a clock in it that is used to anticipate daily needs," says Fulton, your blood pressure and heart rate drop at nighttime and surge in the morning when your feet hit the ground and blood must fight against gravity.

    "Your metabolic needs at night are different than your metabolic needs when you are awake," says Stepp. "Some of them are more; some of them are just different."

    [B]Sleep is supposed to be a period of rest and recovery for each of our cells just like it is for us overall. "You are doing regeneration, you are doing restoration, you are doing repair," Stepp says. At daybreak, genes active at night should be turned off, and genes important for daily activities should be turned on and our metabolism should switch from a restorative to active phase.

    Blood flow adjusts to match these dynamic metabolic needs, and our circadian clocks are sort of intermediaries between metabolism and our cardiovascular system that coordinate changes in metabolism with changes in cardiovascular gene function.

    The MCG scientists have evidence that obesity can break these links between metabolism and cardiovascular regulation. Excessive food consumption, particularly foods that are high in sugar and carbohydrates, some of which our body also breaks down into glucose, dampens clock function and imperils cardiovascular health. "It's certainly an accelerant," Fulton says of high glucose.

    They have documented both high glucose levels and significant circadian dysfunction in a mouse model of hyperphagia. These obese mice have tremendous appetites, high glucose and high blood pressure that does not dip at night when it should, and most importantly, dysfunction of the single layer of endothelial cells that line blood vessels. Normally endothelial cells provide a smooth surface for blood to pass over and play a key role in enabling blood vessels to dilate in response to greater blood volume so blood pressure doesn't increase too much.

    Endothelial dysfunction, a focus of their cardiovascular studies, is a major initiator of atherosclerosis, and what many of us think of as heart disease. Dysfunctional endothelial cells become inflamed, sticky and produce more damaging reactive oxygen species and less nitric oxide, which impairs blood vessel dilation. The result can be a tortuous passageway for blood, sticky walls where cells pile up and coronary artery disease.

    When the MCG scientists disrupt the gears of circadian clocks in mice using genetic approaches or environmental modifications, including jet lag light cycles, both approaches result in loss of clock function and increase the risk of endothelial dysfunction and disease. Now Fulton and Stepp want to know more about how the clocks lose timing and how best to intervene.

    They have bred the obese mice with a clock reporter, a gear of the circadian clock linked to a fluorescent protein that lights up when the gear is turned, so they can better track clock activity.

    Using these clock reporter mice, they saw huge downturns in circadian rhythms and clock-related genes in obese mice and high levels of glucose in the blood upstream of these events.

    "The first thing we want to know is can we understand why the clock is rundown in obesity," says Stepp. "The second thing is what mediates the effects of circadian disruption on cardiovascular disease, and if we fix that disruption, get the amplitude back up, does it fix the cardiovascular problems."

    If intermittent fasting, which should help restore the normal peaks and valleys of glucose levels, or the clock-fixer drugs they are using for these studies interfere with progression to cardiovascular problems, they should have some answers.

    They and others already have evidence that the small, clock-fixer molecule they are using, nobiletin, enhances the amplitude of and reverses the reduction of clock function in obesity. Whether or not that improves cardiovascular function, is one of the things they want to learn more about now.

    That includes checking whether high glucose and resulting clock dysfunction work through the increased expression of galectin-3, a receptor associated with cardiovascular disease that they have seen in their mouse model, to produce expression of the gene NOX1, which converts oxygen to damaging super oxide, in endothelial cells.

    They still are not certain which clock(s) are most central to this problem. Everywhere they have looked—heart, kidney, liver, blood vessels and endothelial cells—they have seen these rundown clocks. For now they are focusing on clocks in the endothelial cells, where they think a lot of the problems start. They don't expect to identify a specific clock(s) in these studies, but if their findings continue to hold they will start knocking out clocks in other cells in future studies.

    They think the problem quite literally is about timing, says Fulton. Proper signaling requires a peak and trough and constant overstimulation by too much glucose has the body instead trying to turn clocks off.

    The scientists note that if you have a healthy musculature despite obesity, it mitigates, at least for a time, the impact of high glucose on the vasculature. Muscle is a first and fast user of glucose, quickly pulling it out of the circulation. "If it goes into the muscle, it never comes out again," says Stepp. "It gets used or stored for later." Obese mice, like humans, lose muscle mass. In some of their initial studies, they preserved muscle mass in obese mice, which also prevented cardiovascular damage.

    They note that both aging, when muscle naturally loses volume even in individuals who remain active, and spinal cord injuries or other conditions that leave us immobile, have some of the same cardiovascular risks as obesity.

    While circadian-related cardiovascular risk also is heightened by lifelike scenarios like shiftwork or chronic jet lag in even a lean mouse, it is way worse for an obese one, Stepp says.

    Adult obesity results from factors that include consuming more calories than are expended, medications and other exposures as well as genetics, including gene variants that increase hunger and food intake, according to the Centers for Disease Control and Prevention. It is associated with poorer mental health, reduced quality of life and contributes to the leading causes of death in the United States including diabetes, heart disease, stroke and some types of cancer. Obesity itself is considered a major risk factor for cardiovascular disease, and a major risk as well for diabetes and high blood pressure, which are other top cardiovascular risks.

    Reduced food intake in old mice can no longer improve health

    Reduced food intake helps both animals and humans to improve health in old age and can prolong life. But when do you have to change your diet to achieve this benefit in old age? Scientists from the Max Planck Institute for Biology of Ageing, the Excellence Cluster for Ageing Research at the University of Cologne, the Babraham Institute in Cambridge and UCL have now shown that mice only become healthier if they start food reduction early and eat less before entering old age. The scientists conclude that healthy behavior must be established earlier in life in order to improve health in old age and extend lifespan.
    Ostatnio edytowane przez htw ; 22-10-19 o 14:25
    correlation doesn't imply causation

  2. #917
    Sztywny Pal Azji
    May 2014
    2 552
    Czy fala elektromagnetyczna wpływa na działanie jelit (pierwszego mózgu) ? TAK
    Jeśli komuś się wydawało, że w lecie sytuacja jest inna - jelita mają się lepiej i tak dalej to nie fatamorgana.
    Nie przedstawiono jeszcze ścieżki odpowiedzialnej, ale oś SKÓRA - JELITA jest już potwierdzona.

    This is the first study to show that skin exposure to UVB light alters the gut microbiome in humans.
    OCTOBER 24, 2019
    Where the sun doesn't shine? Skin UV exposure reflected in poop

    The sun can indeed shine out of your backside, suggests research. Not because you're self-absorbed, but because you've absorbed gut-altering UV radiation.

