Cardiac pathology after valve replacement by disc prosthesis: A study of 61 necropsy patients

Clinical and necropsy observations are described in 61 patients who had one or more cardiac valves replaced with a discoid prosthesis of the Hufnagel type. The most common (31 percent) cause of death among the 45 patients who died early (less than 65 days after operation) appeared to be prosthetic disproportion; that is, the prosthesis was too big for the aorta or ventricular cavity into which it was inserted so that inadequate space was present between the margins of the disc and the endocardium of ventricle or intima of aorta. Prosthetic thrombosis occurred in only 3 of the 45 patients who died early, but poppet movement appeared considerably altered in each. In contrast, thrombi were observed on a prosthesis in 14 of the 16 patients who died late (4 to 47 months [average 21] postoperatively), but in none did the thrombi appear of sufficient size to alter poppet function. Excessive bleeding occurred in 11 (24 percent) of the 45 early deaths and was primarily related to the insertion of a patch in the root of the aorta. Uncorrected valvular disease either by itself or by its ability to alter function of the prosthesis appeared responsible for death in 6 (13 percent) of the 45 patients who died early and in 2 (6 percent) of the 16 who died late. Insertion of a mitral poppet disc in a patient with uncorrected aortic regurgitation, even of mild degree, may be hazardous because the aortic regurgitant jet stream may interfere with proper function of the mitral disc. Likewise, insertion of a poppet disc only in the aortic valve position in a patient with combined aortic and mitral regurgitation may considerably increase the degree of mitral incompetence because the aortic prosthesis is intrinsically obstructive.Disc wear or variance was observed in all but one prosthesis in place for more than 1 year. Although hemolytic anemia of significant degree was not observed in any of the 16 patients who died late, the occurrence of renal hemosiderosis in 13 of the 16 patients indicates that the poppet disc prosthesis is considerably traumatic to erythrocytes. Thus, this type of prosthesis is not an ideal substitute cardiac valve. It clots, despite anticoagulant therapy, it is intrinsically stenotic, portions of it, that is, the disc, degenerate, and it causes hemolysis to erythrocytes.     

Maternal and child health workforce profile and density in China since 1949: a systematic review

Background

Routine sources of information on the maternal and child health workforce in China are without clear definition and categorisation. The aim of the study was to systematically review all the evidence on China's maternal and child health workforce profile (ie, level of education, training, qualification, and professional title), and determine the density of the maternal and child health workforce.

乙脑E蛋白主要抗原片段与结核杆菌hsp70在毕赤酵母中的融合表达

目的构建乙脑E蛋白主要抗原片段与结核杆菌热休克蛋白70（Mycobacterium tuberculosis heat shock protein70，Mt．hsp70）基因融合表达载体，并研究其在巴斯德毕赤酵母中的表达情况，为改善发展新的乙脑疫苗打基础。方法以酵母表达载体pPICZa-A为基本单位构建E蛋白基因主要抗原片段与hsp70的融合表达载体，融合基因以酶切位点BamHⅠ连接，用电穿孔法转化酵母X-33，用Zeocin平板筛选重组子，经甲醇诱导表达后，SDS-PAGE和免疫印迹分析表达产物。结果E蛋白基因与hsp70的融合表达载体构建成功，SDS-PAGE显示，其相对分子质量为114kD，与实际大小相符，经凝胶薄层扫描分析，表达量为33mg／L，经Western印迹验证，有良好的抗原性。结论E—hsp70融合蛋白在酵母中的表达为下一步研究hsp70是否能作为E蛋白免疫时的理想佐剂作准备。     

Primary empty sella syndrome with visual field defects

A patient with an enlarged, asymmetric sella turcica and visual field defects suggestive of a pituitary or parasellar tumor underwent extensive roentgenographic and pituitary function studies. No abnormalities in pituitary luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, ACTH, prolactin or vasopressin secretion were detected. Growth hormone secretion was provoked by arginine infusion but not by hypoglycemia. Pneumoencephalography revealed air in the sella turcica, and no evidence of tumor. Thus, an enlarged sella turcica in a patient with visual field defects but normal pituitary function may suggest the presence of an “empty sella syndrome.”     

Echinococcus granulosus human infection stimulates low avidity anticarbohydrate IgG2 and high avidity antipeptide IgG4 antibodies

Total IgG and IgG subclasses recognizing carbohydrate and peptidic epitopes from native and periodate treated partially purified hydatid cyst fluid (ppHCFA) and protoscolex somatic antigens (PSA) were tested by ELISA in hydatid patients sera. Binding of the major cross-reactive antiphosphorylcholine antibodies was inhibited with free reagent. A predominant anticarbohydrate antibody response against ppHCFA and PSA is shown. Although the main contributing IgG subclass to the antipeptide response against both antigens was IgG4, IgG1 also significantly contributed to the anti-PSA peptidic epitopes response. Western blot showed that IgG1 antibodies strongly recognized in ppHCFA a periodate susceptible 38 kDa antigen. The IgG4 antibodies mainly recognized the periodate-resistant 12, 16 and 24 kDa antigens. In addition, IgG2 antibodies recognized three strongly periodate-susceptible broad bands (116, 55 and 24 kDa antigens). PSA-specific IgG1 and IgG4 antibodies showed similar patterns of antigen recognition as well as no significant reduction of reactivity after periodate treatment while the IgG2 antibody recognition was strongly affected by this treatment. Furthermore, IgG2 showed significantly lower avidities than IgG1 and IgG4 antibodies recognizing both antigens. In conclusion, hydatid patients showed an enhanced production of low avidity anticarbohydrate IgG2 as well as high avidity antipeptide IgG4 antibodies.     

