ForSa punya logo baru!! Ada komen?
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sayang bener 20 tahun gak nikmatin hidup.
Kutipsayang bener 20 tahun gak nikmatin hidup. tergantung mimpi apa dunk buatku, tidur tuh obat yg paling manjur utk mengatasi segala macam stress dan kekesalan eh tp soal anjing itu, kok bisa ya, apa siklus tidur anjing atau hewan lain (deep sleep dsb itu, mesti cek dulu nih ) berbeda dg manusia ya?
The Harvard Women’s Health Watch suggests six reasons to get enough sleep:- Learning and memory: Sleep helps the brain commit new information to memory through a process called memory consolidation. In studies, people who’d slept after learning a task did better on tests later.
- Metabolism and weight: Chronic sleep deprivation may cause weight gain by affecting the way our bodies process and store carbohydrates, and by altering levels of hormones that affect our appetite.
- Safety: Sleep debt contributes to a greater tendency to fall asleep during the daytime. These lapses may cause falls and mistakes such as medical errors, air traffic mishaps, and road accidents.
- Mood: Sleep loss may result in irritability, impatience, inability to concentrate, and moodiness. Too little sleep can also leave you too tired to do the things you like to do.
- Cardiovascular health: Serious sleep disorders have been linked to hypertension, increased stress hormone levels, and irregular heartbeat.
- Disease: Sleep deprivation alters immune function, including the activity of the body’s killer cells. Keeping up with sleep may also help fight cancer.
Seinget gw sih dulu pas smu diajarin kl waktu tidur metabolisme tubuh kita jd lebih lambat, dan saat itu digunain otak untuk istirahat dan tubuh untuk regenerasi sel-sel yang rusak. So...tidur aja lagi...enak ini.. Bener gak yah?
Yang masih jadi pertanyaan buat gue...ngaruh ngga sih kl kita punya jam tidur yg kebalik? (mis: tidur pagi-siang, ngga tidur malem-pagi).. Atau badan kita release hormon/chemicals tertentu pada malam hari yg ga bagus? *kaya tumbuhan*
Sleep and circadian rhythms: do sleep centers talk back to the clock?A homeostatic control mechanism that monitors and reacts to the need for sleep has been thought to function independently of the brain's circadian clock in previous studies. Now simultaneous recordings of sleep stages and electrical activity in the suprachiasmatic nucleus in behaving animals reveal feedback from sleep centers to the circadian pacemaker.
nature.com/neuro/journal/v6/n10/full/nn1003-1005.htmlKutipSleep and circadian rhythms: do sleep centers talk back to the clock?A homeostatic control mechanism that monitors and reacts to the need for sleep has been thought to function independently of the brain's circadian clock in previous studies. Now simultaneous recordings of sleep stages and electrical activity in the suprachiasmatic nucleus in behaving animals reveal feedback from sleep centers to the circadian pacemaker.bentar, mo baca dulu
Missing out on sleep may cause the brain to stop producing new cells, a study has suggested.The work on rats, by a team from Princeton University found a lack of sleep affected the hippocampus, a brain region involved in forming memories.The research in Proceedings of the National Academy of Science showed a stress hormone causes the effect.A UK expert said it would be interesting to see if too little rather than no sleep had the same consequence.DeficitsThe researchers compared animals who were deprived of sleep for 72 hours with others who were not.They found those who missed out on rest had higher levels of the stress hormone corticosterone. It would be interesting to see if partial sleep deprivation - getting a little bit less sleep every night that you need - had the same effectDr Neil Stanley, sleep expertThey also produced significantly fewer new brain cells in a particular region of the hippocampus.When the animals' corticosterone levels were kept at a constant level, the reduction in cell proliferation was abolished.The results suggest that elevated stress hormone levels resulting from sleep deprivation could explain the reduction in cell production in the adult brain.Sleep patterns were restored to normal within a week.However levels of nerve cell production (neurogenesis) were not restored for two weeks, and the brain appears to boost its efforts in order to counteract the shortage.Writing in PNAS, the researchers led by Dr Elizabeth Gould, said that although the role of nerve cell production in adults remained unknown, "the suppression of adult neurogenesis may underlie some of the cognitive deficits associated with prolonged sleep deprivation."People who experience a lack of sleep experience concentration problems and other difficulties.Sleep expert Dr Neil Stanley, based at the Norfolk and Norwich University Hospital, said the study's findings could not be directly translated to humans because people did not go without sleep for 72 hours, unless they were in extreme circumstances.But he added: "It is an interesting finding. It would be interesting to see if partial sleep deprivation - getting a little bit less sleep every night that you need - had the same effect."
