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普通微生物学常用拉丁文学名细菌假单胞菌属Pseudomonas固氮菌属Azotobacter根瘤菌属Rhizobium慢生根瘤菌属Bradyrhizobium醋杆菌属Acetobacter螺菌属Spirillum沙门氏菌属Salmonella大肠杆菌Escherichia coli欧文氏菌属Erwinia沙雷氏菌属Serratia(又叫赛氏杆菌)粘质沙雷氏菌Serratia marcescens(又叫粘质赛氏杆菌) 变形杆菌属Proteus发酵单胞菌属Zymnomonas拟杆菌属Bacteroides弧菌属Vibrio蛭弧菌属Bdellovibrio韦荣氏球菌属Veillonella脱硫弧菌属Desulfovibrio立克次氏体属Rickettsia衣原体属Chlamydia支原体属Mycoplasma密螺旋体属Treponema球衣菌属Sphaerotilus柄杆菌属Caulobacter浮霉状菌属Planctomyces贝日阿托菌属Beggiatoa黏球菌属Myxococcus着色菌属Chromatium绿菌属Chlorobium鱼腥蓝细菌属Anabaena满江红鱼腥蓝细菌Anabaena azollae念珠蓝细菌属Nostoc螺旋蓝细菌属Spirulina硫杆菌属Thiobacillus土壤杆菌属Agrobacterium亚硝化单胞菌属Nitrosomonas硝酸杆菌属Nitrobacter葡萄球菌属Staphylococcus金黄色葡萄球菌属Staphylococcus aureus八叠球菌属Sarcina微球菌属Micrococcus明串珠菌属Leuconostoc消化球菌属Peptococcus链球菌属Streptococcus肺炎球菌Streptococus pneumoniae 奈氏球菌属Neisseria乳杆菌属Lactobacillus芽胞杆菌属Bacillus苏云金芽胞杆菌Bacillus thuringiensis枯草芽胞杆菌Bacillus subtilis炭疽芽胞杆菌Bacillus anthracis梭菌属Clostridium丙酸杆菌属Propionibacterium棒状细菌属Corynebacterium双歧杆菌属Bifidobacterium分枝杆菌属Mycobacterium诺卡氏菌属Nocardia链霉菌属Streptomyces弗兰克氏菌属Frankia小单胞菌属Micromonospora高温放线菌属Thermoactinomyces马杜拉放线菌属Actinomadura古细菌甲烷杆菌属Methanobacterium甲烷球菌属Methanococcus盐杆菌属Halobacter盐球菌属Halococcus热网菌属Pyrodictium热原体属Themoplasma真菌裂殖酵母属Schizosaccharomyces酵母属Saccharomyces酿酒酵母Saccharomyces cerevisiae汉逊酵母属Hansenula红酵母Rhodotorula假丝酵母属Candida球拟酵母属Torulopsis绵霉属Achlya毛霉属Mucor根霉属Rhizopus葡枝根霉（黑根霉）Rhizopus stolonifer 脉胞菌属Neurospora银耳属Tremella伞菌属Agaricus香菇属Lentinus木耳属Auricularia平菇Pleurotus ostreatus 曲霉属Aspergillus青霉属Penicillium藻类小球藻属Chlorella水绵属Spirogyra羽纹硅藻属Pinnularia舟形藻属Navicula原生动物眼虫属Euglena变形虫属Amoeba草履虫属Paramecium疟原虫属Plasmodium病毒慢病毒属Lentivirus引起HIV 核型多角体病毒属Nucleopolyhedrovirus 烟草花叶病毒属TobamovirusT4噬菌体属T4-like viruses马铃薯纺锤形块茎类病毒属Pospivioid羊搔痒因子Scrapie agent。
anorexia nervosa in female adolescents endocrine and bone
INVITED REVIEWAnorexia nervosa in female adolescents:endocrine and bone mineral density disturbancesM T Mun˜oz and J ArgenteDivision of Pediatric Endocrinology,Hospital Universitario Infantil Nin˜o Jesu´s,Avda Mene´ndez Pelayo65,E-28009Madrid,Spain (Correspondence should be addressed to J Argente;Email:argenteFEN@terra.es)AbstractAnorexia nervosa(AN)is a chronic childhood psychiatric illness that involves a reduction in caloricintake,loss of weight and amenorrhea,either primary or secondary.The diagnostic criteria for ANhave been established by the American Psychiatric Association.The prevalence of this diseaseamongst adolescents and young adults is between0.5and1%and the incidence of new cases peryear is approximately5-10/100000between15and19years of age.A number of endocrine and metabolic disturbances have been described in patients with AN includingamenorrhea–oligomenorrhea,delayed puberty,hypothyroidism,hypercortisolism,IGF-I deficiency,electrolyte abnormalities,hypoglycemia and hypophosphatemia,among others.In addition to pro-longed amenorrhea,osteopenia and osteoporosis are the most frequent complications leading to clini-cally relevant fractures and increased fracture risk throughout life.Patients exhibit an alteration inthe hypothalamic–pituitary–gonadal axis,which is responsible for the menstrual disorders.Theincrease in gonadotropin secretion that can be observed after ponderal recuperation suggests thatmalnutrition could be the most important mechanism involved in the decrease in gonadotropinsecretion.The loss of fat tissue as a consequence of nutrient restriction has been associated with hypoleptinemiaand abnormal secretion of peptides implicated in food control(neuropeptide Y,melanocortins andcorticotropin-releasing factor,among others).A review of the endocrine abnormalities,disturbances in neurotransmitters,as well as a detailed ana-lysis of bone markers and bone mineral density in patients with AN is described.European Journal of Endocrinology147275–286IntroductionAnorexia nervosa(AN)is a childhood psychiatric disorder that is characterized by patient-induced and -maintained weight loss that leads to progressive mal-nutrition and specific pathophysiological signs(distur-bance of body image and fear of obesity).The diagnostic criteria for AN according to the American Psychiatric Association(1)are as follows:(a)refusal to maintain body weight at or above a minimally normal weight for age and height;(b)intense fear of gaining weight or becoming fat,even though under-weight;(c)disturbance in the way in which one’s body weight or shape is experienced,undue influence of body weight or shape on self-evaluation,or denial of the seriousness of the current low body weight; and(d)in postmenarcheal females,amenorrhea (absence of at least three consecutive menstrual cycles).Based on the presence or not of bulimic symp-toms,AN appears in two specific subtypes,restricting and binge-eating/purging(1).Although pure forms can rarely be seen,the preva-lence of this disease in adolescents and young adults is between0.5and1%.The incidence of new cases per year is approximately5-10/100000per year between15and19years of age(2).A recent study of a Spanish female population with ages between12 and21years showed a prevelance of0.3%for AN, 0.8%for bulimia and3.1%for non-specified eating dis-orders,resulting in a total sum of4.1%of the popu-lation suffering from some type of eating disorder(3). Complications in many organ systems can be seen, including the cardiovascular and peripheral vascular systems,gastrointestinal,hematological,renal,skeletal, endocrine and metabolic systems,amongst others. These alterations are not only related to the state of malnutrition,but also to the conduct used by these patients to control their weight.The endocrine and metabolic disturbances include amenorrhea–oligo-menorrhea,delayed puberty,hypothyroidism,hyper-cortisolism,insulin-like growth factor(IGF)-I deficiency,electrolyte abnormalities,hypoglycemiaEuropean Journal of Endocrinology(2002)147275–286ISSN0804-4643 q2002Society of the European Journal of Endocrinology Online version via and hypophosphatemia,amongst others,with numer-ous studies of AN patients indicating hypothalamic dys-function as a possible basis.We have here reviewed the endocrine and metabolic aspects of this eating disorder with a special emphasis on bone mineral disturbances.Appetite-regulating peptidesThe hypothalamus is important in the control of energy metabolism.In effect,it is responsible for the sensation of hunger and satiety and,therefore,energy intake.In addition,via modulation of the sympathetic nervous system,it is also involved in thermogenesis and energy expenditure.A variety of neuropeptides control these functions (4).Numerous substances synthesized in different parts of the body send afferent signals back to these hypothalamic centers to modify,either positively or negatively ,appetite or energy expenditure.Regulation of acute eating behavior incorporates a system of satiety signals that originate from the food