淡色库蚊抗溴氰菊酯品系CYP4E2r6基因的克隆与生物信息学分析

目的 从淡色库蚊抗溴氰菊酯品系Ⅳ龄幼虫扩增并分析CYP4E2r6基因，为蚊虫抗药性的研究、检测和防治筛选靶标。方法 根据已扩增的CYP4E2r6基因片段（长470bp，GenBank登录号为CB074945）的序列设计2条特异引物，从淡色库蚊抗溴氰菊酯品系Ⅳ龄幼虫提取RNA，反转录成cDNA，以cDNA为模板，用5’-RACE和3＇-RACE方法，各获得722bp、617bp片段。进行序列拼接并对所得新基因进行登录和生物信息学分析。结果获得了1条3’端含polyA尾，长1025bp的CYP4E2r6基因大片段（GenBank登录号为AY309972），编码289个氨基酸，与果蝇细胞色素P450氨基酸的同源性为55％。编码蛋白的理论分子质量单位为32．9ku，等电点为5．8。结论 获得了CYP4E2r6基因大片段，为进一步获取全长基因并研究该基因的功能奠定了基础。     

Human Hepatic Alcohol Dehydrogenase and Human Erythrocyte Catalase Do Not Metabolize the Cytochrome P-4502E1 Substrate, Chlorzoxazone

Studies of cytochrome P-4502E1 (CYP2E1)-mediated oxidation of ethanol have been hampered by the lack of a suitable probe for in vivo human studies. Chlorzoxazone, a prescribed skeletal muscle relaxant, is metabolized to 6-hydroxychlorzoxazone by CYP2E1 and has been advocated as a specific probe of this enzyme on the basis of microsomal studies. The applications of this probe may include delineating the contribution of CYP2E1 to in vivo human ethanol metabolism. However, the activity of nonmicrosomal enzymes in metabolizing chlorzoxazone is unknown. Alcohol dehydrogenase (ADH), predominantly a hepatic cytosolic enzyme, may be more important than CYP2E1 in the oxidation of ethanol to acetaldehyde. The contribution of catalase in the in vivo oxidation of ethanol to acetaldehyde is controversial. To determine if either of these enzymes metabolizes chlorzoxazone and whether ethanol oxidation by either enzyme is inhibited by chlorzoxazone or its metabolite, multiple in vitro studies were performed. ADH enzyme kinetics were performed with human recombinant β₁β₁ and β₃β₃ ADH with ethanol and chlorzoxazone (0.5 to 2.5 mM). Neither ADH isoenzyme exhibited NAD⁺-dependent oxidation of chlorzoxazone, but displayed Michaelis-Menten kinetics for ethanol with K_m values of 89 μM and 34 mM, for β₁β₁, and β₃β₃, respectively. Typical in vivo concentrations of chlorzoxazone and its metabolite, 6-hydroxychlorzoxazone, did not alter β₁β₁, or β₃β₃ ADH-mediated oxidation of ethanol to acetaldehyde. Studies of human hepatic nonmicrosomal enzyme activity were expanded to include all nonmicrosomal NAD⁺-dependent hepatic enzymes by starch gel electrophoresis assessment. Human hepatic enzymatic activity in the presence of chlorzoxazone was similar to that observed in the control sample (no added substrate), suggesting a lack of metabolism by NAD⁺-dependent enzymes. Similarly, human erythrocyte catalase, in the presence of a hydrogen peroxide generating system, did not metabolize chlorzoxazone. Furthermore, neither chlorzoxazone nor 6-hydroxychlorzoxazone altered the catalase-induced formation of acetaldehyde from ethanol. These data are consistent with chlorzoxazone as a specific probe of CYP2E1 that may be useful to alcohol researchers.     

ENPROSTIL AND RANITIDINE: COMPARATIVE EFFICACY AND SAFETY IN PATIENTS WITH DUODENAL ULCER

Abstract This randomised, double-blind, double-dummy, multiclinic study of duodenal ulcer healing compared the efficacy and safety of enprostil with ranitidine. The six week trial admitted 164 patients with endoscopically demonstrated duodenal ulcer. Ratings of symptoms and adverse events were collated from patients' daily diaries, and endoscopy was repeated to verify healing after four weeks and, if appropriate, after six weeks. Medication used was enprostil (35 μg capsule) or ranitidine hydrochloride (150 mg tablet) with matching placebos twice daily. After six weeks, 81 % of patients treated with enprostil and 95% of those treated with ranitidine had healed ulcers, a statistically significant difference (p = 0.007). There were no differences between treatment groups for the number of days until the daytime ulcer pain completely ceased. Night-time ulcer pain ceased significantly earlier in the group receiving ranitidine (p = 0.019) and was less severe during the week before the last visit (p = 0.001); daytime pain for ranitidine users was also less severe (p = 0.020) during this week. Mild to moderate adverse experiences were reported by 44% of enprostil and 35% of ranitidine patients. There were no severe adverse events. In conclusion, both enprostil and ranitidine were found to be safe and effective in the treatment of duodenal ulcer. However, the ranitidine regimen used in this trial produced better results than the enprostil regimen.     

Pacemaker pseudodysfunction with a coronary sinus pacemaker

A permanent transvenous coronary sinus pacemaker functioned effectively for 22 months both as an atrial and ventricular pacemaker. Slow atrial flutter resulted in failure of the pacemaker to capture the myocardium and thus incorrectly suggested pacemaker dysfunction. Transtelephonic evaluation of this phenomenon was particularly difficult and could have resulted in unnecessary replacement of the pacing unit