女性腹部脂肪抽吸手术前后焦虑抑郁状态调查

目的探讨女性腹部脂肪抽吸手术前后焦虑、抑郁情绪反应的发生率及变化情况。方法采用焦虑自评量表、抑郁自评量表对行腹部脂肪抽吸女性病人76例及随机抽取正常青年女性104人为调查对象。结果术前焦虑状态、抑郁状态发生率分别为28.96%、23.67%,术后焦虑状态、抑郁状态发生率分别为23.69%、18.40%,分别与对照组比较均存在显著性差异（P〈0.05）,手术前后焦虑自评量表、抑郁自评量表评分比较,术后焦虑量表评分明显低于术前（P〈0.05）,高于对照组（P〈0.05）,而术后抑郁自评量表与术前比较无显著性差异（P〉0.05）。结论女性腹部脂肪抽吸手术前普遍存在焦虑、抑郁情绪障碍,在病人术前和术后应加强心理干预。     

Loss of claudin-1 expression induces epithelial-mesenchymal transition through nuclear factor-κB activation in colorectal cancer

Objective

The aim of this study was to elucidate the clinicopathological significance and prognostic role of loss of claudin-1 in colorectal cancer (CRC).

Relationship between normal heart size and body indices in Korean

We provided a curve-fit equation to predict the normal heart weight (g) in Koreans by examining 422 autopsies (215 males and 207 females, from newborn to age 77 yr) who were relatively in good general condition. Heart weight was well correlated with body surface area (m2), body weight (kg), and body height (cm) but poorly with age in both sex. Heart weight progressively increased from birth to the earlier 3rd and 4th decades in male and female, respectively, and then gradually decreased; mean heart weight of all age group was greater in male than in female and significantly different from birth to 4th decade. In both sex, heart weight exponentially increased in accordance with the increase of body height, body weight, and body surface (in male, heart weight=0.00312 x body height(2.239), r2=0.750, p<0.0001; in female, heart weight=0.00443 x body height(2170), r2=0.781, p<0.0001; in male, heart weight=9.22 x body weight(0.853), r2=0.770, p<0.0001; in female, heart weight=9.00 x body weight0.855, r2=0.820, p<0.0001; in male, heart weight=155.18 x body surface area1.290, r=0.808, p<0.0001; in female, heart weight=124.13 x body surface area1.242, r=0.834, p<0.0001). These results indicate that heart weight is better correlated with body surface area than with body weight; however, body weight should be a better determinant of a predicted heart weight, since body surface area is entirely dependent on body height and body weight.     

Ultrastructural study of hepatic mitochondrial abnormality in swine treated with clofibrate

Administration of clofibrate frequently reduces serum cholesterol levels in hypercholesterolemic swine to near the base level within a few weeks even when the hypercholesterolemic diet is continued. The current study was designed to investigate hepatic ultrastructural changes that might be associated with the hypocholesterolemic effect of clofibrate. Characteristic ultrastructural changes were observed in 17% of hepatocellular mitochondria after 6 wk of clofibrate treatment. The most frequent mitochondrial alteration was the presence of discrete bundles of tubular or spiral structures which appeared at random in orientation. The number of microbodies increased moderately but no structural changes were noted.     

Morphine prevents glutamate-induced death of primary rat neonatal astrocytes through modulation of intracellular redox

This study is designed to investigate the effect of morphine on glutamate-induced toxicity of primary rat neonatal astrocytes. Glutamate decreases the intracellular GSH level, and thereby induces cytolysis of astrocytes and C6 glial cells accompanied by apoptotic features. Glutamate-induced cytotoxicity is protected by morphine and antioxidants such as GSH and NAC, whereas MK-801, an antagonist of glutamate receptor NMDA does not protect astrocytes against glutamate toxicity. Also, morphine antagonist, naloxone, as well as selective ligands for opioid receptor subtypes, including DAMGO, DPDPE, and U69593, do not inhibit the protective effect of morphine on glutamate-induced cytotoxicity. Morphine significantly prevents the depletion of GSH by glutamate and thereby inhibits the generation of H2O2 in a dose-dependent manner. Furthermore, morphine prevents the change of mitochondrial permeability transition by glutamate. Taken together, we suggest that morphine protects the primary rat neonatal astrocytes from glutamate toxicity via modulation of intracellular redox status.     