ingested.Cholecystokinin,bombesin,gastrin-releasing peptide,amongst others,are involved in this signaling system and reach the brain via peripheral innervation or the circulation to activate their receptors in the brain (5).Long-term energy balance is regulated via a system comprised of different hormones secreted in proportion to corporal adiposity ,such as leptin and insulin,that act at the level of the central nervous system (CNS).These respond to changes in body fat by activating ana-bolic or catabolic pathways (6),the first through pro-duction of neuropeptide Y (NPY),which stimulates food intake,and the second via the hypothalamic mel-anocortin system,which reduces food intake and stimulates weight loss (7)(Fig.1).Leptin is synthesized by adipose tissue and is involved in the regulation of food intake and energy expenditure.The mechanisms of action of this hormone are largely unknown,but many studies demonstrate that its pri-mary target is the hypothalamus (8).Plasma levels of leptin and its secretory pattern vary during the night and day and are influenced by food intake (9).Acting at the level of the hypothalamus,leptin effects a decrease in appetite,which in turn results in weight loss and activation of the gonadal axis by stimulating gonadotropin-releasing hormone (GnRH)secretion.Mutation analysis of the coding region and part of the promoter region of the leptin gene in patients with AN has yielded negative results,suggesting that involvement of this gene in the etiology of AN is unlikely (10).NPY is produced throughout the CNS and acts as a central stimulator of feeding.Its actions,incrementing ingestion and decreasing thermogenesis (11)are,hence,opposite that of leptin.The neuropeptide YY5and YY1receptors in rats and humans are assumed to play a major role in NPY-induced food intake.The neuropeptide YY5receptor gene (NPYY5R)is expressed in brain regions known to be involved in the central regulation of feeding behavior,including the lateral hypothalamus,the paraventricular nucleus and the arcuate nucleus (12).Systematic mutation screening within the coding region of the NPYY5R revealed a rare Glu-4-Ala variant in a single patient with AN.This allele was transmitted from the mother who had no history of any eating disorder.Association and transmission disequilibrium studies pertaining to vari-ations and polymorphisms within the NPYY1R and NPYY5R and AN were negative (13).Glucocorticoids are also implicated in energy regu-lation.Via their effects on NPY,they act as endogenous antagonists of leptin and insulin (14).Other neuropep-tides that stimulate food intake and energy storage are melatonin-concentrating hormone and orexin A and B,which increase in response to fasting and stimulate appetite (15).The melanocortins (MC)are peptides derived from the precursor pro-opiomelanocortin (POMC)and act on specific receptors.The endogenous MC most implicated in food intake and body weight is a -melanocyte-stimulating hormone,which has a high affinity for the MC receptors,especially MC3and MC4(16).Mutation screening of the coding region of MC4receptors in patients with AN and bulimia nervosa revealed two common polymorphisms in both groups.Allele and genotype frequencies did not differ between these groups and probands of different weight extremes (17).Serotonin (5-hydroxytryptamine;5-HT)is involved in a broad range of biological,physiological and behavioral functions.Its actions are regulated by bio-synthetic enzymes (tryptophan hydroxylase),specific receptors,as well as by an inactivation system involv-ing neuronal re-uptake (serotonin transporter)(18).The serotonergic system has been implicated in the development of eating disorders (19).PolymorphismsFigure 1Model of energy balance regulation.a -MSH,a -melano-cyte-stimulating hormone;CRH,corticotropin-releasing hormone.276M T Mun ˜oz and J ArgenteEUROPEAN JOURNAL OF ENDOCRINOLOGY (2002)147within different5-HT receptor genes and the trypto-phan hydroxylase gene have been analysed and an association between the21438A allele of the 21438G/A polymorphism within the promoter region of the5-HT2A receptor gene and AN has been reported(20,21).However,others studies could not confirm this association(22).Nacmias et al.(23) reported an association between the21438A allele and AN of the restricting subtype,whereas allele fre-quencies in patients with the binge/purging subtype did not differ from those of controls.Aubert et al.(24) found that the21438A allele was associated with lower energy intake and lower alcohol consumption in obese individuals,afinding which they assumed to be consistent with the higher frequency of the A allele in patients with AN.These studies suggest that patients with AN have enhanced5-HT2A receptor binding and provide further evidence for a serotonin-ergic dysfunction in eating disorders,but these results need further confirmation(25).Hypothalamic–pituitary–adrenal axis Adrenocorticotropin(ACTH)and the endogenous opioids are derived from the same precursor,POMC. Increased ACTH secretion is preceeded by activation of the POMC system.The opioid system has both direct and indirect influences over food intake and the level of physical activity.In laboratory animals,opioid administration stimulates appetite via receptors in the paraventricular nucleus and opioid antagonists such as naloxone reduce appetite(26).Corticotropin-releasing hormone(CRH),synthesized in neurons of the para-ventricular nucleus,is regulated,at least in part,by leptin and insulin and its administration i.c.v.induces a reduction in food intake and weight loss(27).We and others have observed that plasma cortisol levels in female adolescents with AN are often elevated while its circadian rhythm is conserved(28).Dexa-methasone can partially suppress this hypercortisol-emia,which is similar to that observed in patients with depression and Cushing’s disease.Recently, Foppiani et al.(29)demonstrated that DDAVP does not stimulate ACTH and cortisol in AN patients.This fact could be due to a down-regulation of hypophyseal 1-deamino-8D-arginine vasopressin(DDAVP)V3recep-tors in AN(29).In acute situations of AN,the dexa-methasone test has no medical significance;however, in patients that are recovering weight it may have prognostic value(30).Refeeding studies of anorexic patients have shown that,irrespective of the initial weight,weight gains as low as10%are associated with the normalization of cortisol secretion(29).The mean plasma half-life of cortisol is prolonged (31)and ACTH levels are within the normal range, but the ACTH response to CRH is inferior to that of con-trol patients(32).Putignano et al.