inflammation _____

A female student， aged 18 years，w ho fell on her buttocks in a bicycle accident presents with swollen soft tissue， hot skin， and tenderness in the left buttock. The doctor suspects inflammation， where the patient has traumatic inflammation besides bacterial infection. Which of the following is NOT among the possible pathologic responses? 资料：Because of the biochemical reactions in your body that occur with every type of food you eat on a daily bases, some foods age you faster than your real age, while other foods help to fight aging.Three of the processes that go on inside your body that have a major impact on your rate of aging are called “glycation”, “inflammation” and “oxidation”.When we talk about aging, we’re not just talking about wrinkles on your skin or how thick your hair is, we’re also talking about factors that you can’t see, such as how well your organs function, and whether your joints are degrading.The passage is probably___. 资料：Because of the biochemical reactions in your body that occur with every type of food you eat on a daily bases, some foods age you faster than your real age, while other foods help to fight aging.Three of the processes that go on inside your body that have a major impact on your rate of aging are called “glycation”, “inflammation” and “oxidation”.When we talk about aging, we’re not just talking about wrinkles on your skin or how thick your hair is, we’re also talking about factors that you can’t see, such as how well your organs function, and whether your joints are degrading.According to the passage, aging is about all the following except--. 根据以下材料，回答Hair loss can be destructive for themillions of men and women who experience it. Now scientists are reporting thata substance from honeybee hives might contain clues for developing a potentialnew therapy. They found that the material, called propolis, encouraged hairgrowth in mice. The study appears in A CS′ Journal of Agricultural and FoodChemistry. Ken Kobayashi and colleagues note that propolis is a resin-likematerial that honeybees use to seal small gaps in their hives. Not only does itwork as a physical barrier, but it also contains active compounds that fightfungal and bacterial invasions. People from ancient times had noticed propolis′special properties and used it to treat tumors, inflammation and wounds. Morerecently, research has shown that the substance promotes the growth of certaincells involved in hair growth though no one had yet tested whether that in turnwould result in new locks. Kobayashi ′ s team wanted to find out.When the researchers tested propolis onmice that had been shaved or waxed, the mice that received the treatment regrewtheir fur faster than those that didn′t. The scientists also noticed that afterthe topical application, the number of special cells involved in the process ofgrowing hair increased. Although they tried the material on mice that couldgrow fur rather than balding mice, the researchers note that hair lossconditions often result from abnormal inflammation. Propolis contains anti-inflammatorycompounds, so they expert it could help treat balding conditions.They add that further testing is needed tosee if the beehive material affects human hair follicles.What may cause hair loss according tothe passage? 根据以下材料，回答Hair loss can be destructive for themillions of men and women who experience it. Now scientists are reporting thata substance from honeybee hives might contain clues for developing a potentialnew therapy. They found that the material, called propolis, encouraged hairgrowth in mice. The study appears in A CS′ Journal of Agricultural and FoodChemistry. Ken Kobayashi and colleagues note that propolis is a resin-likematerial that honeybees use to seal small gaps in their hives. Not only does itwork as a physical barrier, but it also contains active compounds that fightfungal and bacterial invasions. People from ancient times had noticed propolis′special properties and used it to treat tumors, inflammation and wounds. Morerecently, research has shown that the substance promotes the growth of certaincells involved in hair growth though no one had yet tested whether that in turnwould result in new locks. Kobayashi ′ s team wanted to find out.When the researchers tested propolis onmice that had been shaved or waxed, the mice that received the treatment regrewtheir fur faster than those that didn′t. The scientists also noticed that afterthe topical application, the number of special cells involved in the process ofgrowing hair increased. Although they tried the material on mice that couldgrow fur rather than balding mice, the researchers note that hair lossconditions often result from abnormal inflammation. Propolis contains anti-inflammatorycompounds, so they expert it could help treat balding conditions.They add that further testing is needed tosee if the beehive material affects human hair follicles.What′s the main idea of the passage? 