    This is the first study to show that skin exposure to UVB light alters the gut microbiome in humans. Published in Frontiers in Microbiology, the analysis suggests that vitamin D mediates the change—which could help explain the protective effect of UVB light in inflammatory diseases like MS and IBD.

    Ratifying rodent studies

    Sun exposure, vitamin D levels and the mix of bacteria in our gut are each associated with risk of inflammatory conditions like MS and IBD. Scientists hypothesize that a causal chain links the three.
    Exposure to UVB in sunlight is well-known to drive vitamin D production in the skin, and recent studies suggest that vitamin D alters the human gut microbiome. However, that UVB therefore causes gut microbiome changes, via vitamin D production, has so far been shown only in rodents.
    In a new clinical pilot study, researchers tested the effect of skin UVB exposure on the human gut microbiome.
    Healthy female volunteers (n=21) were given three one-minute sessions of full-body UVB exposure in a single week. Before and after treatment, stool samples were taken for analysis of gut bacteria—as well blood samples for vitamin D levels.

    Rich as feces

    Skin UVB exposure significantly increased gut microbial diversity, but only in subjects who were not taking vitamin D supplements during the (winter) study (n=12).

    "Prior to UVB exposure, these women had a less diverse and balanced gut microbiome than those taking regular vitamin D supplements," reports Prof. Bruce Vallance, who led the University of British Columbia study. "UVB exposure boosted the richness and evenness of their microbiome to levels indistinguishable from the supplemented group, whose microbiome was not significantly changed."

    The largest effect was an increase in the relative abundance of Lachnospiraceae bacteria after the UVB light exposures.

    "Previous studies have linked Lachnospiraceae abundance to host vitamin D status," adds Vallance. "We too found a correlation with blood vitamin D levels, which increased following UVB exposure."

    This indicates that vitamin D at least partly mediates UVB-induced gut microbiome changes.

    The results also showed some agreement with mouse studies using UVB, such as an increase in Firmicutes and decrease in Bacteroidetes in the gut following exposure.
    Getting to the bottom of UVB's protective effect
    "In this study we show exciting new data that UVB light is able to modulate the composition of the gut microbiome in humans, putatively through the synthesis of vitamin D," Vallance sums up.
    The study is not designed to show the exact mechanism by which the microbiome changes occur, but both UVB and vitamin D are known to influence the immune system.
    "It is likely that exposure to UVB light somehow alters the immune system in the skin initially, then more systemically, which in turn affects how favorable the intestinal environment is for the different bacteria," suggests Vallance.

    "The results of this study have implications for people who are undergoing UVB phototherapy, and identifies a novel skin-gut axis that may contribute to the protective role of UVB light exposure in inflammatory diseases like MS and IBD."

    Gut instincts: Researchers discover first clues on how gut health influences brain health

    New cellular and molecular processes underlying communication between gut microbes and brain cells have been described for the first time by scientists at Weill Cornell Medicine and Cornell's Ithaca campus.

    Over the last two decades, scientists have observed a clear link between autoimmune disorders and a variety of psychiatric conditions. For example, people with autoimmune disorders such as inflammatory bowel disease (IBD), psoriasis and multiple sclerosis may also have depleted gut microbiota and experience anxiety, depression and mood disorders. Genetic risks for autoimmune disorders and psychiatric disorders also appear to be closely related. But precisely how gut health affects brain health has been unknown.

    Half of all commonly used drugs profoundly affecting the gut microbiome, warn experts

    A new study presented at UEG Week 2019 reports that 18 commonly used drug categories extensively affect the taxonomic structure and metabolic potential of the gut microbiome. Eight categories of drugs were also found to increase antimicrobial resistance mechanisms in the study participants.

    The drug categories found to have the biggest impact on the microbiome include:

    Proton pump inhibitors (PPIs)—used to treat dyspepsia, which affects between 11 percent and 24 percent of the European population. PPIs are also used to treat peptic ulcer, H. Pylori eradication, gastro reflux and Barrett's esophagus.

    Metformin—used as a treatment for type 2 diabetes, affecting 10 percent of European adults

    Antibiotics—used to treat bacterial infections, taken by 34 percent of the European population each year

    Laxatives—used to treat and prevent constipation, affecting 17 percent of European adults

    Snacking: the modern habit that could be putting your health and waistline at risk

    Cakes, biscuits and energy bars are, for many people, just staples of everyday life—the snacks that keep them going through the day.

    But most people don't realize just how easy it is to over-consume calories while snacking. Women are advised by the government to consume 2,000 calories a day and men 2,500. And the NHS suggests aiming to have a balance of 400 calories for breakfast, 600 calories for lunch and 600 calories for the evening meal—leaving the remainder for drinks and health snacks.

    But research from the Behaviour Insight Team, also known unofficially as the "Nudge Unit", found that adults may be consuming an average of 3,000 calories a day without realizing, partly due to snacking.

    dziecięca otyłość wpływa na zdolności poznawcze:

    Childhood obesity linked to structural differences in key brain regions

    Obesity in children is associated with differences in brain structure in regions linked to cognitive control compared to the brains of children who are normal weight, according to new research from the University of Cambridge.
    correlation doesn't imply causation

  3. #918
    Sztywny Pal Azji
    May 2014
    2 552
    Jutro wchodzimy w czas solarny czyli normalny. Pozdrawiam Wszystkich !

    Ekspozycja na spektrum o długości 450–500 nm w nocy upośledza wychwyt glukozy i powoduje, że następnego dnia wybierasz pożywienie w którym znajdzie się więcej cukru - nagle chuj strzela Twoją silną wolę.

    23 października 2019
    Blue light at night acutely impairs glucose tolerance and increases sugar intake in the diurnal rodent Arvicanthis ansorgei in a sex‐dependent manner

    In our modern society, the exposure to light at night (LAN) has increased considerably, which may impact human health negatively. Especially exposure to light at night containing short wavelength emissions (~450–500 nm) can disrupt the normal function of the biological clock, altering sleep‐wake cycles and inducing metabolic changes. Recently, we reported that light at night acutely impairs glucose tolerance in nocturnal rats. However, light at night in nocturnal rodents coincides with their activity period, in contrast to artificial light at night exposure in humans. The aim of this study was to evaluate the acute effects of blue (λ = 490 ± 20 nm) artificial light at night (bALAN) on glucose metabolism and food intake in both male and female diurnal Sudanian grass rats (Arvicanthis ansorgei) fed either regular chow or a free choice high‐fat high sucrose diet (HFHS). In both chow and HFHS fed male Arvicanthis, 1‐hour of bALAN exposure induced a higher glucose response in the oral glucose tolerance test (OGTT) accompanied by a significant decrease in plasma insulin. Furthermore, in HFHS fed animals, bALAN induced an increase in sucrose intake during the dark phase in males but not in females. Additionally, 1‐h of bALAN increased the nonfasted glucose levels together with plasma corticosterone in female grass rats. These results provide new and further evidence for the deleterious effects of exposure to short wavelength emission‐containing artificial light at night on glucose metabolism in a diurnal rodent in a sex‐dependent manner.