(33)demonstrated that,in untreated AN patients,plasma and salivary cortisol and urinary free cortisol concentrations are increased,and cortisol suppression after the dexa-methasone suppression test is decreased in both plasma and saliva.These alterations were less pro-nounced in AN patients who were being treated(33). This hypercortisolemia could reflect a defect at the level of the hypothalamus,or even higher up,that results in the hypersecretion of CRH.Taken together, these observations suggest a situation of CRH hyper-secretion or peripheral cortisol resistance(34). Hypothalamic–pituitary–ovarian axisPatients with AN exhibit isolated hypogonadotropic–hypogonadism of hypothalamic origin and uncertain etiology.Multiple factors could play a role,including hypothalamic dysfunction,weight reduction,sex ster-oid or neurotransmitter alterations and excess physical exercise,among others.Women with AN exhibit low basal levels of gonadotropins,as well as low estradiol levels,indicating abnormal functioning of the hypo-thalamic–pituitary–gonad axis(35).We have demon-strated that spontaneous secretion of luteinizing hormone(LH)during24h is decreased in both the fre-quency and the amplitude of the secretory bursts(36). Weight recuperation increases serum levels of both LH and follicle-stimulating hormone,suggesting that malnutrition could be implicated in the regulation of gonadotropin secretion.Disturbances in neurotrans-mitters implicated in GnRH regulation,including the dopaminergic system and endogenous opioids,have been described(37).Whether these alterations are pri-mary or secondary to malnutrition remains to be elucidated.Malnutrition could be responsible for the delayed puberty and reduction in growth in AN patients,as the shut-down of these two systems has been inter-preted as an adaptation mechanism to a reduction in nutrients.Puberty is delayed if the symptoms of AN start during the prepubertal period.In contrast,if the illness begins once development has already started, puberty is detained and the growth spurt delayed and reduced(38).Finally,if symptoms appear when pub-erty has ended,secondary amenorrhea is present. One of the signals that begins the process of adaptation to malnutrition is hypoinsulinemia,which is present asa consequence of low glucose and amino acid levels(39).Furthermore,growth hormone(GH)abnormal-ities and low IGF-I levels contribute to poor growth in prepubertal patients,leading to a reduction in their final height(Fig.2).Reliable data are not available to establish the percentage of growth lost in these patients,with the exception of one study where it was estimated that3cm is lost in some patients in relation-ship to their target height(40).Anorexia nervosa:endocrine and BMD abnormalities277EUROPEAN JOURNAL OF ENDOCRINOLOGY(2002)147Leptin is also involved in gonadal development and reproductive function.Its receptors are expressed in the anterior pituitary and gonads,and the biological significance of this is a current object of investigation (41).It is suggested that leptin is involved in the regu-lation of GnRH secretion and plays a role in the initiation and maintainance of gonadal function in humans (42).Whether leptin is only a permissive factor or plays a central role in the onset of puberty remains unknown.Problems in the functioning of the reproductive system,including a reduction in serum sex-steroid levels,are frequent in subjects with reduced fat stores (43,44),as occurs in patients with AN.This decrease in gonadal function could be related to the reduced serum leptin levels as a result of the loss of fat tissue.In contrast to this hypothesis,we have observed that in patients with AN during partial weight recuperation there is no significant increase in leptin levels or in the recovery of gonadal function,at least simultaneously (9)(Fig.3).It is possible that a longer weight recuperation period is necessary for this to occur.Some studies suggest that body mass index (BMI)is the most important control factor for the secretion of leptin in situations of modified food intake (45)and that there is a loss in circadian rhythms in patients with AN (46).One aspect of great interest is whether leptin is necessary for therecovery of menstruation in these patients (47);however,more investigation is necessary in order to answer this question.There is a clear association between melatonin levels and gonadal function in humans,with women with hypothalamic amenorrhea having elevated nocturnal melatonin levels (48).Patients with AN also have elevated nocturnal levels of 6-sulfatoximela-tonin (the principal metabolite excreted in the urine)both at diagnosis and after weight recuperation if the amenorrhea persists (49,50).This could be due to insufficient weight gain or the need for a longer period of weight recuperation.The percentage of total body fat can now be evalu-ated by using dual-energy X ray absorptiometry and,in patients with AN and moderate malnutrition,the percentage of total body fat appears to be a better indicator of the nutritional state than BMI.There is a significant correlation between leptin levels and the percentage of total body fat that is not found between BMI and leptin (51,52).It has been reported that if patients with AN recuperate weight to obtain at least 90%of the weight adequate for their height,their men-strual cycles will return within the following 6months.It therefore follows that one of the decisive factors for the normalization of gonadal function is recovery of the nutritional state and body mass(53).Figure 2Hormonal response to malnutrition.T 3,tri-iodothyronine.278M T Mun ˜oz and J ArgenteEUROPEAN JOURNAL OF ENDOCRINOLOGY (2002)147GH–IGF-I axisMost studies indicate that a large percentage of patients with AN have elevated basal and GH-releasing hormone (GHRH)-stimulated GH levels (54).A number of abnormalities in GH response to different stimuli have been described (decreased response after hypoglycemia,clonidine,hexarelin and dexamethasone),as well as paradoxical hormone responses (elevated GH after thyrotropin-releasing hormone (TRH),thyrotropin (TSH)or i.v .glucose),although these responses are het-erogeneous (55–57).Few studies have analyzed spon-taneous GH secretion (SGHS)in AN patients.Scacchi et al.(58)reported that increased GH secretion could be the result of an increased frequency of secretory bursts superimposed on enhanced tonic GH secretion.We studied SGHS in a group of anorexic patients at the time of diagnosis and two different times during weight recuperation and found that at the time ofdiagnosis SGHS is heterogeneous (59).In 40%of these subjects,mean 24-h GH secretion was greater than 3ng/ml (the lower limit of normality)and the remaining 60%had levels below the normal range.The difference between these groups and the controls was due to modification in the amplitude of the GH peaks and not to the frequency .In both groups,recup-eration of at least 10%of their initial weight resulted in the normalization of the parameters of SGHS.More recently ,Støving et al.