Wah...admin nya dedicated bener... Nanya sendiri, jawab sendiri, dan slalu datang dgn info2 dan temuan reference2 baru..Salut buat om admin! Keep up the good work, min. *oops...out of topic*Kalo 'no sleep = no new brain cells', hipersomnia bahaya gak ya?
Udah selesai blom bacanya... itu artikel musti bayar, gak bisa akses
Models of sleep regulation have emphasized two distinct processes: a sleep homeostat and a circadian process. A circadian process is a clocklike mechanism responsible for the tendency to sleep during certain phases of 24-hour cycle, independent of prior sleep and wakefulness. The sleep homeostat is responsible for monitoring and reacting to the need for sleep, causing the urge to sleep to depend on prior amounts of sleep or wakefulness. Because, after staying up for the whole night, the increase in alertness you feel in the morning is usually followed by a very sleepy afternoon (=sleep rebound after deprivation), scientists have agreed that ultimately the sleep homeostat and the circadian system must interact to regulate the propensity, duration, and intensity of sleep. The paper I quoted previously (“Sleep and circadian rythms: do sleep centers talk back to the clock?â€) showed the first physiological evidence that sleep homeostat can actually regulate the neural activities involved in circadian process. Newer review (1) has been able to model the major pathways that translate the output from brain’s sleep homeostat into the circadian rythms of sleep, feeding, corticosteroid secretion, and body temperature. The circadian rythms have been shown to have flexibility in organizing daily schedules. For example, animals that are given food only during normal sleep cycle soon invert their circadian cycle to be awake when the food is presented. It is also becoming clear that the drive for sleep is also shaped by emotional and cognitive inputs. Under some condition, such as in shift work or during an emergency situation, this ability to overcome the more basic drives can be adaptive. The cognitive and emotional systems might suppress some mechanisms (suppress the firing of VLPO neurons, thus disinhibiting the orexin and tuberomammilary neurons; read a bit more in flip-flop switch below) to overcome homeostatic sleep pressure. However, when emotional states such as stress prevent sleep, the process can be maladaptive (e.g. insomnia). The flip-flop switch hypothesis:The flip-flop switch illustrates the relationship between the VLPO (en.wikipedia.org/wiki/Ventrolateral_preoptic_nucleus) and components of the ascending arousal (wakefulness) system (receptors and their neurotransmitters e.g. serotonin, noradrenergic afferents, histaminergic tuberomammilary nucleus /TMN, including orexin neurons). Such a switch, like in electrical circuit, produces sharp transition between sleep and wakefulness. This has obvious advantages in animal, since moving about while not fully alert would pose numerous risks such as becoming an easy target for predators. However, flip-flop switches might also undergo unwanted state transitions when the switch is pushed close to its transition point by environmental perturbation (e.g. monotony while driving, an innocuous sound while sleeping). Orexin neurons may act to stabilize the flip-flop switch and prevent unwanted transitions by activating the monoaminergic systems and keep the switch in the arouse position during wakefulness.Sumber:1. Saper CB, Cano G, Scammell TE. "Homeostatic, circadian, and emotional regulation of sleep". J Comp Neurol. 2005 Dec 5;493(1):92-8Bacaan lain yg jg menarik:2. Borbely AA, Achermann P. "Sleep homeostasis and models of sleep regulation". J Biol Rhythms. 1999 Dec;14(6):557-683. Mistlberger RE. "Circadian regulation of sleep in mammals: role of the suprachiasmatic nucleus". Brain Res Brain Res Rev. 2005 Nov;49(3):429-54.