    Twój silnik również podlega rytmowi:

    batokina odpowiedzialna za beżowienie odnaleziona:

    Proteomics-Based Comparative Mapping of the Secretomes of Human Brown and White Adipocytes Reveals EPDR1 as a Novel Batokine

    Adipokines secreted from white adipose tissue play a role in metabolic crosstalk and homeostasis, whereas the brown adipose secretome is less explored. We performed high-sensitivity mass-spectrometry-based proteomics on the cell media of human adipocytes derived from the supraclavicular brown adipose and from the subcutaneous white adipose depots of adult humans. We identified 471 potentially secreted proteins covering interesting categories such as hormones, growth factors, extracellular matrix proteins, and proteins of the complement system, which were differentially regulated between brown and white adipocytes. A total of 101 proteins were exclusively quantified in brown adipocytes, and among these was ependymin-related protein 1 (EPDR1). EPDR1 was detected in human plasma, and functional studies suggested a role for EPDR1 in thermogenic determination during adipogenesis. In conclusion, we report substantial differences between the secretomes of brown and white human adipocytes and identify novel candidate batokines that can be important regulators of human metabolism.

    correlation doesn't imply causation

  4. #919
    Sztywny Pal Azji
    May 2014
    2 552
    Lato na Arktyce, gdzie ciemności nie ma może być trudne jednak dzięki utrzymaniu ustalonego czasu na posiłek i rutyna snu może utrzymać prawie normalny rytm aktywności melatoniny i ekspresję genów zegarowych.

    The Effect of a Common Daily Schedule on Human Circadian Rhythms During the Polar Day in Svalbard: A Field Study

    All Arctic visitors have to deal with extreme conditions, including a constant high light intensity during the summer season or constant darkness during winter. The light/dark cycle serves as the most potent synchronizing signal for the biological clock, and any Arctic visitor attending those regions during winter or summer would struggle with the absence of those entraining signals. However, the inner clock can be synchronized by other zeitgebers such as physical activity, food intake, or social interactions. Here, we investigated the effect of the polar day on the circadian clock of 10 researchers attending the polar base station in the Svalbard region during the summer season. The data collected in Svalbard was compared with data obtained just before leaving for the expedition (in the Czech Republic 49.8175°N, 15.4730°E). To determine the circadian functions, we monitored activity/rest rhythm with wrist actigraphy followed by sleep diaries, melatonin rhythm in saliva, and clock gene expression (Per1, Bmal1, and Nr1D1) in buccal mucosa samples. Our data shows that the two-week stay in Svalbard delayed melatonin onset but did not affect its rhythmic secretion, and delayed the activity/rest rhythm. Furthermore, the clock gene expression displayed a higher amplitude in Svalbard compared to the amplitude detected in the Czech Republic. We hypothesize that the common daily schedule at the Svalbard expedition strengthens circadian rhythmicity even in conditions of compromised light/dark cycles. To our knowledge, this is the first study to demonstrate peripheral clock gene expression during a polar expedition.

    Activity rhythms of subjects in Czech Republic (CZE) and in Svalbard (SVB).
    A) Mean daily activity of eight subjects in the Czech Republic and in Svalbard. The activity was recorded by MotionWatch for 12 days and displayed as a mean ± SEM in 30 min bins over 24 h. For clarity, part of the day (00:00 to 7:00) was re-plotted. In the Czech Republic, the activity counts are represented by black dots and a black line, and in Svalbard by blue boxes and a blue line. B) Activity acrophase plotted for each subject. Black dots represent the acrophase for each subject in the Czech Republic; blue boxes present the acrophase in Svalbard.

    Wiele elementów zegara dobowego reguluje działanie kilku neuroprzekaźników. Jest więc prawdopodobne, że potencjalne mutacje genów zegarowych mogą nasilać ryzyko chorób psychicznych.

    regularna nawet delikatna ekspozycja na promieniowanie ultrafioletowe zmniejsza objawy NAFLD wywołaną dietą wysoko-tłuszczową.

    Regular exposure to non-burning ultraviolet radiation reduces signs of non-alcoholic fatty liver disease in mature adult mice fed a high fat diet: results of a pilot study

    Obesity often emerges in middle age, increasing risk for metabolic disorders. Our previous preclinical experiments identified that chronic exposure to non-burning ultraviolet radiation, like that achieved through sun exposure, prevented weight gain and signs of metabolic dysfunction in young adult mice fed a high fat diet. Our objective was to perform a pilot study to estimate the effect size of ongoing exposure to sub-erythemal (non-burning, low dose) UVB (1 kJ/m2) radiation on measures of adiposity, food intake and physical activity in ‘mature’ adult C57Bl/6J male mice fed a high fat diet for 12 weeks.

    The severity of liver steatosis, fibrosis and inflammation were reduced in older adult mice exposed twice a week to ultraviolet radiation (from 29 weeks of age), compared to mock-irradiated mice, with some evidence for reduced hepatic mRNAs for tnf and tgfß1 (not fatp2 nor fasN). Power analyses suggested that up to 24 mice per treatment would be required in future experiments to detect a significant effect on some markers of adiposity such as body weight gain. Our studies suggest frequent exposure to low levels of sunlight may reduce the severity of hepatic steatosis induced in older adults living in environments of high caloric intake.

    nie samym chlebem żyją drobnoustroje mikrobioty jelitowej:

    Intersection of the Gut Microbiome and Circadian Rhythms in Metabolism

    czerwone mięso w bułce nie koniecznie dobre połączenie:

    Gut microbiota response to red meat associated carbohydrates may affect human health

    podobno odszukali Eden, metaboliczną Ewę (Linia L0)
    właśnie dlatego Kenijczycy dominują na długich dystansach. Ich mitochondria są bardzo mocno i blisko siebie upakowane i perfekcyjnie zamieniają glukozę na ATP.