(60)analyzed SGHS in eight patients with AN by using the deconvolution method and found that the half-life of GH in these patients is normal.The integrated concentration of GH was ten times greater in AN patients compared with controls.The frequency of the GH peaks,their duration and the amount of GH secreted in each peak,as well as basal GH levels,were elevated.These parameters all correlated negatively with BMI.These observations suggest that the alterations in GH secretion in these patients are due to modifications in its neuroendocrine control,with an increase in GHRH release and decreased somatostatin tone.The GH pat-tern in conjunction with the negative correlation between basal and pulsatile GH secretion and BMI suggests that the alterations in GH secretion observed in AN are directly related to malnutrition (59).One possible mechanism could involve the reduced IGF-I levels produced by malnutrition.Gianotti et al.(61)showed that a low IGF-I dose inhibits,though does not normalize,spontaneous and stimulated GH secretion in patients with AN.These findings indicate the existence of a defective hypothalamic control of GH release (61).This would effect a reduction in the negative feedback action that IGF-I exerts on GH secretion at the level of both the hypothalamus and the pituitary (60).Another variable that could be involved in the alterations in GH secretion is the hypoestrogenism that accompanies amenorrhea.It has been suggested that malnutrition underlies the increase in the amount of GH secreted in each pulse and that hypoestrogenism is responsible for the increased pulse frequency .However,these studies are still insufficient to draw definite conclusions.Recently it has been demonstrated that a gastrointes-tinal peptide hormone,ghrelin,stimulates GH secretion in rats and humans.Ghrelin also plays an important role in the regulation of energy balance.Plasma ghrelin levels are regulated by acute and chronic changes in energy balance, e.g.fasting increases while feeding decreases circulating ghrelin concentrations (62).Otto et al.(63)showed that plasma ghrelin levels in patients with AN are significantly increased and rapidly normalize after partial weight recovery .While decreased leptin levels in AN patients might simply reflect reduced body fat mass,increased gastric ghrelin secretion in AN might,however,reflect a physiological effort to compensate for the lack of nutritional intake and stored energy(64).Figure 3(A)Mean circulating leptin plasma levels (^S.E.M.)in women with AN,at the time of diagnosis,after recovery of 8%of their original body weight and after regaining at least 10%of their original body weight (approximately 1year after starting treat-ment).These are compared with their age-and sex-matched controls (Tanner V females);one-way ANOVA,*P ,0:0001;NS,not significant.(B)Linear correlation between fasting serum leptin levels and body mass index,expressed as standard deviation (BMI (SD)),in women with AN,at the time of diagnosis and after at least partial recovery of their original body weight.Patients with AN at the time of diagnosis (X ),patients with AN after 8%recu-peration of their original weight (A )and patients with AN after recuperation of $10%of their original weight (K ).Anorexia nervosa:endocrine and BMD abnormalities 279EUROPEAN JOURNAL OF ENDOCRINOLOGY (2002)147Serum GH-binding protein(GHBP)levels in patients with AN are dramatically reduced(58,65,66)and tend to normalize with weight recuperation(58,67). This reduction in GH receptors is most likely one of the principal causes of GH resistance.It has been suggested that in malnutrition the low GHBP levels could be related to hypoinsulinemia,alterations in thy-roid function or hypoestrogenism(68,69).On the other hand,many studies have demonstrated a correlation between serum GHBP levels and BMI or the percentage of body fat,and more specifically,with visceral fat(70). Given that it has not been demonstrated that circulating GHBP is uniquely or even preferentially derived from liver GH receptors,it is possible that other tissues, such as adipose tissue,could contribute to plasma GHBP levels.If this is the case,the extreme reduction in adipose tissue in patients with AN could result in the observed decrease in serum GHBP levels(71,72). Patients with AN have extremely reduced serum IGF-I levels that tend to normalize with weight recu-peration(58,73);however,the time necessary for this to occur,as observed in other forms of malnutrition, may be prolonged(74).Circulating IGF-I is largely dependent on GH,but it is also very sensitive to nutri-tional changes.In AN patients,serum IGF-I levels do not correlate with GH secretion(58),which suggests that the decrease in IGF-I is independent of GH and probably directly due to the state of malnutrition. Thus,the coexistence of reduced IGF-I levels and normal or elevated GH secretion suggests that these patients exhibit resistance to GH action.The available data in respect to serum levels of free IGF-I are limited and contradictory.Some authorsfind them to be normal(58),while others report them to be decreased(75);however,in both cases weight recu-peration tended to increase free IGF-I levels.A similar phenomenon is seen with IGF-II levels.We(58)and others(59)found serum IGF-II levels to be normal at the time of diagnosis and to increase with weight recuperation.In contrast,Counts et al.(66)reported IGF-II levels to be decreased,although not significantly, and to normalize with weight recuperation.Serum levels of free IGF-II are reported to be decreased in patients with AN and to increase with weight recuper-ation(59).Patients with AN have elevated serum IGF-binding protein(IGFBP)-1and IGFBP-2levels that tend to nor-malize with weight recuperation(58,66).Both factors are reported to be GH independent and very sensitive to nutritional regulation.The increase in IGFBP-1in these patients is most likely related to hypoinsulinism, although other metabolic or hormonal factors,such as increased glucagon and glucocorticoids levels,as well as decreased intracellular glucose or other specific substrates,may be involved(76).In AN,as in other forms of malnutrition,the increase in IGFBP-2most likely depends on the combined influence of caloric-pro-tein restriction,hypoinsulinism and GH resistance(76).Serum IGFBP-3levels are decreased in AN patients as a consequence of GH resistance and tend to normal-ize after weight recuperation(58,66).Indeed,all of the components of the trimolecular complex formed by the union between IGFBP-3,IGF and the acid-labile sub-unit(ALS)are decreased(68).Given that these proteins are all GH dependent and regulated by the nutritional state,this is not unexpected.IGFBP-3decreases signifi-cantly with caloric restriction,but in adults only with protein restriction(77).In contrast to that observed in other catabolic situations,increased proteolysis of IGFBP-3has not been observed in AN(78). Although present in the serum in low