Sleep can be defined as a state of immobility with greatly reduced responsiveness, which can be distinguished from coma or anaesthesia by its rapid reversibility. An additional defining characteristic of sleep is that when it is prevented, the body tries to recover the lost amount. The functions of mammalian sleep still remain unclear. However, the argument that sleep serves a vital function is compelling. Sleep deprivation in rodents and flies can cause death more quickly than food deprivation (although sleep lost does not have equal effects in all animals). Also the fact that sleep debt can be accumulated suggests that sleep serves important functions that require some portion of the missed sleep amount to be made up. Although motivated humans can overcome sleepiness for short periods, they cannot perform at high levels for sustained periods. Daily sleep amounts vary substantially from mammal to mammal. Some animals, such as bats and opossums, sleep for 18–20 hours a day. Others, such as the elephant and giraffe, sleep for as little as 3–4 hours a day. One might expect species in each mammalian order to have a similar sleep pattern because of their genetic, behavioural and anatomical similarities. This is not the case. Differences in order do not simply explain differences in sleep amounts. Primates as a group do not have sleep characteristics that distinguish them from Rodentia, Insectivora or other orders. Humans, in particular, do not seem to have amounts or aspects of REM sleep or NREM sleep that distinguish them from other species, although they do have less sleep (more waking) than most omnivores. One aspect of sleep strongly linked to body mass and brain size is the duration of the sleep cycle, that is, the average time taken to cycle from NREM sleep onset, through REM sleep, to waking. Small animals have shorter sleep cycles, and cycle times range from about 8 minutes in the short-tailed shrew (Blarina brevicauda) to 1.8 hours in the Asiatic elephant (Elephas maximus). The reason for this robust correlation is not known. Possible explanations include the inverse correlation of metabolic rate with body mass and brain mass, the thermal inertia of the brain and body, the time required for diffusion of substances through the brain parenchyma or the time required to complete a particular anabolic or catabolic biochemical task.Theories of REM sleep function While most theories suggest a role for non-rapid eye movement (NREM) sleep in energy conservation and in nervous system recuperation; REM sleep, the state in which our most vivid dreams occur, has inspired a multitude of functional theories. The identification of the ‘dream state’ as a periodic physiological process during sleep has encouraged the addition of physiological and psychological theories to the more mystical theories of the ancients. REM sleep is ‘paradoxical’ in the sense that although an animal in REM sleep is behaviourally sleep, brain metabolic and neuronal activity are high, respiration and heart rate are variable, rapid eye movements and twitches of the extremities occur and males frequently develop erections. These phenomena and the vivid dreams that humans report upon awakening from REM sleep have made the function of this state particularly mysterious and intriguing. Although behavioural immobility and reduced overall body metabolic rate relative to active waking are maintained, why has this state evolved whencontinued NREM sleep, with its reduction in brain metabolic activity, would seem to be more efficient at achieving the recuperative and energy-saving effects of sleep?Memory consolidation The idea that either REM or NREM sleep is ‘absolutely required’ for memory consolidation has received much attention recently. Certainly disturbed sleep is not conducive to concentration and learning, but an essential role for sleep in memory consolidation remains unprovenREM sleep and development REM sleep amount is positively correlated with total sleep amount and negatively correlated with body weight. However, if one statistically controls for body weight or brain weight, REM sleep amount is most strongly correlated with immaturity at birth. Altricial mammals, those that are immature at birth, tend to have more REM sleep than mammals that are mature at birth, or precocial. This tendency is marked in the neonatal period. But perhaps more remarkable is that altricial animals continue to have more REM sleep as adults. The platypus has 8 hours of REM sleep per day as an adult and the neonate cannot thermoregulate, locomote, acquire food or defend itself at birth and lives attached to its mother. The ferret, likewise, is immature at birth, and the adult has over 6 hours of