根据以下材料，回答Hair loss can be destructive for themillions of men and women who experience it. Now scientists are reporting thata substance from honeybee hives might contain clues for developing a potentialnew therapy. They found that the material, called propolis, encouraged hairgrowth in mice. The study appears in A CS′ Journal of Agricultural and FoodChemistry. Ken Kobayashi and colleagues note that propolis is a resin-likematerial that honeybees use to seal small gaps in their hives. Not only does itwork as a physical barrier, but it also contains active compounds that fightfungal and bacterial invasions. People from ancient times had noticed propolis′special properties and used it to treat tumors, inflammation and wounds. Morerecently, research has shown that the substance promotes the growth of certaincells involved in hair growth though no one had yet tested whether that in turnwould result in new locks. Kobayashi ′ s team wanted to find out.When the researchers tested propolis onmice that had been shaved or waxed, the mice that received the treatment regrewtheir fur faster than those that didn′t. The scientists also noticed that afterthe topical application, the number of special cells involved in the process ofgrowing hair increased. Although they tried the material on mice that couldgrow fur rather than balding mice, the researchers note that hair lossconditions often result from abnormal inflammation. Propolis contains anti-inflammatorycompounds, so they expert it could help treat balding conditions.They add that further testing is needed tosee if the beehive material affects human hair follicles.Which of the following is wrong aboutpropolis? 根据以下材料，回答Hair loss can be destructive for themillions of men and women who experience it. Now scientists are reporting thata substance from honeybee hives might contain clues for developing a potentialnew therapy. They found that the material, called propolis, encouraged hairgrowth in mice. The study appears in A CS′ Journal of Agricultural and FoodChemistry. Ken Kobayashi and colleagues note that propolis is a resin-likematerial that honeybees use to seal small gaps in their hives. Not only does itwork as a physical barrier, but it also contains active compounds that fightfungal and bacterial invasions. People from ancient times had noticed propolis′special properties and used it to treat tumors, inflammation and wounds. Morerecently, research has shown that the substance promotes the growth of certaincells involved in hair growth though no one had yet tested whether that in turnwould result in new locks. Kobayashi ′ s team wanted to find out.When the researchers tested propolis onmice that had been shaved or waxed, the mice that received the treatment regrewtheir fur faster than those that didn′t. The scientists also noticed that afterthe topical application, the number of special cells involved in the process ofgrowing hair increased. Although they tried the material on mice that couldgrow fur rather than balding mice, the researchers note that hair lossconditions often result from abnormal inflammation. Propolis contains anti-inflammatorycompounds, so they expert it could help treat balding conditions.They add that further testing is needed tosee if the beehive material affects human hair follicles.The underline sentence in thefirst paragraph means ___________. 资料：Because of the biochemical reactions in your body that occur with every type of food you eat on a daily bases, some foods age you faster than your real age, while other foods help to fight aging.Three of the processes that go on inside your body that have a major impact on your rate of aging are called “glycation”, “inflammation” and “oxidation”.When we talk about aging, we’re not just talking about wrinkles on your skin or how thick your hair is, we’re also talking about factors that you can’t see, such as how well your organs function, and whether your joints are degrading.What may make you feel 10 years older than your real age? When we eat may be just as important as what we eat. A new study shows that mice that eat when they should be sleeping gain more weight than mice that eat at normal hours. Another study sheds light on why we pack on the pounds in the first place. Whether these studies translate into therapies that help humans beat obesity remains to be seen, but they give scientists clues about the myriad factors that they must take into account.　　Observations of overnight workers have shown that eating at night disrupts metabolism and the hormones that signal we’re sated. But no one had done controlled studies on this connection until now. Biologist Fred Turek of Northwestern University in Evanston, Illinois, and graduate student Deanna Arble examined the link between a high-fat diet and what time of day mice eat. A control group of six nocturnal mice ate their pellets (60％ fat by calories, mostly lard) during the night. Another group of six ate the same meal during the day, Turek says, which disrupts their circadian rhythm—the body’s normal 24-hour cycle.　　