    Nasi dalecy przodkowie, około 200 tysięcy lat temu, znaleźli sobie dobre warunki rozwoju na południe od dorzecza Zambezi, na terenie obecnej Botswany - pisze na łamach czasopisma "Nature" międzynarodowy zespół naukowców. Wyniki opublikowanych przez nich badań genetycznych wskazują na to, że przedstawiciele Homo sapiens sapiens żyli tam około 70 tysięcy lat, a do rozproszenia na inne tereny nakłoniły ich 130 do 110 tysięcy lat temu między innymi zmiany klimatyczne. Te migracje przyczyniły się potem do genetycznej, etnicznej i kulturowej różnorodności naszego gatunku.
    Czytaj więcej na
    Ostatnio edytowane przez htw ; 31-10-19 o 19:53
    correlation doesn't imply causation

  5. #920
    Sztywny Pal Azji
    May 2014
    2 552
    When you eat may matter more than what you eat: study

    There's evidence that the old expression "eat breakfast like a king, lunch like a prince and dinner like a pauper" could use some tweaking. With one important revision, this approach could help not just for better health, but also for losing weight.

    A study in the American Journal of Clinical Nutrition found that when you eat rather than what you eat could have the bigger impact.

    pomysł poszerzenie świadomości czyli pisanie na etykietach śmieciowego jedzenia ile dana porcja ma kalorii nie wypalił, ciekawe

    Calorie labels in fast food outlets linked to small drop in calories purchased

    Labelling menus with the calorie content of individual dishes and drinks in fast food outlets is associated with a small immediate decrease in average calories purchased, according to a study using data from a large US restaurant company published by The BMJ today.

    But this was followed by a gradual weekly increase over the next year, implying that calorie labelling alone "may not be enough to make sustainable reductions in calorie intake in fast food restaurants," say the researchers.

    sowy bardziej czułe na dobroczynne działanie UVB

    Narrow-band ultraviolet B (NB UV-B) exposures improve mood in healthy individuals differently depending on chronotype.

    Our results indicate that four suberythematous exposures to NB UV-B can induce a change in
    perceived mood and 25(OH)D 3 as well as IL-6 levels. Mood improved more in evening chrono-
    types than morning chronotypes. Our findings support the hypothesis that UVR-exposed human
    skin transmits cues via reciprocal molecular inter- actions that affect mood regulation in the brain and contribute to behavior and the timing of daily activities. However, the demonstration of the exact mechanisms remains a major challenge.

    Odkryto w mózgu rejon odpowiedzialny za zachowania impulsywne, neurony z rejonu bocznego podwzgórza przekazują sygnały rejonom brzusznym hipokampa

    Nie możesz przestać sięgać po cukierki? Tracisz pieniądze w grach hazardowych? Naukowcy zaczynają lepiej rozumieć mechanizm, który za tym stoi. Zespół pod kierunkiem badaczy z University of Southern California odkrył rejon mózgu, który steruje zachowaniami impulsywnymi. Jak pisze na łamach czasopisma „Nature Communications”, zrozumienie jego działania może pomóc osobom, które nie mogą powstrzymać się od przejadania, mają problemy z hazardem, uzależnieniem od narkotyków, czy alkoholu. Są szanse, że ta wiedza pomoże też pacjentom cierpiącym na chorobę Parkinsona.

    może ktoś z czytających ma niskiego teścia ?

    Absent Diurnal Variation in Serum Testosterone in Young Men With Testosterone Deficiency

    Although healthy young men demonstrate diurnal pattern of serum testosterone (T), minimal information is available regarding diurnal variation in young men with T deficiency.

    Blood samples were obtained over a 24-hour period at 08:00, 11:00, 14:00, 17:00, 20:00, and 08:00 the following morning. Men were categorized as normal or low T if serum T > 300ng/dL or >300ng/dL at 08:00, respectively.

    Twenty-one volunteers (mean age 31.7y, range 18-49) were studied. Eleven had normal T and ten had low T, all with normal LH concentrations. The low T group was older (mean 33.4y vs 30.1y), with higher BMI (mean 32.6kg/m 2 vs 27.5kg/m 2); these differences were not significant. Highest overall mean T concentration was observed at 08:00 and lowest at 14:00. Mean T levels in the normal group declined between 08:00 and 14:00 from 423ng/dL to 358ng/dL (15% decline; p=0.0003). Mean T for the low T group was 228ng/dL at 08:00 and 218ng/dL at 14:00 (4% decline; p=0.54). Calculated free T paralleled total T, with a decline of 14% (p<0.001) for the normal T group and 5% (p=0.52) for the low T group. Two of eleven men in the normal group did not demonstrate diurnal variation. No individual with baseline T>400ng/dL demonstrated T <300ng/dL at any time point.

    Men with low T concentrations failed to demonstrate diurnal variation with 24h blood sampling. We speculate that similar central mechanisms may be involved in the pathophysiology leading to secondary T deficiency as well as the loss of circadian rhythmicity.
    było już 100x ale jakby ktoś zapomniał:
    correlation doesn't imply causation

  6. #921
    Sztywny Pal Azji
    May 2014
    2 552
    Sleep restriction increases free fatty acids in healthy men

    Effects of Low-Fat and High-Fat Meals, with and without Dietary Fiber, on Postprandial Endothelial Function, Triglyceridemia, and Glycemia in Adolescents

    Melatonin supplementation and pro-inflammatory mediators: a systematic review and meta-analysis of clinical trials

    Thirteen eligible studies with 22 datasets with total sample size of 749 participants were included in the meta-analysis. Melatonin supplementation significantly decreased TNF-α and IL-6 levels [(WMD = − 2.24 pg/ml; 95% CI − 3.45, − 1.03; P < 0.001; I2 = 96.7%, Pheterogeneity < 0.001) and (WMD = − 30.25 pg/ml; 95% CI − 41.45, − 19.06; P < 0.001, I2 = 99.0%; Pheterogeneity < 0.001)], respectively. The effect of melatonin on CRP levels was marginal (WMD = − 0.45 mg/L; 95% CI − 0.94, 0.03; P = 0.06; I2 = 96.6%, Pheterogeneity < 0.001).