concentrations, both IGFBP-4and IGFBP-5are very important in the pro-cess of bone formation,where at the cellular level they regulate the actions of the IGFs.In AN,serum levels of both of these IGFBPs are dramatically reduced and do not normalize with partial weight recuperation(79). The biological significance of the changes in IGFBPs that occur in AN or malnutrition is difficult to explain, in part because the physiological roles of the binding proteins are not totally understood.The decrease in serum IGFBP-3,and therefore the trimolecular complex IGFBP-3–IGF–ALS,impedes the retention of IGF in the vascular space,favoring the decrease in plasma levels (59).On the other hand,the increase in IGFBP-1and IGFBP-2,two proteins with low molecular weights that can cross the vascular barrier,would favor even more the movement of the IGFs to the tissues where they can act.Therefore,modification of the serum and tissue levels of the IGFBPs could be one of the mechanisms by which malnutrition regulates the con-centration and actions of the IGFs and the somatotrope axis(68).Hypothalamic–pituitary–thyroid axis The majority of patients with AN present a condition called‘low T3syndrome’characterized by low tri-iodothyronine(T3),normal or low thyroxine(T4)and normal TSH(80).We have observed that T3levels are reduced at the time of diagnosis and normalize with weight gain,while T4and TSH levels are within the normal range at both time-points(81).The extremely reduced T3levels in these patients is due to the exist-ence of altered peripheral deiodination that preferen-tially transforms T4into the inactive metabolite, reverse T3.These thyroid alterations normalize with weight recuperation(82).Stoving et al.(83)determined thyroid volume by ultrasonographic methods in patients with AN and demonstrated that this gland is markedly reduced in comparison with age-and sex-matched controls.This thyroid atrophy is not due to low TSH levels,as TSH levels are usually normal in AN.However,thyroid size is influenced by IGF-I,and the low IGF-I levels in these patients could contribute to thyroid atrophy280M T Mun˜oz and J Argente EUROPEAN JOURNAL OF ENDOCRINOLOGY(2002)147 。
用作嗜中性白细胞弹性蛋白酶抑制剂的2-吡啶酮衍生物及其用途[发明专利]
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专利名称：用作嗜中性白细胞弹性蛋白酶抑制剂的2－吡啶酮衍生物及其用途
专利类型：发明专利
发明人：彼得·汉森,卡罗里娜·劳威兹,汉斯·洛恩,安东尼奥斯·尼基蒂迪斯
申请号：CN200480027517.4
申请日：20040915
公开号：CN1856467A
公开日：
20061101
专利内容由知识产权出版社提供
摘要：本发明提供了新颖的式(I)的化合物以及其光学异构体、外消旋体以及互变体，以及其可药用盐，其中R、R、R、R、G、G、L、Y和n如说明书中定义；以及其制备方法、包含这些化合物的组合物以及其在治疗中的用途。
所述的化合物为嗜中性白细胞弹性蛋白酶抑制剂。
申请人：阿斯利康(瑞典)有限公司
地址：瑞典南泰利耶
国籍：SE
代理机构：北京市柳沈律师事务所
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丁香榄提取物在皮肤病治疗中的应用研究
丁香榄提取物在皮肤病治疗中的应用研究皮肤病是指影响皮肤及其附属器官的各种疾病，包括感染性疾病、自身免疫性疾病、过敏性疾病等。
随着社会发展和生活水平的提高，人们对皮肤病的关注和治疗需求也越来越高。
传统草药中的丁香榄被发现在皮肤病治疗中具有良好的应用前景。
本文将重点介绍丁香榄提取物在皮肤病治疗中的应用研究进展。
丁香榄，学名Syzygium aromaticum，属于植物界桃金娘科，常见于东南亚地区。
丁香榄富含挥发油、鞣质、酚类物质等成分，具有抗菌、抗炎、抗氧化等多种药理作用。
首先，丁香榄提取物在抗菌方面显示出较好效果。
很多皮肤病如痤疮、酒渣鼻等是由细菌感染引起的。
研究显示，丁香榄提取物中的挥发油成分对多种细菌具有较强的抑制作用，包括金黄色葡萄球菌、大肠杆菌等常见致病菌。
这表明丁香榄提取物可以作为皮肤病治疗中的抗菌药物应用于临床。
其次，丁香榄提取物在抗炎方面也具备一定的疗效。
很多皮肤病如湿疹、银屑病等都伴随着明显的炎症反应。
研究发现，丁香榄提取物中的酚类物质具有较强的抗炎作用，可以有效抑制炎症介质的释放，减轻炎症反应，并具有较好的抗纤维化作用。
因此，丁香榄提取物可以应用于治疗和缓解炎症相关的皮肤病。
此外，丁香榄提取物还具备良好的抗氧化性能。
氧化应激是多种皮肤病的共同病理机制，包括皮肤衰老、色斑等。
研究显示，丁香榄提取物中的鞣质成分具有明显的抗氧化作用，可以清除自由基、减缓细胞脂质过氧化以及促进胶原蛋白生成等，从而有助于改善和预防氧化损伤相关的皮肤病。
此外，丁香榄提取物还显示出一定的抗过敏作用。
过敏性皮炎是常见的皮肤病类型之一，常伴随着瘙痒、红斑和水疱等症状。
研究发现，丁香榄提取物中的成分能够降低免疫细胞的活化程度，减少过敏介质的释放，从而缓解过敏反应和瘙痒症状。
因此，丁香榄提取物在过敏性皮肤病的治疗中也具备一定的潜力。
值得注意的是，尽管丁香榄提取物在皮肤病治疗中具有多种优势和潜力，但仍然存在一些不足之处。
微生物学课程思考题
微生物学课程思考题《微生物学》课程复习思考题绪论1.什么是微生物？它包括哪些类群？2.人类迟至19世纪才真正认识微生物其中主要克服了哪些重大障碍？3.微生物有哪五大共性？其中最基本的是哪一个？为什么？4.什么是微生物学？学习微生物学的任务是什么？5. 用一个具体事例说明人类与微生物的关系，为什么说微生物是人类的敌人，更是我们的朋友？（建议将一些具体事例延伸成为展板制作的题目）6. 为什么微生物能成为生命科学研究的“明星”?7. 为什么说巴斯德和柯赫是微生物学的奠基人?（请不要简单罗列二个人的工作，而应该对他们的工作及意义进行评论）第一章1.试图示G+和G-细菌细胞壁的主要构造井简要说明其异同。
2.试图示肽聚糖的模式构造，并指出G+和G-细茵肽聚糖结构的差别。
3.试述革兰氏染色法的机制并说明此法的重要性。
4.渗透调节皮层膨胀学说是如间解释芽袍耐热机制的？5.裂异形胞原体与始体．类支原体，浚酶体袍囊，磁小体。
第二章1.试解释菌物、真菌、酵母茵、霉菌和章菌。
2.试简介菌丝、茵丝体、菌丝球、真酵母、假酵母、芽痕、蒂痕、真菌丝、假菌丝等名词。
3.霉菌的营养菌丝恻气生菌丝各有何特点？它们分别可分化出哪些特化构造？4.试列表比较各种真菌胞子的特点。
5.细菌、放线菌、酵母菌和霉菌四大类微生物的菌落有何不同？为什么？第三章1.什么是真病毒？什么是亚病毒？2.病毒的一般太小如何？试图示病毒的典型构造。
3.病毒粒有哪几种对称形式？每种对称又有几类特殊外形？试各举一例。
4.什么叫烈性噬菌体？简述其裂解性生活史。
5.什么是一步生长曲线？它可分几期？各期有何特点？6.试解释溶源性、溶源菌、温和噬菌体。
第四章1.什么叫能源？试以能源为主、碳源为辅对微生物的营养类型进行分类。
2.什么叫生长因子？它包括哪几类化合物？微生物与生长因子的关系有哪几类？试举例加以说明。
3.什么叫水活度（a）？它对微生物的生命活动有间影响？对人类的生产实践w和日常生活有何意义？4.什么是选择性培养基？试举一例并分析其中的原理。
暹罗炭疽菌中脂滴包被蛋白Cap20与乙酸激酶CsAck的互作研究
暹罗炭疽菌中脂滴包被蛋白Cap20与乙酸激酶CsAck的互作研究作者：王娜王记圆李潇张宇刘文波林春花缪卫国来源：《热带作物学报》2022年第03期摘要：暹羅炭疽菌（Colletotrichum siamense）是一种重要的病原真菌，是我国橡胶树炭疽病（Colletotrichum leaf disease， CLD）的田间优势病原种，也是热带、亚热带地区许多其他农林作物炭疽病的主要病原种。
脂滴是细胞的中性脂，存在于绝大多数真核细胞中，是细胞内甘油三酯的主要贮存形式。
脂滴在细胞内可以参与脂质代谢、膜转运、蛋白降解和信号传导等。
包被蛋白（perilipin）是脂滴表面最丰富的脂质相关蛋白，主要存在于动植物体内，对细胞内脂滴代谢起着重要的调控作用。
Cap20是暹罗炭疽菌中包被蛋白的同源蛋白，前期证实Cap20是一个致病相关蛋白，它参与了炭疽菌附着胞膨压形成、脂滴数量和致病性。
了解其互作蛋白和互作的生物学意义可能为深入了解脂滴包被蛋白参与的致病分子机制具有重要意义。
课题组前期通过酵母双杂交技术在暹罗炭疽菌cDNA文库中筛选到一个与Cap20互作的候选蛋白乙酸激酶，本研究克隆了该乙酸激酶的编码基因，并进行了蛋白结构和同源蛋白聚类分析。
结果表明，乙酸激酶编码基因的DNA大小为1312 bp，包括一个内含子，cDNA为1248 bp，编码415个氨基酸，含有一个乙酸激酶结构域，命名为CsAck。
然后构建含6×his标签的原核表达载体PET32a-CsAck，利用其和含GST标签的pGEX6p-1-Cap20（先前构建）进行蛋白表达和纯化，获得含有6×His标签的融合蛋白CsAck和含有GST标签的Cap20。
通过Pull down 验证了Cap20和CsAck蛋白之间的体外互作。
最后，构建含有潮霉素转移酶基因HPH的表达载体PXY203-CsAck-S和含有氯嘧磺隆抗性基因ILV1的表达载体pCB1532-GFP-Cap20，将它们共同转化暹罗炭疽菌野生型菌株获得转化子。
诺丽酵素在重度吸烟者体内的抗氧化活性研究
诺丽酵素在重度吸烟者体内的抗氧化活性研究美国罗克福德UIC医学院美国曼尼托巴大学社区健康科学学院医学系加拿大温尼伯地区保监局美国海巴戟控股有限公司研究发展部摘要：研究方法诺丽酵素经动物体外扣体内试验显示具有抗氧化活性。
本研究以285名重度吸烟者为研究对象，以常用的安慰剂为临床对照试验，对诺丽酵素(TNJ)在人体中的抗氧化活性进行了为期30天的临床研究。
参与研究的重度吸烟者被随机分为3个小组，即对照组（每日摄取118 mL安慰剂）、实验组l（每日摄取29.5 mL诺丽酵素）、实验组2（每日摄取29.5 mL诺丽酵素），并对三个组实验前后血液中超氧阴离子自由基(SAR)和脂质过氧化物(LO OH)含量进行测定与比较[研究结果]经过30天的临床实验，发现实验组2的供试者体内的SAR平均由0.26±0.14μrnol/ ml. 下降至19土0.10μmol/ml．LOOH平均由0.53±0.19 μmol/mL下降至0.40±0.10 μmol/mL;实验组3的供试者体内的SAR平均由0.26±0.22μmo/mL下降至0.18±0.11μmol/mL，LOOH平均由0.55±0.21μmol/mL下降至0.40±0.14μmol/ml；而在对照组供试者体内SAR和LOOH含量没有发生明显的变化。
[研究结论]诺丽酵素在重度吸烟者体内具有抗氧化活性，与该研究领域先前相关的研究结果相符。
前言吸烟会导致人体产生大量的氧离子自由基，引发，系列与吸烟相关的疾病二据研究统计，人们每吸一口烟，大约会产生1017个氧化分子，这些氧化分子在体内被激发活化，形成血液中的脂质过氧化产物，如脂质过氧化物(LOOH)及超氧化物阴离子自由基(SAR)．由此可见，吸烟会大大增加血液中脂质过氧化物(LOOH)及超氧化物阴离子自由基(SAR)的含量。
诱导脂质过氧化过程在很大程度上依赖于细胞膜上多不饱和脂肪酸的自由基反应，不饱和键自催化或酶解进一步形成脂质过氧化物脂质过氧化物的产生能够迅速分解醛和烯醇等DN A结合因子，导致机体细胞的内源性损伤。
1900-2011诺贝尔生理学或医学奖获得者名录
获奖时国籍 美国 英国 澳大利亚 英国 英国 美国 联邦德国 法国 法国 法国 美国 美国 瑞典 美国 美国 美国 美国 美国 美国 美国 美国 美国
5
获奖原因
1963
霍奇金，A.L. 赫胥黎，A.F.
研究神经冲动沿神经纤维传递
1964
布洛赫，K. 吕南，F. 雅各布，F.
发现胆固醇和脂肪酸的代谢
1965
1901——2011 诺贝尔生理学或医学奖获得者
年份 1901 1902 1903 1904 1905 1906 1907 1908 1909 1910 1911 1912 1913 1914 1915～ 1918 1919 1920 中译名 贝林，E.von 罗斯，R. 芬森，N.R. 巴甫洛夫，I.P. 科赫，R. 高尔基，C. 拉蒙–卡哈尔，S. 拉韦朗，A. 埃尔利希，P. 梅契尼科夫，I.I. 柯赫尔，E.T. 科塞尔，A. 古尔斯特兰德，A. 卡雷尔，A. 里歇，C.R. 巴拉尼，R. 无人获奖 博尔代，J. 克罗伊，A. Bordet Jules (Schack) August (Steenberg) Krogh 比利时 丹麦
1958
塔特姆，E.L. 莱德伯格，J.
1959
奥乔亚，S. 科恩伯格，A. 伯内特，F.M. 梅达沃，P.B. 贝凯西，G.von 克里克，F.H.C.
1960 1961 1962
发现器官移植的免疫性 研究内耳功能 发现脱氧核糖核酸的分子结构
年份
中译名 沃森，J.D. 威尔金斯，M. 埃克尔斯，J.C.
1934
迈诺特，G.R. 墨菲，W.P.
发现肝质食物治疗贫血
1935 1936
施佩曼，H. 戴尔，H.H.
