抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

The metabolic syndrome has received increased attention in the past few years. This statement from the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) is intended to provide up-to-date guidance for professionals on the diagnosis and management of the metabolic syndrome in adults.

The metabolic syndrome is a constellation of interrelated risk factors of metabolic origin— metabolic risk factors —that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD).1 Patients with the metabolic syndrome also are at increased risk for developing type 2 diabetes mellitus. Another set of conditions, the underlying risk factors , give rise to the metabolic risk factors. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria to be used in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general they include a combination of both underlying and metabolic risk factors.

The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics commonly manifest a prothrombotic state and a pro-inflammatory state as well. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B (apoB), increased small LDL particles, and a reduced level of HDL cholesterol (HDL-C). The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of ASCVD risk factors, but one that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to which components of the syndrome are …

https://www.lipidcenter.com/pdf/metabolic.pdf

Diagnosis and Management of the Metabolic Syndrome An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement

The current obesity epidemic poses a major public health issue since obesity predisposes towards several chronic diseases BMI and total adiposity are positively correlated with cardiometabolic disease risk at the population level However, body fat distribution and an impaired adipose tissue function, rather than total fat mass, better predict insulin resistance and related complications at the individual level Adipose tissue dysfunction is determined by an impaired adipose tissue expandability, adipocyte hypertrophy, altered lipid metabolism, and local inflammation Recent human studies suggest that adipose tissue oxygenation may be a key factor herein A subgroup of obese individuals - the 'metabolically healthy obese' (MHO) - have a better adipose tissue function, less ectopic fat storage, and are more insulin sensitive than obese metabolically unhealthy persons, emphasizing the central role of adipose tissue function in metabolic health However, controversy has surrounded the idea that metabolically healthy obesity may be considered really healthy since MHO individuals are at increased (cardio)metabolic disease risk and may have a lower quality of life than normal weight subjects due to other comorbidities Detailed metabolic phenotyping of obese persons will be invaluable in understanding the pathophysiology of metabolic disturbances, and is needed to identify high-risk individuals or subgroups, thereby paving the way for optimization of prevention and treatment strategies to combat cardiometabolic diseases

/pdf/the-metabolic-phenotype-in-obesity-fat-mass-body-fat-1f28h51lv5.pdf

The Metabolic Phenotype in Obesity: Fat Mass, Body Fat Distribution, and Adipose Tissue Function

Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement.

The metabolic syndrome

Localization of leptin receptor (OB-R) gene expression in mouse brain by in situ hybridization

Molecular biology and nutrition: the quest for integration.

Rapid chemiluminescent detection of facilitative glucose transporter mRNAs (GLUTs 1-4) with digoxigenin end-labelled oligonucleotides.

402 Spiegelman, B., eds.), vol. 133, pp. 219-236, Alan R. Liss, New York 8 Ibrahimi, A., Bertrand, B., Bardon, S., Amri, E., Grimaldi, P., Ailhaud, G. and Dani, C. (1993) Biochem. J. 289, 141-147 9 Breviaro, F., d’hiello, E. M., Golay, J., Peri, G., Bottazzi, B., Bairoch, A., Saccone, S., Marzella, R., Predazzi, V., Rocchi, M., Della Valle, G., Dejana, E., Mantovani, A. and Introna, M. (1992) J. Biol. Chem. 267,22190-22197 10 Lee, G. W., Lee, T. H. and Vilcek, J. (1993) J. Immunol. 150, 1804-1812 1 1 Amri, E., Bonino, F., Ailhaud, G., Abumrad, N. and Grimaldi, P. A. (1995) J. Biol. Chem. 270, 23672371 12 Amri, E., Ailhaud, G. and Grimaldi, P. A. (1994) J. Lipid Res. 35, 930-937 13 Nandan, D., Clarke, E. P., Ball, E. H. and Sanwal, B. D. (1990) J. Cell. Biol. 110, 1673-1679 14 Vassaux, G., Gaillard, D., Ailhaud, G. and NCgrel, R. (1992) J. Biol. Chem. 267, 11092-1 1097 15 Vassaux, G., Gaillard, D., Darimont, C., Ailhaud, G. and NCgrel, R. (1992) Endocrinology 131, 2393-2398

Uncoupling protein in brown adipose tissue: molecular differentiation of the adipose tissues

Delta 9-Tetrahydrocannabinol (20 mg/kg i.p.) and propranolol (20 and 50 mg/kg i.p.) produced marked falls in the rectal temperatures of mice kept at an ambient temperature of 22 degrees C. Propranolol (50 mg/kg i.p.) also decreased the thermogenic activity of brown fat, as measured by a decrease in the level of [3H]GDP binding to mitochondria obtained from mouse interscapular brown adipose tissue. In contrast, delta 9-tetrahydrocannabinol (20 mg/kg i.p.) did not affect mitochondrial GDP binding even though the dose used was one shown previously to depress heat production. GDP binding was also unaffected by this cannabinoid in brown adipose tissue taken from mice that had been kept at 13 degrees C instead of 22 degrees C. In mice kept at 34 degrees C, isoprenaline (0.25 and 1.0 mg/kg s.c.) induced a marked rise in rectal temperature and increased the level of GDP binding to brown fat mitochondria. Propranolol (50 mg/kg i.p.) prevented the hyperthermic response to isoprenaline, the mice becoming hypothermic instead. Delta 9-Tetrahydrocannabinol (20 mg/kg i.p.) had no effect on isoprenaline-induced hyperthermia. We conclude from these data that there is no significant involvement of brown adipose tissue in the hypothermic response of mice to delta 9-tetrahydrocannabinol.

Evidence that the hypothermic response of mice to delta-9-tetrahydrocannabinol is not mediated by changes in thermogenesis in brown adipose tissue.

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