    The results of the present meta-analysis support that melatonin supplementation could be effective on ameliorating of inflammatory mediators.
    From circadian clocks to non-alcoholic fatty liver disease

    Introduction: The circadian rhythm is an integral regulator of various endocrine processes in the body, including sleep-wake cycles, hormonal regulation, and metabolism. In addition to metabolic, genetic, and environmental factors, a dysregulated circadian rhythm resulting from lifestyle changes has been implicated in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). An accumulating body of evidence also supports strong association between NAFLD and metabolic disorder, the pathogenesis of which is related to periodic fluctuations in hormonal homeostasis. It is clear that endocrine and circadian rhythms are tightly interconnected. Generally, the circadian rhythm regulates flux patterns of physiological functions. The present review will discuss the modulation of bodily processes by the circadian rhythm with specific attention to the regulation of NAFLD by leptin and related hormones.
    correlation doesn't imply causation

  7. #922
    Sztywny Pal Azji
    May 2014
    2 552
    20 sekund przed wejściem do NREM zalewamy się rytmicznie płynem mózgowo-rdzeniowy.

    Niezwykłe pulsowanie mózgu podczas snu wolnofalowego

    Podczas snu wolnofalowego w mózgu zachodzą niesamowite sprzężone zjawiska. Gdy neurony się wyciszają, po kilku sekundach następuje odpływ krwi z głowy, a na jej miejsce napływa płyn mózgowo-rdzeniowy (ang. cerebrospinal fluid, CSF). Obmywa on mózg rytmicznymi, pulsującymi falami.

    początki dziecięcej otyłości rodzą się już w brzuszku mamusi, zegary się rozjeżdżają, ośrodek głodu i sytości (neurony AgRP) zostaje upośledzony, jednym słowem jest super.

    Maternal Obesity during Pregnancy Alters Daily Activity and Feeding Cycles, and Hypothalamic Clock Gene Expression in Adult Male Mouse Offspring

    Abstract: An obesogenic diet adversely affects the endogenous mammalian circadian clock, altering daily activity and metabolism, and resulting in obesity. We investigated whether an obese pregnancy can alter the molecular clock in the offspring hypothalamus, resulting in changes to their activity and feeding rhythms. Female mice were fed a control (C, 7% kcal fat) or high fat diet (HF, 45% kcal fat) before mating and throughout pregnancy. Male offspring were fed the C or HF diet postweaning, resulting in four offspring groups: C/C, C/HF, HF/C, and HF/HF. Daily activity and food intake were monitored, and at 15 weeks of age were killed at six time-points over 24 h. The clock genes Clock, Bmal1, Per2, and Cry2 in the suprachiasmatic nucleus (SCN) and appetite genes Npy and Pomc in the arcuate nucleus (ARC) were measured. Daily activity and feeding cycles in the HF/C, C/HF, and HF/HF offspring were altered, with increased feeding bouts and activity during the day and increased food intake but reduced activity at night. Gene expression patterns and levels of Clock, Bmal1, Per2, and Cry2 in the SCN and Npy and Pomc in the ARC were altered in HF diet-exposed offspring. The altered expression of hypothalamic molecular clock components and appetite genes, together with changes in activity and feeding rhythms, could be contributing to offspring obesity.

    a na Malezji cierpią na niedobór witaminy D -

    Risk factors of vitamin D deficiency among 15-year-old adolescents participating in the Malaysian Health and Adolescents Longitudinal Research Team Study (MyHeARTs)

    UVB moduluje mikrobiom jelitowy:

    Skin Exposure to Narrow Band Ultraviolet (UVB) Light Modulates the Human Intestinal Microbiome
    Ostatnio edytowane przez htw ; 05-11-19 o 14:56
    correlation doesn't imply causation

  8. #923
    Sztywny Pal Azji
    May 2014
    2 552

    Stressed to the max? Deep sleep can rewire the anxious brain

    When it comes to managing anxiety disorders, William Shakespeare's Macbeth had it right when he referred to sleep as the "balm of hurt minds." While a full night of slumber stabilizes emotions, a sleepless night can trigger up to a 30% rise in anxiety levels, according to new research from the University of California, Berkeley.
    correlation doesn't imply causation

  9. #924
    Sztywny Pal Azji
    May 2014
    2 552
    jak UVB dotyka cholesterolu na skórze?

    Cytat Zamieszczone przez htw Zobacz posta

    Narrow-band ultraviolet B (NB UV-B) exposures improve mood in healthy individuals differently depending on chronotype.

    a jak wrzucisz gotowca ?

    NOVEMBER 7, 2019
    Vitamin D and Omega 3 supplements do not reduce risk of systemic inflammation

    "People commonly think that these supplements can prevent inflammatory diseases, but when a patient asks their doctor, 'Should I take this supplement?' doctors often don't know what to advise because there haven't been large scale clinical trials. VITAL provides a large dataset to address these questions," said corresponding author Karen Costenbader, MD, MPH, director of the Lupus Program in the Division of Rheumatology, Inflammation and Immunity. "In this case, there isn't a strong message that either supplement will reduce risk of systemic inflammation, at least not the biomarkers of disease."

    The VITAL study is a randomized, double-blind, placebo-controlled trial in which investigators tested the effects of supplements of vitamin D (2000 IU/day), omega 3s (1 gm/day) or both. For this analysis, Costenbader and colleagues tested levels of three known biomarkers of inflammation at the start of the trial and after one year of taking supplements or a placebo. They were interleukin-6 (IL-6), tumor necrosis factor-receptor 2, and high sensitivity C-reactive protein (hsCRP).

    The team found that neither supplement reduced the biomarkers at one year. Surprisingly, among those taking the vitamin D supplement, instead of decreasing, IL-6 levels rose by 8.2 percent. The investigators also report that among participants who had lower fish intake at the start of the trial, hsCRP levels did decline for those taking the omega-3 supplement.

    Melatonin and its ubiquitous anticancer effects

    Melatonin (N-acetyl-5-methoxy-tryptamine), which is generally considered as pleiotropic and multitasking molecule, secretes from pineal gland at night under normal light or dark conditions. Apart from circadian regulations, Melatonin also has antioxidant, anti-ageing, immunomodulation and anticancer properties. From the epidemiological research, it was postulated that Melatonin has significant apoptotic, angiogenic, oncostatic and anti-proliferative effects on various oncological cells. In this review, the underlying anticancer mechanisms of Melatonin such as stimulation of apoptosis, Melatonin receptors (MT1 and MT2) stimulation, paro-survival signal regulation, the hindering of angiogenesis, epigenetic alteration and metastasis have been discussed with recent findings. The Melatonin utilization as an adjuvant with chemotherapeutic drugs for the reinforcement of therapeutic effects was also discussed. This review precisely emphasizes the anticancer effect of Melatonin on various cancer cells. This review exemplifies the epidemiology and anticancer efficiency of Melatonin with prior attention to the mechanisms of actions.