番荔枝内酯抗肿瘤课件115
阿诺宁各组分的抗肿瘤活性和急性毒 性比较研究
阿诺 宁 (Anouning)是中国科学院华南植物园从国产番荔枝 科植物番荔枝Annona squamosa L. 种子中发现的具有高抗癌活性的番荔枝内醋有效部位药物， 其由质量分数大于90%的5一6个番荔枝内酷化合物和质量分 数小于10% 的未知成分组成。其中单体化合物squamocin 质量分数约占50%一60%，bullatacin质量分数约占9.0%一 15%。阿诺宁具有强的广谱的抗肿瘤作用，且用量小.将阿诺 宁(简称为A)分为两个部分，即其主 要成分组分(由squamocin和bullatacin以质量比约5:1比例组 成，简称为B)和非主要成分组分(除去squamocin和 bullatacin后的剩余部分，简称为C)
番荔枝提取物对早孕大鼠的作用
〔英〕/Damasceno D C⋯/Phytomedicine一2002，9(7)一 667^-67 作 者 研 究了超剂量的番荔枝Annonasquamosa Linn.种子 水提取物是否导致孕鼠流产，干扰大鼠的生殖行为，以及摄 人提取物是否与可能的大鼠胚胎植人的变化相关。 在鼠胎植人前期给予超剂量的番荔枝种子水提取物既不引起 子宫内膜形态学改变，也不干扰孕鼠的生殖能力。
细胞株
人鼻咽癌细胞(CNEZ)、人肝癌细胞(Bel一7402)、人口腔癌 细胞(KB)和人乳腺癌细胞(MCF一7);多药耐药性 multidrugresistance，MDR)细胞:对阿霉素耐药110.6倍的人 乳腺癌细胞(MCF一7/Adr)、对长春新碱(VCR)耐药100倍的 人口腔癌细胞(KBV200)，人体正常脐血管内皮细胞 (ECV3O4);人体正常肝细胞(Chang Liver cell，CLC)
医学寄生虫学-寄生虫英文单词
Parasitology 寄生虫学Fasiolopsis buski 布氏姜片吸虫Parasite 寄生虫Paragonimus westermani卫氏并殖吸虫Parasitosis 寄生虫病Schistosomajaponicum 日本血吸虫lifecycle 生活史schistosomiasis 血吸虫病host 宿主Oneomelania 钉螺definitiveorfinalhost 终宿主cestode(Class Cestoda) 绦虫intermediatehost 中间宿主Taenia solium 链状带绦虫reserviorhost 储蓄宿主Taenia saginata 肥胖带绦虫paratenichost 转续宿主Cystieercus 囊尾蚴infectivestage 感染期cysticercosis 囊虫病epidemiology 流行病学Echinococcusgranulosus细粒棘球绦虫pathogenesis 致病机理hydatidcyst 棘球蚴concomitantimmunity 伴随免疫Protczca 原生动物亚界premunition 带虫免疫Entamoeba histolytica 溶组织内阿米巴carrier 带虫者trophozoite 滋养体ectopicparasitism 异位寄生cyst 包囊helminth 蠕虫opportunisticprotozoan 机会致病原虫nematode(Class Nematoda) 线虫(纲) malaria 疟疾Ascaris lumbricoides 似蚓蛔线虫Plasmodium vivax 间日疟原虫adultworm 成虫ringform 环形滋养体ovum(p1．ova) 卵细胞sporozoite 子孢子directsmear 直接涂片法relapse 复发Trichuris trichiura 毛首鞭形线虫recrudescence 再燃hookworm 钩虫flagellate 鞭毛虫．Ancylostoma duodonale 十二指肠钩口线虫Leishmania donovani 杜氏利什曼原虫Necator americanus 美洲板口线虫Kala-azar 黑热病larve(p1．1arvae) 幼虫leishimaniasis 利什曼病brinefloration 盐水浮集法Trichimonus vaginalis 阴道毛滴虫Trichinella spiralis 旋毛形线虫Giadia lamblia 蓝氏贾第鞭毛虫filariasis 丝虫病Toxoplasma gondii 刚地弓形虫microfilaria 微丝蚴Pneumocystis carinii 卡氏肺孢子虫Wuchereria bancrofti 班氏吴策线虫tachymite 速殖于Brugia malayi 马来布鲁线虫bradyzoite 缓殖子noctunalperiodicity 夜现周期性PhylumArthropoda 节肢动物门Enterobius vermicularis 蠕形住肠线虫insect 昆虫trematodeematoda) 吸虫(钢) vector 媒介sucker 吸盘metamorphosis 变态oralsucker 口吸盘entomology 昆虫学ventralsucker 腹吸盘tick 蜱miracidum 毛蚴mosquito 蚊cercaria 尾蚴metacercaria 后尾蚴、囊蚴Clonorchis sinensis 华枝睾吸虫。
药名菌名
89 89 89 63 64 44 63 91 91 91 8 91 91 73 91 63 91 63 73 11 91
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E.casseliflavus E.cecorum E.cancerogenus E.cloacae E.coli E.dissolvens E.dispar E.durans E.coli, EIEC E.coli, EPEC E.coli, ETEC E.faecalis E.fergusonii E.faecium E.gallinarum E.gergoviae E.gilvus E.hermannii E.hormaechei E.hoshinae E.ictaluri E.intermedium E.lentum E.limosum E.malodoratus E.mundtii E.hirae E.nimipressuralis E.pseudoavium E.raffinosus E.sakazakii E.tarda E.vulneris F.groupⅡb C.indologenes C.meningosepticum F.mortiferum F.necrophorum F.nucleatum F.odoratum P.oryzihabitans F.varium G.capitatum G.haemolysans G.morbillorum G.penicillatum H.alvei H.alvei biogroup 1 H.aphrophilus
不饱和脂肪酸与炎症性肠病因果关系的孟德尔随机化分析
不饱和脂肪酸与炎症性肠病因果关系的孟德尔随机化分析*李 健1 高建淑1,2 赵可可1,2 高鸿亮1,2#新疆医科大学第一附属医院消化病二科1（830054） 新疆医科大学研究生学院2背景：炎症性肠病（IBD ）是一种慢性复发性胃肠道炎症性疾病，包括溃疡性结肠炎（UC ）和克罗恩病（CD ）。
目前尚不清楚不饱和脂肪酸与IBD 之间是否存在因果关系。
目的：采用两样本孟德尔随机化分析探究不饱和脂肪酸与IBD 之间的因果关系。
方法：不饱和脂肪酸和IBD 的全基因组关联研究（GWAS ）数据均来源于网络公开数据库。
采用逆方差加权分析法进行两样本孟德尔随机化分析，使用加权中位数法和MR⁃Egger 回归分析验证因果效应，以OR 及其95% CI 评价不饱和脂肪酸与IBD 风险的因果关系。
结果：ω⁃6脂肪酸与CD 无直接因果关系，与UC 有直接因果关系，逆方差加权分析结果显示ω⁃6脂肪酸基因水平每增加一个标准差，UC 风险增加16%（OR =1.16，95% CI : 1.00~1.36，P =0.04）。
而ω⁃3脂肪酸、单不饱和脂肪酸与IBD 之间均未发现因果关系。
结论：ω⁃6脂肪酸可能仅与UC 存在因果关系，ω⁃3脂肪酸、单不饱和脂肪酸与IBD 之间均未发现因果关系。
关键词 脂肪酸类，不饱和； 脂肪酸类，ω⁃6； 炎症性肠病； 结肠炎, 溃疡性； Crohn 病； 孟德尔随机化分析Causal Association Between Unsaturated Fatty Acids and Inflammatory Bowel Disease: A Mendelian Random ⁃ization Analysis LI Jian 1, GAO Jianshu 1,2, ZHAO Keke 1,2, GAO Hongliang 1,2. 1The Second Department of Gastroenterology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi (830054); 2Graduate School of Xinjiang Medical University, UrumqiCorrespondence to:GAOHongliang,Email:*************************.cnBackground: Inflammatory bowel disease (IBD) is a chronic recurrent inflammatory disease of gastrointestinal tract including ulcerative colitis (UC) and Crohn's disease (CD). It is unclear whether there is a causal association between unsaturated fatty acids and IBD. Aims: A two ⁃sample Mendelian randomization analysis was used to explore the causal association between unsaturated fatty acids and IBD. Methods: The data of the genome⁃wide association study (GWAS) of unsaturated fatty acids and IBD were obtained from web ⁃based public databases. Two ⁃sample Mendelian randomization analysis was performed by using inverse⁃variance weighted analysis, and weight median estimator and MR⁃Egger regression were conducted to validate the association of the causal effect. The causality of unsaturated fatty acids on the risk of IBDwas evaluated by OR and 95% CI . Results: No direct causal association was found between ω⁃6 fatty acids and CD, and a direct causal association was found with UC. Inverse⁃variance weighted analysis showed a 16% increase in the risk of UC for each standard deviation increase in ω⁃6 fatty acid gene levels (OR =1.16, 95% CI : 1.00⁃1.36, P =0.04). However, no causal association was found between ω⁃3 fatty acids, monounsaturated fatty acids and IBD. Conclusions: ω⁃6 fatty acids may be onlycausally associated with UC, and no causal association is found between ω⁃3 fatty acids, monounsaturated fatty acids and IBD.Key words Fatty Acids, Unsaturated; Fatty Acids, Omega⁃6; Inflammatory Bowel Disease; Colitis, Ulcerative; Crohn Disease; Mendelian Randomization AnalysisDOI ： 10.3969/j.issn.1008⁃7125.2023.01.003*基金项目：新疆维吾尔自治区自然科学基金杰出青年科学基金项目（2022D01E25）炎症性肠病（inflammatory bowel disease, IBD ）是一种免疫介导的胃肠道慢性炎症性疾病，包括溃疡性结肠炎（ulcerative colitis, UC ）和克罗恩病（Crohn's disease, CD ），临床特征以腹痛和腹泻为主。