After 6 weeks, the off-schedule mice weighed almost 20％ more than the controls, Turek and Arble report today in?Obesity, supporting the idea that consuming calories when you should be sleeping is harmful. Turek and Arble acknowledge that the disrupted mice ate a tad more and were a tad more sluggish, but the differences could not account for all of the weight gain.　　In the second study, a different team of researchers investigated the link between weight and the immune system. Hundreds of genes seem to affect the accumulation of fat, but one that helps protect us from infection might help us lose weight with little effort, biochemist Alan Saltiel of the University of Michigan, Ann Arbor, and colleagues suggest today in?Cell. The researchers tested me weight-adding abilities of a protein called IKK∈, which is linked with obesity, diabetes, and chronic, low-1evel inflammation. For 3 months, the team fed six When we eat may be just as important as what we eat. A new study shows that mice that eat when they should be sleeping gain more weight than mice that eat at normal hours. Another study sheds light on why we pack on the pounds in the first place. Whether these studies translate into therapies that help humans beat obesity remains to be seen, but they give scientists clues about the myriad factors that they must take into account.　　Observations of overnight workers have shown that eating at night disrupts metabolism and the hormones that signal we’re sated. But no one had done controlled studies on this connection until now. Biologist Fred Turek of Northwestern University in Evanston, Illinois, and graduate student Deanna Arble examined the link between a high-fat diet and what time of day mice eat. A control group of six nocturnal mice ate their pellets (60％ fat by calories, mostly lard) during the night. Another group of six ate the same meal during the day, Turek says, which disrupts their circadian rhythm—the body’s normal 24-hour cycle.　　After 6 weeks, the off-schedule mice weighed almost 20％ more than the controls, Turek and Arble report today in?Obesity, supporting the idea that consuming calories when you should be sleeping is harmful. Turek and Arble acknowledge that the disrupted mice ate a tad more and were a tad more sluggish, but the differences could not account for all of the weight gain.　　In the second study, a different team of researchers investigated the link between weight and the immune system. Hundreds of genes seem to affect the accumulation of fat, but one that helps protect us from infection might help us lose weight with little effort, biochemist Alan Saltiel of the University of Michigan, Ann Arbor, and colleagues suggest today in?Cell. The researchers tested me weight-adding abilities of a protein called IKK∈, which is linked with obesity, diabetes, and chronic, low-1evel inflammation. For 3 months, the team fed six When we eat may be just as important as what we eat. A new study shows that mice that eat when they should be sleeping gain more weight than mice that eat at normal hours. Another study sheds light on why we pack on the pounds in the first place. Whether these studies translate into therapies that help humans beat obesity remains to be seen, but they give scientists clues about the myriad factors that they must take into account.　　Observations of overnight workers have shown that eating at night disrupts metabolism and the hormones that signal we’re sated. But no one had done controlled studies on this connection until now. Biologist Fred Turek of Northwestern University in Evanston, Illinois, and graduate student Deanna Arble examined the link between a high-fat diet and what time of day mice eat. A control group of six nocturnal mice ate their pellets (60％ fat by calories, mostly lard) during the night. Another group of six ate the same meal during the day, Turek says, which disrupts their circadian rhythm—the body’s normal 24-hour cycle.　　After 6 weeks, the off-schedule mice weighed almost 20％ more than the controls, Turek and Arble report today in?Obesity, supporting the idea that consuming calories when you should be sleeping is harmful. Turek and Arble acknowledge that the disrupted mice ate a tad more and were a tad more sluggish, but the differences could not account for all of the weight gain.　　In the second study, a different team of researchers investigated the link between weight and the immune system. Hundreds of genes seem to affect the accumulation of fat, but one that helps protect us from infection might help us lose weight with little effort, biochemist Alan Saltiel of the University of Michigan, Ann Arbor, and colleagues suggest today in?Cell. The researchers tested me weight-adding abilities of a protein called IKK∈, which is linked with obesity, diabetes, and chronic, low-1evel inflammation. For 3 months, the team fed six Passage 1Lonely people, it seems, are at greater risk than the gregarious of developing illnessesassociated with chronic inflammation, such as heart disease and certain cancers. A paper publishedlast year in the Public Library of Science, Medicine, shows the effect on mortality of loneliness iscomparable with that of smoking and drinking after examining the results of 148 previous studiesand