    The relationship between sleep duration, sleep quality and dietary intake in adults

    To determine the relationship of specific macro- and micro-nutrients and food groups with sleep duration and sleep quality in adults. This cross-sectional descriptive study was conducted on 2446 adults aged between 20 and 64 years in Turkey. The participants’ socio-demographic characteristics, anthropometric measurements, and dietary intake (24-h recall) were taken. The Pittsburgh Sleep Quality Index was used to assess sleep quality. In the study, 48.9% of the participants were male and 51.1% were female, with an average age of 38.7 ± 12.70 years. Total protein, meat, and processed meat product consumption rates of long sleepers were found to be lower than those of normal sleepers (p < 0.05). Saturated fat intake of short sleepers was higher than that of long sleepers (p < 0.018). Participants with good sleep quality were found to consume higher carbohydrate, fiber, beta-carotene, vitamin E, thiamine, vitamin B6, total folate, vitamin C, calcium, magnesium, potassium, and iron compared to those with poor sleep quality (p < 0.05). When examined in terms of food groups, fruit consumption was higher in individuals with good sleep quality compared to those with poor sleep quality (p < 0.05). In this study, some macro- and micro-nutrients of the diet were found correlated with sleep duration and quality. Mechanisms mediating the relationship between sleep duration and dietary intake are multi-factorial. Because of the differences in appetite-related hormones, such as leptin and ghrelin, and hedonic factors, future studies will benefit from assessing sleep duration/quality and dietary intake.

    Stress hormone helps control the circadian rhythm of brain cells
    correlation doesn't imply causation

  10. #925
    Sztywny Pal Azji
    May 2014
    2 552
    Utrata masy ciała u ludzi nie jest spowodowana usuwaniem lipidów, ale szybkością pobierania lipidów w tkance tłuszczowej.Im wolniej idzie tym większa szansa, że po latach się utrzyma, takie płyną wnioski z 18 letniego badania.

    Adipose lipid turnover and long-term changes in body weight

    Dietary fat, the gut microbiota, and metabolic health – A systematic review conducted within the MyNewGut project

    Oxygen deficiency rewires mitochondria
    Mitochondria burn oxygen and provide energy for the body. Cells lacking oxygen or nutrients have to change their energy supply quickly in order to keep growing. Scientists from the Max Planck Institute for Biology of Ageing have now shown that mitochondria are reprogrammed under depleted oxygen and nutrients. Tumors of the pancreas may also use this reprogramming mechanism to keep growing despite reduced nutrient and oxygen levels. The researchers believe that proteins in this newly discovered signaling pathway could be a good target for therapies against pancreatic cancer, for which no drug is currently available.

    brak mitofagi najprawdopodobniej odpowiada ze wczesne stadium neurodegeneracji

    Self-cannibalizing mitochondria may set the stage for ALS development
    Ostatnio edytowane przez htw ; 09-11-19 o 16:45
    correlation doesn't imply causation

  11. #926
    Sztywny Pal Azji
    May 2014
    2 552
    11 LISTOPADA 2019
    Evening meals could harm the female heart, study shows

    (HealthDay)—Late dinners and heavy evening snacking do no favors for women's hearts, a new study suggests.

    Researchers at New York City's Columbia University found that those who ate more of their daily calories in the evening had a higher risk of heart disease.
    One cardiologist who looked over the new findings wasn't surprised by the effect.
    "The way metabolism, circadian rhythm, cortisol/insulin cycles work, they do not and cannot support heavy meals in the evening hours," said Dr. Evelina Grayver.

    "Not only are our bodies not meant to digest at late hours, we are also less mobile at night, thus the calories we consume are not being expended as energy," said Grayver, who directs the coronary care unit at North Shore University Hospital in Manhasset, N.Y.

    The new study involved 112 women, average age 33, whose heart health was assessed at the start of the study and then again one year later. The women recorded what they ate for one week at the start of the study and for one week 12 months later.
    Most of the women ate some food after 6 p.m., but those who consumed a higher proportion of their daily calories in the evening tended to have had poorer heart health, say a team led by Nour Makarem, a Columbia associate research scientist.
    In fact, with every 1% increase in calories consumed after 6 p.m., heart health declined accordingly.
    Specifically, women who ate more of their daily calories in the evening were more likely to have higher blood pressure, higher body mass index and poorer long-term control of blood sugar.
    Similar findings occurred with every 1% increase in daily calories consumed after 8 p.m., according to the study, which is to be presented at the American Heart Association's annual meeting, held Nov 16 to 18 in Philadelphia.
    "So far, lifestyle approaches to prevent heart disease have focused on what we eat and how much we eat," Makarem said in an AHA news release. But he said that the when of eating may be important, too.
    There's good news from the study, because shifting the timing of eating is "a simple, modifiable behavior that can help lower heart disease risk," Makarem said.
    Dr. Satjit Bhusri is a cardiologist at Lenox Hill Hospital in New York City. He agreed the findings make sense.
    "Calories are immediate energy," he said. "I always advise patients to eat a lean, low -carbohydrate, early dinner. This simple understanding and mindfulness of when and what to eat, as the study states, can make a major impact on overall cardiovascular health and outcomes."
    Because these findings were presented at a medical meeting, they should be considered preliminary until published in a peer-reviewed journal.

    11 listopada 2019
    Characterising nitric oxide-mediated metabolic benefits of low-dose ultraviolet radiation in the mouse: a focus on brown adipose tissue

    Exposure to sunlight has the potential to suppress metabolic dysfunction and obesity. We previously demonstrated that regular exposure to low-doses of ultraviolet radiation (UVR) reduced weight gain and signs of diabetes in male mice fed a high-fat diet, in part via release of nitric oxide from skin. Here, we explore further mechanistic pathways through which low-dose UVR exerts these beneficial effects.

    We fed mice with a luciferase-tagged Ucp1 gene (which encodes uncoupling protein-1 [UCP-1]), referred to here as the Ucp1 luciferase transgenic mouse (‘Thermomouse’) a high-fat diet and examined the effects of repeated exposure to low-dose UVR on weight gain and development of metabolic dysfunction as well as UCP-1-dependent thermogenesis in interscapular brown adipose tissue (iBAT).