757例体检人群血脂水平调查分析

目的 :了解“健康”体检人群不同年龄组的血脂水平。方法 :对75 7例体检人群的血清甘油三酯 (TG)、总胆固醇 (TC)、高密度脂蛋白胆固醇 (HDL C) ,按年龄分组 ,采用SPSS10 .0软件进行统计分析。结果 :2 0～ 2 9岁组的TG (1.2 8± 0 .63mmol/L)与 3 0～ 3 9岁组(1.5 6± 0 .78mmol/L)和 40～ 49岁组 (1.5 1± 0 .79mmol/L)均有显著性差异 (P <0 .0 1) ;其它各组间无显著性差异。 2 0～ 2 9岁组的TC (4 .5 8± 0 .88mmol/L)与 3 0～ 3 9岁组 (4 .97± 0 .97mmol/L)、40～ 49岁组 (5 .0 0± 1.0 3mmol/L)、5 0～ 5 9岁组 (5 .0 0± 1.0 4mmol/L)、60～ 69岁组 (5 .0 7± 0 .96mmol/L)均有显著性差异 (P <0 .0 1);其它各组间无显著性差异。HDL C水平 70～ 77岁组均显著高于其它各年龄组 ,而其它各年龄组间无统计学差异。TG ,TC ,HDL C的异常率分布在各年龄组间无统计学差异 (P >0 .0 5 )。结论 :75 7例体检人群血脂水平呈升高趋势 ,中青年人群更为明显 ,应当提倡文明饮食和健康的生活方式 ,加强健康教育     

Mutational analysis of Fas ligand gene in human non-Hodgkin lymphoma

Among the systems triggering apoptosis, the Fas-Fas ligand (FasL) system is recognized as a major pathway for the induction of apoptosis in cells and tissues. Ligation of Fas by either an agonistic antibody or FasL transmits a 'death signal' to the target cell, potentially triggering apoptosis. Alterations of genes along the Fas-mediated apoptosis pathway have been reported in many human cancers. However, there have been no data regarding FasL gene mutations in human cancers. We hypothesized that FasL gene mutation might be involved in the development of non-Hodgkin lymphoma (NHL). In this study, we analyzed the entire coding region of the FasL gene for the detection of somatic mutations in a series of 111 NHLs and found that one tumor had a FasL gene mutation in the cytoplasmic domain. To evaluate the functional alterations of the mutant in apoptosis, we overexpressed the mutant in 293T cells, but couldn't find any significant loss of cell death compared to the wild-type FasL. Together, these data suggest that FasL is occasionally mutated in human NHL and that FasL mutations appear to play no role in the pathogenesis of the vast majority of NHLs.     

恶性肿瘤患者红细胞变形性的研究(附153例临床分析)

观察153例恶性肿瘤(MT)患者红细胞变形能力(RCD)明显低于正常人(P<0.01),病情越重,RCD下降越明显。RCD下降与血液粘度增高、RBC膜过氧化性损害加重有关。血液粘度增高及RCD下降有利于肿瘤细胞的附壁、癌性血栓形成,使肿瘤免疫失效,有利于肿瘤生长及转移。认为RCD的检测对了解MT的病情及估计预后有重要意义。改善血流变性、提高RCD、有助于缓解肿瘤生长及转移的预防。     

