Elevated concentrations of linoleic acid in erythrocyte membrane phospholipids in patients with inflammatory bowel disease

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn disease (CD), is a disorder characterized by diffuse inflammation of the gastrointestinal tract. The immune response and inflammation are mediated by polyunsaturated fatty acids and influenced by dietary fats and lipid metabolism. This study examined the qualitative and quantitative fat intake of IBD patients and healthy controls on plasma phospholipid and erythrocyte membrane phospholipid (EMP) fatty acid content. Measurement of the fatty acid composition of plasma phospholipid and EMP were performed in 29 UC patients, 20 CD patients, and 31 healthy controls. Anthropometric characteristics and data on dietary intake were also collected. We observed significantly lower lipid intake in UC and CD patients vs controls. The UC and CD patients had significantly higher levels of linoleic acid in their EMP than did controls. There were no significant differences in the levels of n-3 polyunsaturated fatty acids, but there were significantly higher levels of the n-6 in the EMP of UC and CD patients compared with controls. The significant differences persisted after the data were adjusted for potential confounders and lipid intake. Higher levels of linoleic acids and n-6 fatty acids, which are involved in production of proinflammatory mediators, were found in IBD patients compared with controls, thereby implicating n-6 fatty acids in the pathophysiology of the disease.     

爱维治对烧伤患者心肌组织缺血缺氧的保护作用

目的:研究爱维治对烧伤患者心肌组织缺血缺氧的影响。方法:本研究为随机、开放、对照性多中心研究。选择烧伤总面积在30%~70%总体表面积(TBSA)且血清乳酸值异常的患者作为研究对象,将70例患者随机分为两组:试验组(n=36)给予爱维治30 mL 生理氯化钠溶液250 mL,静脉滴注,qd,给药7 d;对照组(n=34)仅给予生理氯化钠溶液250 mL,静脉滴注,qd,共7 d。取患者用药前、用药后48 h,72 h和7 d的血样,以血清乳酸值、心肌型肌酸激酶同工酶和肌钙蛋白作为主要监测指标,评价爱维治对烧伤后患者心肌组织的影响。结果:两组血清乳酸值、心肌型肌酸激酶同工酶、肌钙蛋白阳性率在观测期内均有下降,但试验组下降的时间早且幅度大,有统计学意义。结论:爱维治能够有效而且快速改善大面积烧伤患者心肌组织缺血缺氧状况。     

景蜂胶囊对小鼠抗应激作用的实验研究

景蜂胶囊是由红景天、枸杞、高原油菜蜂花粉、党参、女贞子多糖和黄芪多糖组成的中药制剂。本文报道该制剂对小鼠抗应激的作用。     

Pleural flap closure of pericardial defects following intrapericardial pneumonectomy.

Persistent pericardial defects following intrapericardial pneumonectomy are, historically, the major cause of iatrogenic cardiac herniation. This complication is uniformly fatal when unrecognized and untreated and has been associated with a 43% mortality even with surgical correction. Suture approximation of all small defects is recommended, and a technique for routine pleural flap closure of moderate to large-sized defects is described.     

Activation of hepatic guanylate cyclase by nitrosyl-heme complexes: Comparison of unpurified and partially purified enzyme

The objective of this study was to evaluate the effects of several agents on activation of both unpurified and partially purified hepatic soluble guanylate cyclase by performed NO (nitric oxide or nitrosyl)-heme complexes. Guanylate cyclase was activated by NO complexes of the heme compounds, hematin, hemoglobin, myoglobin, catalase and cytochrome c, and also by the reaction product of NO and ferredoxin, a non-heme, iron sulfur electron transfer protein. NO-lipoxygenase, which contains non-heme iron, did not activate guanylate cyclase. NO-heme complexes activated unpurified enzyme almost equally well in the presence of either Mg²⁺ or Mn²⁺. However, activation of purified (350- to 750-fold) guanylate cyclase was markedly greater with Mg²⁺ than with Mn²⁺. At concentrations that did not alter basal enzymatic activity, Ca²⁺ markedly inhibited guanylate cyclase activation in the presence of Mg²⁺ but not of Mn²⁺. Hemoproteins inhibited activation of unpurified and purified enzyme by NO-heme complexes, and increasing the concentrations of the latter overcame the inhibition. Gel filtration studies indicated that uncomplexed and NO-complexed hematin bind to common or adjacent sites on guanylate cyclase. Whereas dl-dithiothreitol enhanced activation, ferricyanide, cystine, o-iodosobenzoic acid and ethacrynic acid inhibited activation of guanylate cyclase by NO-heme complexes. The data indicate that the effects of these diverse agents on guanylate cyclase activation by preformed NO-heme are similar to their effects on enzyme activation by NO and nitroso compounds, both of which readily form NO-heme complexes. Therefore, the effects of these diverse agents may be on guanylate cyclase rather than on NO-heme formation.     