    Repeated exposure to low-dose UVR suppressed the development of glucose intolerance and hepatic lipid accumulation via dermal release of nitric oxide while also reducing circulating IL-6 (compared with mice fed a high-fat diet only). Dietary nitrate supplementation did not mimic the effects of low-dose UVR. A single low dose of UVR increased UCP-1 expression (by more than twofold) in iBAT of mice fed a low-fat diet, 24 h after exposure. However, in mice fed a high-fat diet, there was no effect of UVR on UCP-1 expression in iBAT (compared with mock-treated mice) when measured at regular intervals over 12 weeks. More extensive circadian studies did not identify any substantial shifts in UCP-1 expression in mice exposed to low-dose UVR, although skin temperature at the interscapular site was reduced in UVR-exposed mice. The appearance of cells with a white adipocyte phenotype (‘whitening’) in iBAT induced by consuming the high-fat diet was suppressed by exposure to low-dose UVR in a nitric oxide-dependent fashion. Significant shifts in the expression of important core gene regulators of BAT function (Dio2, increased more than twofold), fatty acid transport (increased Fatp2 [also known as Slc27a2]), lipolysis (decreased Atgl [also known as Pnpla2]), lipogenesis (decreased Fasn) and inflammation (decreased Tnf), and proportions of macrophages (increased twofold) were observed in iBAT of mice exposed to low-dose UVR. These effects were independent of nitric oxide released from skin.

    zaczeło się od:

    An Unexpected Role: UVA-Induced Release of Nitric Oxide from Skin May Have Unexpected Health Benefits

    Appetite control and exercise: Does the timing of exercise play a role?


    •Exercise differently affect energy intake and appetite depending on its timing

    •Morning exercise seems to have better effect on energy intake

    •The closer exercise is to the meal, the greater are the beneficial effects

    The prevention and management of chronic diseases, particularly overweight and obesity, relies on multidisciplinary strategies mainly combining dietary approaches with physical activity. Recently, the timing of exercise (time of the day as well as delay/position relative to a meal) has been suggested as an important parameter to consider when prescribing physical activity. Some studies have for instance shown the interest of the timing of exercise on the glycemia, sleep and body composition regulation. However, the impact of exercise-timing on appetite control and energy intake remains unclear. This is why, the present paper questions whether physical exercise, depending on its timing during the day and related to a meal, can affect energy intake, appetite sensations and food reward. Although evidences remain actually limited, exercising during the morning; and particularly close to lunch, might have a better impact on overall energy balance through reduced subsequent energy intake, without leading to compensatory intakes at the following meals. Importantly, dealing with the timing of exercise to optimize energy balance (and affect energy intake and appetite) does not only require to consider its time during the day (morning vs. afternoon or evening), but also and maybe mainly its order/position (pre vs. post) and delay regarding meals. While the actual literature remains limited in this area, the present paper tends to highlight the importance of considering the timing of exercise to optimize our impact on the overall energy balance, and to encourage the elaboration of further studies to better understand and determine the potential effect of this timing of exercise, in order to find the best combination between the different exercise characteristics, intensity, duration, modality, to empower these effects.

    Bedroom lighting environment and incident diabetes mellitus: a longitudinal study of the HEIJO-KYO cohort.

    Light information received by the brain influences human circadian timing and metabolism; low-level light at night (LAN) significantly increased body mass and led to prediabetes in mice. We hypothesized that LAN exposure increases the diabetes risk in humans. The aim of the present study was to evaluate a longitudinal association between LAN exposure and the incidence of diabetes in a general population.

    In our prospective cohort study, bedroom light intensity was measured at 1-min intervals in 678 elderly participants without diabetes at baseline. The average light intensity recorded between bedtimes and rise times over two consecutive nights was used in the analysis.

    During follow-up (median, 42 months), 19 of the 678 participants (mean age, 70.6 years) developed diabetes. Poisson regression models revealed that the incidence rate for diabetes was significantly higher in the LAN group (average ≥ 5 lux, N = 128) than the dark group (average < 5 lux, N = 550) (incidence rate ratio, 3.74; 95% confidence interval (CI), 1.55-9.05; p = 0.003). Further propensity score adjustments in relation to LAN produced consistent results (incidence rate ratio, 3.19; 95% CI, 1.38-7.35; p = 0.007). When the cut-off value of LAN was decreased to 3 lux, the relationship remained significant (incidence rate ratio 2.74; 95% CI, 1.19-6.33; p = 0.018).

    Our findings suggest that LAN exposure increases the incidence of diabetes in a general elderly population. Further research involving a large cohort with new-onset diabetes is warranted to elucidate these findings.

    zajebista animacja:

    Hours of daylight as a function of day of the year and latitude
    Ostatnio edytowane przez htw ; 11-11-19 o 18:25
    correlation doesn't imply causation

  12. #927
    18:25 - to już grubo po zachodzie słońca, a Ty przed komputerem.
    łumrzesz na śmierć.

  13. #928
    Sztywny Pal Azji
    May 2014
    2 552
    w punkt !
    ale nie musisz się o mnie martwić, mój sprzęt jest prawie idealnie melanopsynowo zaadaptowany
    lecz dziękuję za troskę.
    Ostatnio edytowane przez htw ; 12-11-19 o 07:48
    correlation doesn't imply causation

  14. #929
    a adoptuj sobie kogo chcesz,ja pod pierzynę Ci nie będę zaglądał, oby sprzęt działał.

    Ostatnio edytowane przez Mastif ; 12-11-19 o 07:54

  15. #930
    Sztywny Pal Azji
    May 2014
    2 552
    Przewlekły stres psychospołeczny tłumi produkcję dopaminy

    U ludzi, którzy przez długi czas zmagają się przeciwnościami psychospołecznymi, są np. ofiarami przemocy, upośledzeniu ulega zdolność produkowania ilości dopaminy koniecznych do poradzenia sobie z sytuacjami stresowymi.
    Wyniki, które ukazały się w piśmie eLife, wyjaśniają, czemu długotrwała ekspozycja na traumę psychologiczną i przemoc może stanowić czynnik ryzyka choroby psychicznej czy uzależnień.
    Wiedzieliśmy, że chroniczne przeciwności psychospołeczne mogą skutkować podatnością na choroby psychiczne, np. depresję czy schizofrenię. Dotąd brakowało nam jednak precyzyjnego mechanistycznego wyjaśnienia, w jaki sposób dochodzi do zwiększenia ryzyka - opowiada dr Michael Bloomfield z Uniwersyteckiego College'u Londyńskiego.
    By się tego dowiedzieć, naukowcy zebrali grupę 34 ochotników. Połowę cechowała duża kumulatywna ekspozycja na przeciwności psychospołeczne. Resztę próby stanowiła dopasowana pod względem wieku i płci grupa kontrolna (z niską kumulatywną ekspozycją).
    Wszyscy przeszli procedurę wywołania ostrego stresu społecznego za pomocą Montréal Imaging Stress Task (MIST). Dwie godziny później badanym wstrzyknięto znacznik, który pozwalał prześledzić produkcję dopaminy w mózgu za pomocą pozytonowej tomografii emisyjnej (PET).
    Okazało się, że u osób z grupy kontrolnej produkcja dopaminy korelowała (była proporcjonalna) ze stopniem postrzeganego zagrożenia i reakcją fizjologiczną na ostry stres. U ochotników z dużą ekspozycją kumulatywną na przeciwności psychospołeczne percepcja zagrożenia była zaś wyolbrzymiona, a synteza dopaminy w prążkowiu upośledzona. Stłumione były również inne fizjologiczne reakcje na stres; ciśnienie i poziomy kortyzolu nie rosły np. w takim stopniu jak w grupie kontrolnej.