controlled for factors such as age and pre-existing illness.Steven Cole of the University of California, Los Angeles, thinks he may know why this is so.He told the American Association for the Advancement of Science meeting in Washington, D.C.,about his work studying the expression of genes in lonely people. Dr. Cole harvested samples ofwhite blood cells from both lonely and gregarious people. He then analysed the activity of theirgenes, as measured by the production of a substance called messenger RNA. This molecule carriesinstructions from the genes telling a cell which proteins to make. The level of messenger RNA frommost genes was the same in both types of people. There were several dozen genes, however, thatwere less active in the lonely, and several dozen others that were more active. Moreover, both theless active and the more active gene types came from a small number of functional groups.Broadly speaking, the genes less active in the lonely were those involved in staving off viralinfections. Those that were more active were involved in protecting against bacteria. Dr. Colesuspects this could help explain not only why the lonely are iller, but how, in evolutionary terms, thisodd state of affairs has come about.The crucial bit of the puzzle is that viruses have to be caught from another infected individualand they are usually species-specific. Bacteria, in contrast, often just lurk in the environment, andmay thrive on many hosts. The gregarious are therefore at greater risk than the lonely of catchingviruses, and Dr. Cole thus suggests that past evolution has created a mechanism which causes whitecells to respond appropriately. Conversely, the lonely are better off ramping up their protectionagainst bacterial infection, which is a bigger relative risk to them.What Dr. Cole seems to have revealed, then, is a mechanism by which social environmentreaches inside a person′ s body and tweaks its genome so that it responds appropriately. It is not thatthe lonely and the gregarious are genetically different from each other. Rather, their genes areregulated differently, according to how sociable an individual is. Dr. Cole thinks this regulation ispart of a wider mechanism that tunes individuals to the circumstances they find themselves in.What message does Dr. Cole seem to convey by the mechanism Passage 1Lonely people, it seems, are at greater risk than the gregarious of developing illnessesassociated with chronic inflammation, such as heart disease and certain cancers. A paper publishedlast year in the Public Library of Science, Medicine, shows the effect on mortality of loneliness iscomparable with that of smoking and drinking after examining the results of 148 previous studiesand controlled for factors such as age and pre-existing illness.Steven Cole of the University of California, Los Angeles, thinks he may know why this is so.He told the American Association for the Advancement of Science meeting in Washington, D.C.,about his work studying the expression of genes in lonely people. Dr. Cole harvested samples ofwhite blood cells from both lonely and gregarious people. He then analysed the activity of theirgenes, as measured by the production of a substance called messenger RNA. This molecule carriesinstructions from the genes telling a cell which proteins to make. The level of messenger RNA frommost genes was the same in both types of people. There were several dozen genes, however, thatwere less active in the lonely, and several dozen others that were more active. Moreover, both theless active and the more active gene types came from a small number of functional groups.Broadly speaking, the genes less active in the lonely were those involved in staving off viralinfections. Those that were more active were involved in protecting against bacteria. Dr. Colesuspects this could help explain not only why the lonely are iller, but how, in evolutionary terms, thisodd state of affairs has come about.The crucial bit of the puzzle is that viruses have to be caught from another infected individualand they are usually species-specific. Bacteria, in contrast, often just lurk in the environment, andmay thrive on many hosts. The gregarious are therefore at greater risk than the lonely of catchingviruses, and Dr. Cole thus suggests that past evolution has created a mechanism which causes whitecells to respond appropriately. Conversely, the lonely are better off ramping up their protectionagainst bacterial infection, which is a bigger relative risk to them.What Dr. Cole seems to have revealed, then, is a mechanism by which social environmentreaches inside a person′ s body and tweaks its genome so that it responds appropriately. It is not thatthe lonely and the gregarious are genetically different from each other. Rather, their genes areregulated differently, according to how sociable an individual is. Dr. Cole thinks this regulation ispart of a wider mechanism that tunes individuals to the circumstances they find themselves in.Broadly speaking, the genes more active in the lonely__________ . Passage 1Lonely people, it