The use of a bedside assay for plasma B-type natriuretic peptide as a biomarker in the management of patent ductus arteriosus in premature neonates

OBJECTIVE: To test the utility of the bedside plasma concentration of B-type natriuretic peptide (BNP) assay as a screen for patent ductus arteriosus (PDA) in premature neonates. STUDY DESIGN: Newborn infants admitted to the neonatal intensive care unit (NICU) had paired echocardiography and BNP measurements at enrollment and every 4 to 5 days. RESULTS: Twenty neonates (gestational age approximately 28.6 weeks and birth weight approximately 1161 g) had 81 paired echocardiography and BNP determinations. BNP ranged from 5 to 3900 pg/mL. Fifty-six of 81 echocardiograms showed PDA. Significant correlations were found between BNP and ductal size and degree of shunting. Correlation was greater in infants >2 days of age. BNP >300 pg/mL predicted significant PDA, whereas BNP <105 pg/mL predicted absence of significant PDA. CONCLUSION: Bedside measurement of BNP correlates with magnitude of PDA in premature newborns, particularly beyond day 2, and may be useful in guiding diagnostic and management strategies.     

Evidence that unsaturated fatty acids are potent inhibitors of renal UDP-glucuronosyltransferases (UGT): kinetic studies using human kidney cortical microsomes and recombinant UGT1A9 and UGT2B7

Renal ischaemia is associated with accumulation of fatty acids (FA) and mobilisation of arachidonic acid (AA). Given the capacity of UDP-glucuronosyltransferase (UGT) isoforms to metabolise both drugs and FA, we hypothesised that FA would inhibit renal drug glucuronidation. The effect of FA (C2:0-C20:5) on 4-methylumbelliferone (4-MU) glucuronidation was investigated using human kidney cortical microsomes (HKCM) and recombinant UGT1A9 and UGT2B7 as the enzyme sources. 4-MU glucuronidation exhibited Michaelis-Menten kinetics with HKCM (apparent K(m) (K(m)(app)) 20.3 microM), weak substrate inhibition with UGT1A9 (K(m)(app) 10.2 microM, K(si) 289.6 microM), and sigmoid kinetics with UGT2B7 (S(50)(app)440.6 microM) Similarly, biphasic UDP-glucuronic acid (UDPGA) kinetics were observed with HKCM (S(50) 354.3 microM) and UGT1A9 (S(50) 88.2 microM). In contrast, the Michaelis-Menten kinetics for UDPGA observed with UGT2B7 (K(m)(app) 493.2 microM) suggested that kinetic interactions with UGTs were specific to the xenobiotic substrate and the co-substrate (UDPGA). FA (C16:1-C20:5) significantly inhibited (25-93%) HKCM, UGT1A9 or UGT2B7 catalysed 4-MU glucuronidation. Although linoleic acid (LA) and AA were both competitive inhibitors of 4-MU glucuronidation by HKCM (K(i)(app) 6.34 and 0.15 microM, respectively), only LA was a competitive inhibitor of UGT1A9 (K(i)(app) 4.06 microM). In contrast, inhibition of UGT1A9 by AA exhibited atypical kinetics. These data indicate that LA and AA are potent inhibitors of 4-MU glucuronidation catalysed by human kidney UGTs and recombinant UGT1A9 and UGT2B7. It is conceivable therefore that during periods of renal ischaemia FA may impair renal drug glucuronidation thus compromising the protective capacity of the kidney against drug-induced nephrotoxicity.