抑制血管通透性及凋亡的方法[发明专利]
![抑制血管通透性及凋亡的方法[发明专利]](https://img.taocdn.com/s3/m/6306d6e8b52acfc788ebc9af.png)
基于建构主义学习理论的中小学信息技术“CPU”专题学习网站的设计发布时间：2021-03-19T15:14:24.053Z 来源：《中小学教育》2020年第34期作者：念存菊[导读] 本课题研究的目的是把建构主义学习理论和中小学信息技术课程标准相整合并应用于专题学习网站的设计与开发中念存菊云南省红河哈尼彝族自治州泸西县第一中学652499摘要：本课题研究的目的是把建构主义学习理论和中小学信息技术课程标准相整合并应用于专题学习网站的设计与开发中，旨在强调学习者的主体作用，为学生创造一个网络化的学习平台.关键字：信息技术；专题学习网站；CPU；中小学1 引言1.1 研究背景中小学生由于年龄小，好玩好动，对网络充满好奇，很多学生愿意把更多的时间用来上网。
抓住中小学生的这个特点，我们可以以网络为平台，搭建专题学习网站，创建一个学生感兴趣的学习环境，尝试将学生正确的引导到网络的教学环境下，不仅满足学生的好奇心，也能让学生学到科学文化知识，从而提高学习质量。
1.2 问题的提出基于学生学习的心理，我们可以尝试利用网络信息技术，创设网络化的学习环境，搭建网络环境下的学习平台，为学生能高效的学习创设条件。
专题学习网站作为新形势下的网络化学习平台，能满足当代中小学生的学习心理，顺应时代的潮流。
中小学信息技术课程标准中要求学生了解计算机的硬件组成，而CPU是计算机的核心部件，控制着计算机的整个运行过程，这就要求学习者对其进行系统的学习。
1.3 国内研究现状及发展趋势“专题学习网站其本质是一种基于网络资源的研究性学习系统，让学习者自己选择和确定研究课题，应用知识和工具去解决实际问题。
专题学习网站不同于一般的网络课件或网络学校，它主要是提供实现研究性学习的学习资源和协作研究学习环境。
专题学习网站必须包括的一般性内容有：专题知识、专题协作学习环境、专题资源库和专题评价。
1.3.1 国内研究现状国内关于中小学的专题学习网站的建设情况是：80.68%已经建设完成，有13.64%的网站的个别功能正在建设中，有5.68%的网站功能框架还未健全，且资源少。
抗真菌剂及益生元的药物组合物与念珠菌性阴道炎的治疗方法[发明专利]
![抗真菌剂及益生元的药物组合物与念珠菌性阴道炎的治疗方法[发明专利]](https://img.taocdn.com/s3/m/5e8189baad02de80d5d840b0.png)
专利名称：抗真菌剂及益生元的药物组合物与念珠菌性阴道炎的治疗方法
专利类型：发明专利
发明人：亚历山大·弗拉基米罗维奇·季科夫斯基,奥格列·瓦连京诺维奇·多罗日科,鲍里斯·阿纳托列维奇·鲁多伊
申请号：CN200880130753.7
申请日：20080930
公开号：CN102123736A
公开日：
20110713
专利内容由知识产权出版社提供
摘要：本发明涉及医学和药学领域，更具体地涉及含有抗真菌剂和益生元的用于治疗念珠菌性阴道炎和外阴阴道炎的阴道栓剂的药物组合物。
用于治疗的组合物成分可起到协同作用：通过益生元来刺激阴道正常菌群的生长；通过现代抗真菌剂来抑制并消除念珠菌属致病真菌。
另外，该组合物主要含有对典型正常菌群，例如乳酸杆菌和双歧杆菌不敏感的抗真菌剂。
用于治疗真菌性或细菌性阴道病、阴道炎和外阴阴道炎的方法是利用抗真菌剂和益生元的药物组合物进行局部用药。
申请人：亚历山大·弗拉基米罗维奇·季科夫斯基
地址：俄罗斯联邦莫斯科圣阿维阿特申那亚79/3,356号
国籍：RU
代理机构：上海智信专利代理有限公司
代理人：邓琪
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西班牙语教程第二册答案
第二册答案第1课II. 把动词变为陈述式过去未完成时1.cog a2.saludaba3.Asistiamos4.Madrugaba5. apeabas6.llegaba7.deten a8.entend as9.desped a 10.Jug a bamosv.1.tenia cultivaba2.conversaban3.nadabamos4.pod a5.asistian se divertian6.se alojaban7.sol era8.ten an era9.era queria 10.estabaVI.1.Mientras curazaba la plaza, me encontr e con una amiga.2.El vistante pregunta si habia un momumento a Cervantes en el parque.3.Me dice que con estecarnet podia yo visitar gratis la exposicion.4.Nos pregunta d o nde se conaepjanos de ciudad.5.Los turistas creen que las cosas les van a resultar muy complicadas.6.Nos se?ala aquel palacio que es inmenso.o el museo de Prado es inmenso, no podemos recorrerlo en una ma?ana.8.El taxita nos lleva a un hostal que cerca de una estaci o n de metro.9.Ella ve a alguien que camina hacia ella.10.No puedo asistir a la clase porque me siento indispuesto.fue 7.toca 8.toca 9.quito 10.Pon 11.Ponganse 12.sigue 13.Seguiste 14.pones 15.segu aXI.1.que2.a3. de que a4.que a5.que6.A de7.de8.en con9.de a 10.a en an IVIII:. el ejercicio hecho la tema conversada la nota copiado los coches producidos la celebracion celebrado el huerto cultivado el cuento contado el invitado alojado en mi casa el pescado cocinadola cosa perdidolos libros repartidoel camino indicadoel monumento admirado la entrada conseguidola ropa metidoIX1. Quitan2. Me voy 3;ir 4.quitar 5.tocar 6.se XII.1.H aga el favor de pasarme las revistas que est2.El muchacho que nada en el rio es mi primo.3.Les voy a presentar a la se?orita G4.Ve a ayudar a tu madre que barre el comedora n en la mesa.o mez que estudi o junto conmigo en una escuela hace varios a?os.5. Puede usted pasarme el diccionario que tiene a su lado?6. Es inreresante el cuento que lee?7. Comemos en ese comedor que quede cerca de la bibioteca.8. Vamos a visitar a la profesora extranjera que trabaja en nuestra facultad. 9. Levant o un viento que me sec . o el sudor10. El doctor le curo la enfermedad el receto una medicina tradicionalXV.su garganta y lengua. Luego le dijo que era un resfriado, pero no muy grave y que no tencasa ella desansaba unos d as y se sent a mejor.第2课II1. Se celebraba una velada cada fin de semana el a?o pasado.2. El hombre cesaba el trabajo cada vez que o a el ruido. i3. Los ni?os difrutaban mucho jugando todos las tardes durante las vacaciones.4. Todos se fijaban en m siempreique etraba.5. Bailabamos cueca,marinera y tango en todas las fiestas en aquel entonces.6. Le aplaud amos mucho todas las vecesque recitaba.7. Sudaba mucho jugando al boloncesto en quellae poca.8. Se desped an de nosotro a la diez todas las noches entonces.9. El m e dico me recetaba medicina tradicional china siempre que me atendia.10. La madre se preocupaba mucho por la hija porque regresaba tarde cadi todas las neches en aquellae poca.III.1. Dijo hac a2.pregunt o ae3tDijoi dol ai 4.dije ten ai 5.entr acababa 6.dijo tenia era 7.Dijo pod a 8.V bailaba 9.contestaba sab a lO.preguntaron gustabaIV.1. Me pregunt o si me importaba esperar un rato.2. Dijiste que un asno pasataba tranquilamente en el prado.3. Contestaron que sent an mucho miedo.4. Le pregunt e por que a eeffiinmo. i5. Repondi o que el hombre que busc o cojeaba un poco.6. le di e queateranz o n.7. Le preguntamos que hab a un monumento a Cervantes en la plaza. 8. Me pregunt o d o nde saenpcoodnseguir entradas.Ana se lavant o tarde ,apyoe r que se sentio indispudetdol a lacabeza y la garganta, ten a la nariz itapada y perdio el apetito.P a rque ten a fi fe bre. Se puso el termo ：m37e.n8tgrorados. Decidi o ir alhospital. El m e dico le atenci o simpaticamente, le auscult o , le tom o el pulso, le tom o la tempa por qu epreocuparse.Ana fue a la farmaria con la receta que el m e dico le recta o le. Lpauseonufenramienryaetcocdiav o in. En9.Contest o que qaerer un p exposicion de Goya.10.Dijieron que era muy complicado el problema.。