seems, are at greater risk than the gregarious of developing illnessesassociated with chronic inflammation, such as heart disease and certain cancers. A paper publishedlast year in the Public Library of Science, Medicine, shows the effect on mortality of loneliness iscomparable with that of smoking and drinking after examining the results of 148 previous studiesand controlled for factors such as age and pre-existing illness.Steven Cole of the University of California, Los Angeles, thinks he may know why this is so.He told the American Association for the Advancement of Science meeting in Washington, D.C.,about his work studying the expression of genes in lonely people. Dr. Cole harvested samples ofwhite blood cells from both lonely and gregarious people. He then analysed the activity of theirgenes, as measured by the production of a substance called messenger RNA. This molecule carriesinstructions from the genes telling a cell which proteins to make. The level of messenger RNA frommost genes was the same in both types of people. There were several dozen genes, however, thatwere less active in the lonely, and several dozen others that were more active. Moreover, both theless active and the more active gene types came from a small number of functional groups.Broadly speaking, the genes less active in the lonely were those involved in staving off viralinfections. Those that were more active were involved in protecting against bacteria. Dr. Colesuspects this could help explain not only why the lonely are iller, but how, in evolutionary terms, thisodd state of affairs has come about.The crucial bit of the puzzle is that viruses have to be caught from another infected individualand they are usually species-specific. Bacteria, in contrast, often just lurk in the environment, andmay thrive on many hosts. The gregarious are therefore at greater risk than the lonely of catchingviruses, and Dr. Cole thus suggests that past evolution has created a mechanism which causes whitecells to respond appropriately. Conversely, the lonely are better off ramping up their protectionagainst bacterial infection, which is a bigger relative risk to them.What Dr. Cole seems to have revealed, then, is a mechanism by which social environmentreaches inside a person′ s body and tweaks its genome so that it responds appropriately. It is not thatthe lonely and the gregarious are genetically different from each other. Rather, their genes areregulated differently, according to how sociable an individual is. Dr. Cole thinks this regulation ispart of a wider mechanism that tunes individuals to the circumstances they find themselves in.What risk may lonely people run according to the first paragraph Passage 1Lonely people, it seems, are at greater risk than the gregarious of developing illnessesassociated with chronic inflammation, such as heart disease and certain cancers. A paper publishedlast year in the Public Library of Science, Medicine, shows the effect on mortality of loneliness iscomparable with that of smoking and drinking after examining the results of 148 previous studiesand controlled for factors such as age and pre-existing illness.Steven Cole of the University of California, Los Angeles, thinks he may know why this is so.He told the American Association for the Advancement of Science meeting in Washington, D.C.,about his work studying the expression of genes in lonely people. Dr. Cole harvested samples ofwhite blood cells from both lonely and gregarious people. He then analysed the activity of theirgenes, as measured by the production of a substance called messenger RNA. This molecule carriesinstructions from the genes telling a cell which proteins to make. The level of messenger RNA frommost genes was the same in both types of people. There were several dozen genes, however, thatwere less active in the lonely, and several dozen others that were more active. Moreover, both theless active and the more active gene types came from a small number of functional groups.Broadly speaking, the genes less active in the lonely were those involved in staving off viralinfections. Those that were more active were involved in protecting against bacteria. Dr. Colesuspects this could help explain not only why the lonely are iller, but how, in evolutionary terms, thisodd state of affairs has come about.The crucial bit of the puzzle is that viruses have to be caught from another infected individualand they are usually species-specific. Bacteria, in contrast, often just lurk in the environment, andmay thrive on many hosts. The gregarious are therefore at greater risk than the lonely of catchingviruses, and Dr. Cole thus suggests that past evolution has created a mechanism which causes whitecells to respond appropriately. Conversely, the lonely are better off ramping up their protectionagainst bacterial infection, which is a bigger relative risk to them.What Dr. Cole seems to have revealed, then, is a mechanism by which social environmentreaches inside a person′ s body and tweaks its genome so that it responds appropriately. It is not thatthe lonely