    To badanie nie stanowi dowodu, że przewlekły stres psychospołeczny wywołuje chorobę psychiczną lub nadużywanie substancji psychoaktywnych na późniejszych etapach życia. Wskazaliśmy jednak prawdopodobny mechanizm, który sugeruje, że chroniczny stres może podwyższać ryzyko choroby psychicznej, zmieniając mózgowy układ dopaminergiczny.
    By lepiej zrozumieć, jak wywołane przeciwnościami psychospołecznymi zmiany w układzie dopaminergicznym mogą zwiększać podatność na choroby psychiczne i uzależnienie, potrzebne są dalsze badania - podsumowuje prof. Oliver Howes z King's College London.,31016

    Niewielka mutacja genetyczna genu COMT wraz z silnie stresującymi sytuacjami z dzieciństwa znacznie zwiększa ryzyko uzależnienia od narkotyków i alkoholu

    Mocno stresujące doświadczenia z dzieciństwa wraz z niewielką mutacją genetyczną genu COMT znacznie zwiększają ryzyko uzależniania od alkoholu lub narkotyków – wynika z nowych badań przeprowadzonych na Uniwersytetu Oklahomy.

    Dlaczego niektórzy ludzie są bardziej podatni na uzależnienia od alkoholu i narkotyków? To pytanie od dawna nurtuje naukowców. Dr William R. Lovallo z Uniwersytetu Oklahomy poświęcił na zgłębienie tego zagadnienia 20 lat badań. Sprawdzał, w jaki sposób geny danej osoby przyczyniają się do uzależnienia. Jego celem było zrozumienie przyczyn uzależnienia i sposoby zapobiegania.

    ćwiczenia zrobią z Ciebie faradaja:

    12 November 2019
    Moderate exercise training reduced the harmful effects of electromagnetic radiation emitted from a cell phone on hematological parameters in male Wistar rats

    Twenty-four male Wistar rats (10 weeks old) were randomly assigned to e exposure to RF-EMR (RF-EMR) group, exercise group RF-EMR plus exercise (RF-EMR + Exercise) group, and control group. The rats in the exposure to RF-EMR groups (RF-EMR and RF-EMR + exercise) were exposed to RF-EMR 3 h/day for 28 days. The rats in the exercise groups (exercise and RF-EMR + exercise) were administered to moderate exercise training 6 days a week for 28 days. After 28 days, animals were sacrificed 24 h following the completion of the experiment, and hematological parameters, including complete blood count, were assessed.

    Exposure to RF-EMR induced a significant decrease in RBC, HGB, HCT, MCV, MCH, and MCHC, and an increase in PLT and WBC in compared with the control group (p < 0.05). However, most of the hematological parameters of the RF-EMR + exercise group were similar to the control group (except for PLT) that showed the inhibitory effect of exercise training against the harmful effects of cell phone radiation.

    28 day moderate exercise training is beneficial to attenuate the harmful effects of RF-EMR emitted from the cell phone.

    i coś o zachodzie:

    Melatonin as a mitochondria-targeted antioxidant: one of evolution’s best ideas

    Fig. 3 Melatonin is believed to exist in most, possibly all, animal and plant species. It predictably evolved 3.0–2.5 billion years ago in photosynthetic cyanobacteria as an antioxidant; this function has been retained to the present day including in humans. Other functions of melatonin, many more than are shown in this figure, appeared at later stages of evolution. Reprinted with permission

    Fig. 8 The targeting of melatonin to the mitochondria; evidence suggests that melatonin enters the mitochondria through specific transporters, PETP 1/2 (oligopeptide transporters). The actions of melatonin in mitochondria are multiple. These actions, particularly including its ability to reduce oxidative damage to critical mitochondrial molecules, preserve the function of these organelles and benefit diseases in which mitochondrial malfunction is a feature. Melatonin increases the efficiency of the electron transport chain (I, II, III and IV) and improves ATP production (ATP synthase). Reactive oxygen species (ROS) produced when electrons leak from the ETC are directly scavenged by melatonin and its metabolite [N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK)]. ROS are also metabolized by mitochondria superoxide dismutase (SOD2) and scavenged by glu

    i antynowotworowa

    11 November 2019
    Melatonin activates cell death programs for the suppression of uterine leiomyoma cell proliferation

    The circadian nature of melatonin has a protective effect on the progression of female reproductive cancers, including in breast and ovarian cancers. However, the effect of melatonin on the growth of uterine leiomyoma is still unclear. In this study, we found that the growth of uterine leiomyoma ELT3 cells was reduced by treatment with melatonin. Treatment with melatonin increased the distribution of sub‐G1 phase and increased DNA condensation in ELT3 cells. Melatonin‐induced apoptosis and autophagy cell death progression was observed in ELT3 cells. Melatonin exerts a highly selective effect on primary normal human uterine smooth muscle (UtSMC) cells. The UtSMC cell cycle was arrested by melatonin treatment through up‐regulation of p21, p27, and PTEN protein expression, but melatonin did not further promote apoptosis program activation. Melatonin reduced cell proliferation in ELT3 cells underlying the activation of melatonin MT1 and MT2 receptors, which in turn down‐regulated the Akt‐ERK1/2‐NFκB signaling pathway. Melatonin reduced ELT3 tumor growth in both xenograft and orthotopic uterine tumor mice models. The extracellular matrix of the tumor was also reduced by melatonin treatment. Taken together, these results suggest that melatonin potentially plays a role in suppression of uterine leiomyoma growth.

    leki które upośledzają metabolizm, może ktoś zainteresowany ?

    Ostatnio edytowane przez htw ; 13-11-19 o 16:13
    correlation doesn't imply causation

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