73例绝经后阴道出血原因及护理措施

绝经后阴道出血(PMB)是指生理性绝经1年以上的阴道出血或血性白带,是老年妇女最常见的症状之一.其中恶性病变多为子宫内膜腺癌、宫颈癌;良性病变多为老年性阴道炎、宫颈糜烂或息肉、宫内节育器、子宫肌瘤等.还有妇女因服用雌激素或外用雌激素药物后亦可引起绝经后出血.我院2008年1月-2009年6月收集妇科门诊及住院的绝经后阴道出血73例,对其病因作回顾性分析及护理措施报告如下.     

多粘菌素B与内毒素相互作用的红外光谱分析

目的利用傅里叶变换红外光谱（fourier transform infrared spectroscopy,FTIR）探讨多粘菌素B（polymyxcin B,PMB）与内毒素的相互作用力。方法利用FTIR分析PMB与内毒素相互作用后的红外光谱图。结果①PMB的N-H伸缩振动：在PMB与内毒素吸附后的图谱中该吸收峰的强度相比PMB的吸收峰强度有所减弱。②C-N的伸缩振动：PMB与内毒素吸附后的图谱中该吸收峰的强度相比PMB的吸收峰强度也有一定程度的减弱。结论PMB作为吸附剂吸附内毒素的作用力是正、负电荷间的静电引力。     

TNFRp55 modulates IL-6 and nitric oxide responses following Yersinia lipopolysaccharide stimulation in peritoneal macrophages

While cytokines are major regulators of macrophage activation following host-pathogen interactions, they also act to limit inflammation to avoid tissue damage. In previous studies we reported the development of progressive Yersinia enterocolitica-induced reactive arthritis (ReA) in mice lacking the tumor necrosis factor receptor p55 (TNFRp55). In this work, we analyzed the response of TNFRp55^−/− macrophages to Y. enterocolitica antigens. We found higher concentration of nitric oxide (NO) in TNFRp55^−/− compared to wild-type macrophages in response to heat-killed Yersinia (HKY) and Yersinia outer membranes (OM). Moreover, Toll-like receptor (TLR)4 expression was increased in OM-stimulated TNFRp55^−/− versus wild-type (WT) macrophages. Accordingly, NO production was inhibited in TLR4-deficient macrophages following stimulation with OM, suggesting that LPS may function as a major OM component implicated in these responses. Thus, augmented NO production together with enhanced expression of inducible nitric oxide synthase (iNOS) and higher IL-6 production, may provide a pro-inflammatory setting in Yersinia LPS-stimulated TNFRp55^−/− macrophages. Augmented synthesis of NO and IL-6 was prevented by treatment with Polymyxin B, or by exposure to a specific NF-κB p65 oligonucleotide antisense, indicating the involvement of TLR4-mediated NF-κB activation in the unleashed pro-inflammatory response triggered by TNFRp55 deficiency. Thus, TNFRp55 modulates macrophage functions in response to Yersinia LPS stimulation through mechanisms involving NO, IL-6 and NF-κB pathways, suggesting an essential regulatory role of TNF via TNFRp55 signaling.     

Burn injuries in Lagos

Eighty-nine cases of burns admitted to the Lagos University Teaching Hospital during an 8-year period (1968–1975) have been studied. The age incidence ranged from 1 day to 54 years. Fifty cases (56·2 per cent) occurred in children below the age of 15 years. Thirty-nine (43·8 per cent) were adults, aged 15 years and above. Sixty-three cases (70·8 per cent) were domestic accidents. There was a mortality rate of 13·5 per cent. There was severe morbidity in the surviving cases, the average admission period in 73 cases being 37 days and the average total healing time in 57 cases being 54 days. The most troublesome late complications were contractures, hypertrophic or keloid scars and failure of repigmentation. Gram-negative bacteria accounted for 64 per cent of the incidence of wound sepsis.Health education has an important role to play in the prevention of burn accidents both in the home and in industry. In particular, it is suggested that cooking above floor level and closer supervision of children should reduce the incidence of domestic bums in younger children, while stricter factory inspection, with rigorous enforcement of industrial safety laws, should reduce the incidence of industrial burn accidents in the working adult population.     

Pro-inflammatory effects of commercial alpha-lactalbumin on RAW 264.7 macrophages is due to endotoxin contamination

This study investigated the effects of alpha-lactalbumin (α-LA) on cellular signaling molecules associated with inflammatory responses in RAW 264.7 macrophages. The results indicated that commercial α-LA could increase prostaglandin E₂ (PGE₂) and the expression of COX-2 via increased phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK) and jun N-terminal kinase (JNK), and increase nitric oxide (NO) and the expression of iNOS via the activation of ERK1/2 and JNK. Furthermore, commercial α-LA could increase nuclear translocation of p65 nuclear factor-kappa B (p65 NF-κB) through stimulation on inhibitor kappa B-alpha (IκB-α) degradation. Since endotoxin also has these effects, we assayed the content of endotoxin in the commercial α-LA. We found to our surprise that endotoxin was there and that α-LA-induced NO and PGE₂ production could be suppressed by polymyxin B, a specific inhibitor of endotoxin. Thus, the pro-inflammatory effects of commercial α-LA might be caused by endotoxin contamination through activation and expression of iNOS and COX-2 which were upregulated by MAPKs or nuclear translocation of p65 NF-κB in RAW 264.7 cells. It is therefore crucial to assess the possibility of endotoxin contamination within any biological product being studied for immune augmenting activities before a meaning result can be obtained.     

固定多粘菌素B的新型吸附剂对血液中细菌内毒素吸附性能的实验研究

研究了固定有多粘菌素B（Polymyxin B,PMB）短肽的聚苯乙烯微球对血浆中细菌内毒素的亲和吸附性能，讨论了不同吸附条件对吸附性能的影响。用纯种大白鼠作为实验动物，建立内毒索血症动物模型。用固定有PMB短肽的聚苯乙烯微球对动物模型进行血液灌流实验，观察该吸附剂血液灌流清除血浆中内毒素的功效，考察了接有PMB短肽的聚苯乙烯微球的血液相容性及其对蛋白的影响。实验结果表明。采用血液灌流吸附疗法成功地清除动物模型血液中的内毒素，而且，固定有多粘菌素B的特异吸附剂具有良好的血液相容性。     

Role of whole saliva in the efficacy of sublingual immunotherapy in seasonal allergic rhinitis

Background

The development of methods to predict the clinical effectiveness of sublingual immunotherapy (SLIT) for allergic diseases is a crucial matter. We sought to determine whether whole saliva, which is the first body component that contacts allergen extracts during SLIT, is associated with the clinical effectiveness of SLIT in Japanese cedar pollinosis.

Supracondylar fracture of the femur following Attenborough stabilized gliding knee arthroplasty

Three cases of supracondylar fracture of the femur following replacement of the knee with the Attenborough stabilized gliding prosthesis are presented. It is felt that the fractures probably occurred due to faulty surgical technique.