and the gregarious are genetically different from each other. Rather, their genes areregulated differently, according to how sociable an individual is. Dr. Cole thinks this regulation ispart of a wider mechanism that tunes individuals to the circumstances they find themselves in.What can we know about viruses and bacteria from the fourth paragraph Passage 1Lonely people, it seems, are at greater risk than the gregarious of developing illnessesassociated with chronic inflammation, such as heart disease and certain cancers. A paper publishedlast year in the Public Library of Science, Medicine, shows the effect on mortality of loneliness iscomparable with that of smoking and drinking after examining the results of 148 previous studiesand controlled for factors such as age and pre-existing illness.Steven Cole of the University of California, Los Angeles, thinks he may know why this is so.He told the American Association for the Advancement of Science meeting in Washington, D.C.,about his work studying the expression of genes in lonely people. Dr. Cole harvested samples ofwhite blood cells from both lonely and gregarious people. He then analysed the activity of theirgenes, as measured by the production of a substance called messenger RNA. This molecule carriesinstructions from the genes telling a cell which proteins to make. The level of messenger RNA frommost genes was the same in both types of people. There were several dozen genes, however, thatwere less active in the lonely, and several dozen others that were more active. Moreover, both theless active and the more active gene types came from a small number of functional groups.Broadly speaking, the genes less active in the lonely were those involved in staving off viralinfections. Those that were more active were involved in protecting against bacteria. Dr. Colesuspects this could help explain not only why the lonely are iller, but how, in evolutionary terms, thisodd state of affairs has come about.The crucial bit of the puzzle is that viruses have to be caught from another infected individualand they are usually species-specific. Bacteria, in contrast, often just lurk in the environment, andmay thrive on many hosts. The gregarious are therefore at greater risk than the lonely of catchingviruses, and Dr. Cole thus suggests that past evolution has created a mechanism which causes whitecells to respond appropriately. Conversely, the lonely are better off ramping up their protectionagainst bacterial infection, which is a bigger relative risk to them.What Dr. Cole seems to have revealed, then, is a mechanism by which social environmentreaches inside a person′ s body and tweaks its genome so that it responds appropriately. It is not thatthe lonely and the gregarious are genetically different from each other. Rather, their genes areregulated differently, according to how sociable an individual is. Dr. Cole thinks this regulation ispart of a wider mechanism that tunes individuals to the circumstances they find themselves in.Dr. Cole made an analysis of the activity of the genes by __________. When we eat may be just as important as what we eat. A new study shows that mice that eat when they should be sleeping gain more weight than mice that eat at normal hours. Another study sheds light on why we pack on the pounds in the first place. Whether these studies translate into therapies that help humans beat obesity remains to be seen, but they give scientists clues about the myriad factors that they must take into account.　　Observations of overnight workers have shown that eating at night disrupts metabolism and the hormones that signal we’re sated. But no one had done controlled studies on this connection until now. Biologist Fred Turek of Northwestern University in Evanston, Illinois, and graduate student Deanna Arble examined the link between a high-fat diet and what time of day mice eat. A control group of six nocturnal mice ate their pellets (60％ fat by calories, mostly lard) during the night. Another group of six ate the same meal during the day, Turek says, which disrupts their circadian rhythm—the body’s normal 24-hour cycle.　　After 6 weeks, the off-schedule mice weighed almost 20％ more than the controls, Turek and Arble report today in?Obesity, supporting the idea that consuming calories when you should be sleeping is harmful. Turek and Arble acknowledge that the disrupted mice ate a tad more and were a tad more sluggish, but the differences could not account for all of the weight gain.　　In the second study, a different team of researchers investigated the link between weight and the immune system. Hundreds of genes seem to affect the accumulation of fat, but one that helps protect us from infection might help us lose weight with little effort, biochemist Alan Saltiel of the University of Michigan, Ann Arbor, and colleagues suggest today in?Cell. The researchers tested me weight-adding abilities of a protein called IKK∈, which is linked with obesity, diabetes, and chronic, low-1evel inflammation. For 3 months, the team fed six mice missing IKK∈ genes a diet of high-fat chow.　　