REM sleep per day. By contrast, the guinea pig has only 1 hour of REM sleep per day as an adult. The guinea pig is born with teeth, claws, fur and open eyes; it thermoregulates at birth, locomotes within an hour of birth and eats solid food within a day of birth. Similarly, the sheep and giraffe are relatively mature at birth and have little REM sleep (less than 1 hour per day) at maturity. Although the nature of sleep states early in the development of the rat differs from adult patterns, the brainstem mechanisms generating REM sleep are present at birth. The extremely high levels of REM sleep seen at birth, followed by a slow decrease to adult levels seen in many terrestrial mammals, must be an important clue to its function. This time course, combined with the observation that neuronal activity levels are high during REM sleep, led to the hypothesis that this sleep state is involved in the development of the brain. REM sleep in adults If we accept that the large amount of REM sleep early in life serves to maintain or establish brain connections during crucial periods of development, what is the function of this state later in life? One idea that has been proposed repeatedly is that REM sleep stimulates the adult brain during sleep to reverse the effects of NREM sleep on immediately subsequent waking behaviour. Animals typically awaken spontaneously from REM sleep. Animals that are awakened from NREM sleep have poor sensory-motor function compared with those awakened from REM sleep. Awakening in a more alert state would convey a substantial selective advantage. In humans, the duration of REM sleep episodes progressively increases throughout the sleep period and is maximal at the expected time of awakening. The initial REM sleep period of the night may last only 5–10 minutes, whereas the last REM sleep period may last more than 25 minutes. The intensity of REM sleep, as measured by the density of eye movements and twitches, the prevalence of erections in males and the vividness of dream reports also increases as the night progresses. REM sleep amounts are maximal near the nadir of the brain and core body temperature cycles. And temperature in several brain regions increases during REM sleep, even though the regulation of body temperature is largely suppressed during REM sleep. It might be also that the normal function of REM sleep is to dampen activity and emotional expression by causing the changes in monoaminergic systems. REM sleep deprivation has antidepressive effects. The monoaminergic systems are well known to be involved in emotional regulation, and most antidepressive medications act through effects on monoaminergic systems and suppress REM sleep.
Lho, aku kira jurnal Nature bisa diakses gratis? Anyway, ini sekedar summary singkat, aku quote dr sana-sini. Nggak detil sih. Lebih asyik baca artikel aslinya tentu. Sayang nggak memungkinkan ya utk ada data base artikel2 koleksi pribadi para member di FS?
The functions of mammalian sleep still remain unclear.
If we accept that the large amount of REM sleep early in life serves to maintain or establish brain connections during crucial periods of development, what is the function of this state later in life?
Tapi blum jelas kan berarti berapa lama kita harus tidur sebenernya? Apa harus 8 jam sehari, 6 jam sehari atau gak perlu tiap hari tidur Agak ngelantur dikit, waktu seperti jam, hari, bulan, tahun, itu kan kita yang buat karena beberapa alasan tertentu. Nah, apa bener ini juga sesuai dengan waktu biologis kita?
Kegunaan tidur sendiri juga blom jelas rasanya (kalo gak salah baca), dia masih pake remain unclear, perhaps, it might be, possible explanation, etc (atau subyektif yahh ini ).
What is shift work sleep disorder (SWSD)?Shift work sleep disorder is a sleep disorder that affects people who frequently rotate shifts or work at night, contrary to the body’s natural circadian rhythms, and cannot adjust to their schedule. It consists of a constant or recurrent pattern of sleep interruption that results in insomnia or excessive sleepiness. Shift work sleep disorder is common in people who work nontraditional hours, usually between 10:00 pm and 6:00 am. How many people suffer from shift work sleep disorder? Nearly six million full-time employees in the US work at night on a regular or rotating basis Approximately one quarter of these night shift workers are estimated to have SWSD What are the symptoms of shift work sleep disorder? The most common symptoms of shift work sleep disorder are insomnia and excessive sleepiness. Other symptoms of shift work sleep disorder include: Difficulty concentrating Headaches Lack of energy Not every shift worker suffers from shift work sleep disorder.