Polyl-histidine

Poly-l-histidine (PHSTD) of molecular weight 26,000 induced the generation of large amounts of Superoxide (O ₂ ^– ) and hydrogen peroxide (H₂O₂) in human neutrophils (PMNs). Despite its low solubility at neutral pH, PHSTD was bound very rapidly to the PMN surfaces. Maximal generation of O ₂ ^– took place with 4–5 ×10^–6 M of PHSTD, starting after a lag of about 25 sec and proceeding for 15–17 min at a rate of 150 nmol/10⁷ PMNs/min, suggesting that this polycation is one of the most potent stimulators of O ₂ ^– generation known, PHSTD was found to be non-toxic for PMNs even at millimolar concentrations. Generation of O ₂ ^– by PHSTD depended on extracellular calcium; it was inhibited by calcium channel blockers and by trifluoperazine, and it triggered a sharp rise in intracellular calcium as determined by the Quin 2 fluorescence technique. The generation of both O ₂ ^– and H₂O₂ by PHSTD was partially inhibited by cytochalasin B or (CYB, CYE). On the other hand, CYB markedly enhanced the generation of both O ₂ ^– and H₂O₂ following stimulation of PMNs either by PHSTD, polyarginine, histone, or by antibody-opsonized group A streptococci. Electron microscopic analysis and NBT reduction tests revealed that both PHSTD and PHSTD-opsonized streptococci were avidly phagocytosed by PMNs. Since CYB totally inhibited internalization of both PHSTD and the PHSTD-opsonized streptococci, it was suggested that these agents stimulated oxygen radical generation mainly on the leukocyte surfaces. Complexes (CX) formed between PHSTD and polyanethole sulfonate (a strong polyanion) or between histone and the polyanion mimicked immune CX in their ability to trigger the generation of large amounts of O ₂ ^– which were inhibited by CYB. Generation of O ₂ ^– and chemiluminescence either by PHSTD or by PHSTD-opsonized streptococci were markedly inhibited by poly-l-glutamate, suggesting that PHSTD acted as a cationic agent which interacted via electrostatic forces with some negatively charged sites in the leukocyte membrane. Generation of H₂O₂ by PHSTD was also markedly inhibited by deoxyglucose, KCN, DASA, as well as by the lipoxygenase inhibitors nordihydroguaiaretic acid, phenidone, and propylgallate. On the other hand, cyclooxygenase inhibitors such as aspirin, indomethacin, and piroxicam were inactive, suggesting that arachidonic acid metabolism via lipoxygenase pathway might have been involved in the activation by PHSTD of the NADPH oxidase in PMNs. PHSTD may mimic the effects of antibodies both as an opsonin and as a potent stimulator of the respiratory burst in PMNs and may thus serve as a model for further study of leukocyte-bacteria interactions in infectious and inflammatory sites and of the pathogenicity of immune complexes.Supported by a research grant from Dr. S. M. Robbins of Cleveland, Ohio.     

Localization of the third component of complement on the cell wall of encapsulated Staphylococcus aureus M: implications for the mechanism of resistance to phagocytosis.

Encapsulated Staphylococcus aureus strains are more virulent than unencapsulated staphylococci, and this phenomenon has been associated with decreased opsonization of encapsulated bacteria by normal human serum. Peptidoglycan, a major cell wall component of S. aureus, has been shown to promote opsonization of this bacterial species by certain components of the serum complement system. However, when the processes of complement activation and opsonization of encapsulated staphylococci have been studied, it has been found that encapsulated bacteria activate complement efficiently and C3 is bacteria associated, yet these organisms are not efficiently phagocytized by human polymorphonuclear leukocytes. In this study, the hypothesis was tested that opsonically active molecules are not on the true external surface of encapsulated organisms but rather are cell wall associated and thus "hidden" from human polymorphonuclear leukocytes. By using immunoelectronmicroscopy, C3 was found to be localized on the cell wall of an encapsulated S. aureus strain after incubation of the organism in normal human serum. When shrinkage of the capsule was prevented by treatment with anticapsular antibody, the C3 was again shown to be cell wall associated and located beneath the bacterial capsule. These results suggest that encapsulated S. aureus may resist phagocytosis because opsonically active C3 molecules are not exposed at the true external surface of the bacterium.