Because IKKE’s main job is immune defense, Saltiel’s team didn’t expect to find weight differences between knockout mice and controls. But the knockout mice did gain significantly less. Best of all, the girth the animals did add was less harmful to their overall health. “The knockout mice don’t gain as much weight but also don’t get diabetes, don’t get insulin resistance, and don’t get accumulation of lipids on the liver,” Saltiel says, all of which contribute to the suite of health problems associated with being overweight. Saltiel calls IKK∈ “an especially appealing drug target for the treatment of metabolic disease.”　　Tom Maniatis, a molecular biologist at Harvard University praises the study but remains skeptical about any drug that would inhibit IKK∈. He helped develop the mice used in the experiment and notes that they are vulnerable to the flu. He suspects that suppressing IKK∈ may help people with diabetes or obesity, “but the first time the swine flu comes along, that’s it.”　　Researchers are also enthusiastic about the circadian rhythm paper Frank Scheet, a neuroscientist at Harvard who studies sleep, was struck that “you could see something happening [to the disrupted mice] in the first week already. That’s consistent with human studies where we found changes in just 3 days.”　　Together, the papers suggest that there’s no simple answer to why people gain weight. Says Turek, “It’s clearly not just calories in versus calories out.”Which of the following statements about IKK∈ is INCORRECT? When we eat may be just as important as what we eat. A new study shows that mice that eat when they should be sleeping gain more weight than mice that eat at normal hours. Another study sheds light on why we pack on the pounds in the first place. Whether these studies translate into therapies that help humans beat obesity remains to be seen, but they give scientists clues about the myriad factors that they must take into account.　　Observations of overnight workers have shown that eating at night disrupts metabolism and the hormones that signal we’re sated. But no one had done controlled studies on this connection until now. Biologist Fred Turek of Northwestern University in Evanston, Illinois, and graduate student Deanna Arble examined the link between a high-fat diet and what time of day mice eat. A control group of six nocturnal mice ate their pellets (60％ fat by calories, mostly lard) during the night. Another group of six ate the same meal during the day, Turek says, which disrupts their circadian rhythm—the body’s normal 24-hour cycle.　　After 6 weeks, the off-schedule mice weighed almost 20％ more than the controls, Turek and Arble report today in?Obesity, supporting the idea that consuming calories when you should be sleeping is harmful. Turek and Arble acknowledge that the disrupted mice ate a tad more and were a tad more sluggish, but the differences could not account for all of the weight gain.　　In the second study, a different team of researchers investigated the link between weight and the immune system. Hundreds of genes seem to affect the accumulation of fat, but one that helps protect us from infection might help us lose weight with little effort, biochemist Alan Saltiel of the University of Michigan, Ann Arbor, and colleagues suggest today in?Cell. The researchers tested me weight-adding abilities of a protein called IKK∈, which is linked with obesity, diabetes, and chronic, low-1evel inflammation. For 3 months, the team fed six mice missing IKK∈ genes a diet of high-fat chow.　　Because IKKE’s main job is immune defense, Saltiel’s team didn’t expect to find weight differences between knockout mice and controls. But the knockout mice did gain significantly less. Best of all, the girth the animals did add was less harmful to their overall health. “The knockout mice don’t gain as much weight but also don’t get diabetes, don’t get insulin resistance, and don’t get accumulation of lipids on the liver,” Saltiel says, all of which contribute to the suite of health problems associated with being overweight. Saltiel calls IKK∈ “an especially appealing drug target for the treatment of metabolic disease.”　　Tom Maniatis, a molecular biologist at Harvard University praises the study but remains skeptical about any drug that would inhibit IKK∈. He helped develop the mice used in the experiment and notes that they are vulnerable to the flu. He suspects that suppressing IKK∈ may help people with diabetes or obesity, “but the first time the swine flu comes along, that’s it.”　　Researchers are also enthusiastic about the circadian rhythm paper Frank Scheet, a neuroscientist at Harvard who studies sleep, was struck that “you could see something happening [to the disrupted mice] in the first week already. That’s consistent with human studies where we found changes in just 3 days.”　　Together, the papers suggest that there’s no simple answer to why people gain weight. Says Turek, “It’s clearly not just calories in versus calories out.”Which of the following statements is CORRECT according to Fred Turek’s research?