什么是热带性肺嗜酸粒细胞浸润症
什么是热带性肺嗜酸粒细胞浸润症
*导读：1943年Weingarten等首先于印度、斯里兰卡等地发现热带性肺嗜酸粒细胞浸润症或称热带性嗜酸粒细胞增多症（tropicaleosinophilia），又称Weingarten综合征。
……
1943年Weingarten等首先于印度、斯里兰卡等地发现热带性肺嗜酸粒细胞浸润症或称热带性嗜酸粒细胞增多症(tropical eosinophilia)，又称Weingarten综合征。
其后在非洲、拉丁美洲、东南亚及我国南方均有发现。
本症主要与丝虫感染有关，男性多于女性，多见于青壮年。
常见临床症状有咳嗽、喘鸣、胸闷乏力、厌食及发热等。
咳嗽剧烈，但痰多粘稠，不易咳出，有时痰中带血。
可有哮喘样发作。
少数患者可有心律失常及消化系统表现。
若不给予有效治疗，病程常迁延反复，数年后可由于肺纤维化出现肺功能不全的表现。
体检可发现肺部哮鸣音及轻度肝、脾、淋巴结肿大。
实验室检查外周血嗜酸粒细胞显著增加，可超过2500/mm3，甚至更高。
IgE 也相应增高。
胸部X线表现为粟粒状或模糊阴影，中下肺野、两侧分布为多。
经治疗后肺部X线异常可很快消失。
但慢性患者常遗留肺间质纤维化。
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Autarquía política de aislamiento económico de un país respecto a la economía de los demás
impuestos y su consumo.
1
IE Business School DICCIONARIO DE ECONOMÍA EC2-102
Ahorro público la cantidad de ingresos fiscales que le queda al Estado una vez pagado su
Administraciones Públicas (también se denomina Gobierno o Estado) es el conjunto de las
Administraciones central, regional y local, así como las Administraciones de la Seguridad Social, quedando excluidas las entidades de titularidad pública que lleven a cabo operaciones comerciales, como las empresas públicas. Las Administraciones Públicas se dedican principalmente a la producción de bienes y servicios que no son de mercado y que entrañan, en muchos casos, redistribución de la renta y de la riqueza nacional.
EC2-102
DICCIONARIO DE ECONOMÍA
Compilación del profesor Rafael Pampillón del IE Business School. Versión original de 16 de febrero de 2007. Última revisión, 1 de febrero de 2008 (R.L.) Editado por el Departamento de Publicaciones del IE. María de Molina 13, 28006 – Madrid, España. ©2007 IE. Prohibida la reproducción total o parcial sin el permiso escrito del IE.
Ahorro parte de la renta actual que no se destina al consumo presente, también se puede definir
como la acumulación de riqueza durante un cierto período de tiempo. El ahorro empresarial es la generación de beneficios y la no-distribución de los mismos por las empresas. El ahorro del gobierno es la diferencia entre sus ingresos y los gastos públicos en bienes y servicios. El ahorro permite que las economías se desarrollen. Normalmente el ahorro se transforma en inversión a través de los intermediarios financieros. Suele ocurrir que, tanto las empresas como el Estado, generan menos ahorro del que necesitan. Por tanto, las empresas y el Sector Público necesitan ahorro de las economías domésticas que son las generadoras netas de ahorro.
Acción título (o valor) que da derecho a la propiedad parcial de una empresa. Las acciones
son títulos de renta variable y comprenden las acciones cotizadas en Bolsa (acciones cotizadas), las acciones no cotizadas y otras formas de participación. Los valores de renta variable suelen generar ingresos en forma de dividendos.
gasto corriente.
Amortización
→ DEPRECIACIÓN.
Apreciación de los stocks subida del valor de las existencias. Asistencia técnica servicios ofrecidos, generalmente por ingenieros y técnicos, para el
Ayuda oficial al desarrollo (AOD) préstamos desembolsados en condiciones muy
favorables y subvenciones concedidas por organismos oficiales de los miembros del Comité de Asistencia para el Desarrollo (CAD), por instituciones multilaterales y por países no miembros del CAD con el fin de propiciar el desarrollo económico y el bienestar en los países pobres. Incluye préstamos con un componente de subvención de por lo menos el 25%. También se puede definir como el conjunto de recursos financieros gubernamentales suministrados por los Países Desarrollados (PD) a los Países en Desarrollo (PED). La AOD se puede conceder a través de tres canales: 1) Directamente por la Unión Europea o bien por los gobiernos estatales, regionales o locales. 2) A través de instituciones financieras multilaterales, como el Banco Mundial. 3) Por medio de las Organizaciones no Gubernamentales de Desarrollo (ONGD). En este último caso, en el de las ONGD, habría que excluir del cómputo de la AOD los recursos privados canalizados por las ONGD. La AOD responde teóricamente a las siguientes características: a) Persigue tres objetivos esenciales: construir la democracia, favorecer el desarrollo económico y proteger el medio ambiente de los PED. b) Reviste un carácter de liberalidad que comporta un elemento de subvención (gratuidad) de al menos un 35%. La liberabilidad puede alcanzar el 100% de la ayuda (ayuda no reembolsable). La AOD puede ser bilateral o multilateral. La cooperación bilateral es la que procede directamente de fuentes gubernamentales y se hace efectiva mediante donaciones o créditos blandos de gobierno de PD a gobierno de PED. Objetivo de las Naciones Unidas es que los países desarrollados alcancen el 0,7% del PNB en ayuda al desarrollo. Muchos PD condicionan su AOD a la exportación de sus bienes y servicios a los PED. El problema del condicionamiento es que los países donantes pueden forzar a los países receptores a pagar más por las importaciones (compras) financiadas con la ayuda que les dan que lo que pagarían en el mercado. En este sentido, la AOD ha sido concebida más como un medio eficaz para aumentar las exportaciones de los PD que para sacar del subdesarrollo a los PED. Qué duda cabe que alguna ayuda al desarrollo podría estar motivada por razones morales y humanitarias hacia los países menos afortunados. Sin embargo, la mayor parte de la AOD está condicionada por razones políticas y económicas de los países donantes.