羊心淋巴流阻断后血清生化指标的改变

为给临床心脏术后监测心淋巴管损伤程度及可能出现的并发症提供参考指标，以手术方法阻断羊心淋巴流并对其血清相关成份进行了测定。实验发现，实验组术后谷草转氨酶（ＳＧＯＴ）、谷丙转氨酶（ＳＧＰＴ）、碱性磷酸酶（ＡＫＰ）、乳酸脱氢酶（ＬＤＨ）均有不同程度的增高，以ＳＧＯＴ增高最为明显，术前均值为４７．５３Ｕ，术后２天增至１０４．２０Ｕ，高峰出现时间最早，多在术后２４小时。血清离子改变中低钾最为突出，血钾在术后２天明显降低（Ｐ＜０．０１），术后７天逐渐恢复，术后１４天恢复至术前水平。血清蛋白改变以球蛋白降低、白蛋白／球蛋白比值升高为主。提示心淋巴循环郁滞可导致心肌细胞损伤、毛细血管通透性和结构的改变。不同酶活性的变化对郁滞的敏感度存在着差异。     

脑血管病患者血清IgE型免疫复合物的检测

本文用胶固素酶联免疫吸附试验检测了１６例缺血性脑血管病（ＩＣＤ）患者，１４例出血性脑血管病（ＨＣＤ）患者和２０例健康正常人的血清ＩｇＥ型循环免疫复合物（ＣＩＤ）水平。结果显示ＩＣＤ组和ＨＣＤ组ＩｇＥ－ＣＩＣ水平明显高于正常组（分别为Ｐ＜０．００１和Ｐ＜０．０５）。ＩＣＤ组与ＨＣＤ组间没有显著差异（Ｐ＞０．０２）。提示脑血管病的发生与ＩｇＥ－ＣＩＣ的形成有关。     

Mutagenicity of benzo(a)pyrenyl-1-sulfate in the Ames test.

Comparison of the mutagenicity of nine isomeric benzo(a)pyrenyl [B(a)P] phenols conjugated with either sulfate or glucuronide was carried out using strain Salmonella typhimurium TA98. Of the nine conjugates tested, only B(a)P-1-sulfate was mutagenic. Accordingly, the mutagenicity of B(a)P-1-sulfate was compared with that of B(a)P and 1-hydroxybenzo(a)pyrene [B(a)P-1-OH] in the presence and absence of rat lung S9 and Aroclor-induced liver S9 with and without an NADPH-generating system. B(a)P-1-sulfate was slightly mutagenic, whereas B(a)P and the 1-hydroxy derivative were nonmutagenic when S9 fractions and NADPH were omitted. Addition of induced liver S9 with NADPH caused mutagenicity with B(a) -1-OH greater than B(a)P greater than B(a)P-1-sulfate. B(a)P-1-sulfate was the only mutagenic species when lung S9 was added. This mutagenicity did not require NADPH. Sodium sulfite, an inhibitor of arylsulfatase, decreased the mutagenicity of B(a)P-1-sulfate. These data suggest that a unique mutagenic species is generated from B(a)P-1-sulfate via arylsulfatase in rat lung.     

Widenings of the myelin lamellae in a typical Guillain–Barré syndrome

The so-called “widenings of the myelin lamellae” are thought to be specific ultrastructural features of peripheral nerve myelin in patients with peripheral neuropathy associated with a monoclonal dysglobulinemia of IgM type and antiglycolipid activity. We report here a case of Guillain–Barré syndrome with no evidence of serum monoclonal dysglobulinemia, presenting the typical widenings of the myelin lamellae in small-diameter myelinated fibers from a sural nerve biopsy. In view of the positive reaction with anti-C3d complement on direct immunofluorescence, an immunological mechanism may be involved in the widenings of the myelin lamellae. © 1994 John Wiley & Sons, Inc.     

An experimental model for canine visceral leishmaniasis

Seven mixed-breed dogs were challenged with either promastigotes or amastigotes of Leishmania donovani infantum strains recently isolated from naturally infected dogs. Different routes and numbers of parasites were utilized and each dog was monitored for at least 1 year post-infection. Anti-parasite specific antibody levels were measured by enzyme-linked immunosorbence, immunofluorescence, crossed-immune electrophoresis and Western blotting on crude antigen. Western blotting on two pure parasite proteins, dp72 and gp70-2, was also done. Mitogenic and antigen-specific stimulation of peripheral blood lymphocytes was monitored; and the haematological, clinical and parasitological parameters measured. Dogs challenged with amastigotes exhibited a more pronounced humoral response to leishmanial antigens. Only in one case was strong antigen-specific proliferation detected. Clinical signs of disease, including hypergammaglobulinaemia, enlarged lymph nodes and the presence of parasites, were also more apparent in the dogs challenged with amastigotes. None of the seven dogs died. Serum antibodies to leishmanial antigens were apparent between 1.5 to 3 months following challenge and correlated with the appearance of enlarged lymph nodes, hypergammaglobulinaemia and the presence of parasites in tissue biopsies. Serum antibodies remained chronically high in these dogs throughout the period of the study. Only one dog (1/3) challenged intravenously with promastigotes and the dog challenged intradermally with amastigotes produced transient antibody responses to leishmanial antigen.     

Altered enzyme activities of xenobiotic biotransformation in kidneys after subchronic administration of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) to rats

Activities of the xenobiotic metabolizing enzymes were measured in the liver, kidney, duodenum and lung microsomes and cytosol fractions of Wistar rats after subchronic administration of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a potent bacterial mutagen in chlorinated drinking water. MX was administered by gavage at the dose level of 30 mg/kg for 18 weeks (low dose), or at the dose level which was raised gradually from 45 mg/kg for 7 weeks via 60 mg/kg for 2 weeks to a clearly toxic dose of 75 mg/kg for 5 weeks (high dose). Microsomal and cytosolic preparations were made and the activities of 7-ethoxyresorufin-O-deethylase (EROD), pentoxyresorufin-O-dealkylase (PROD), NADPH-cytochrome-c-reductase, UDP-glucuronosyltransferase (UDPGT) and glutathione-S-transferase (GST) were measured. Kidneys were affected most. A dose-dependent decrease was observed in EROD (90% in males, 80% in females at the high dose) and in PROD (58% in females, at the high dose) in kidneys. An increase was, however, detected in kidney NADPH-cytochrome-c-reductase (66% in females at high dose), UDPGT (89% in males and 97% in females at high dose) and GST activities (56% in males and 50% in females at high dose). MX caused only a few changes in the enzyme activities of the liver. The EROD activity was decreased 25% to 37%, both in the livers of males and females, but the total content of P450s was not altered. Hepatic GST activity was elevated in females in a dose-dependent manner (31% and 44%). GST activity was elevated in duodenum in females (59%) at the high dose. There were no marked changes in the enzyme activities in the lungs. MX was a weak inhibitor of EROD activity both in the liver and kidney microsomes in vitro, decreasing the EROD activity by 53% and 43%, respectively at the concentration of 0.9 mM. The results indicate that MX decreases the activity of phase I metabolism enzymes, but induces phase II conjugation enzyme activities, particularly in kidneys in vivo. It is possible that these changes contribute to metabolism of MX in kidneys and renders them susceptible to MX in the course of repeated exposure.     

Application of a 3D volume 19FMR imaging protocol for mapping oxygen tension (pO2) in perfluorocarbons at low field

A limited flip angle gradient-echo 3D volume acquisition imaging protocol for mapping partial pressure of oxygen (pO₂) in perfluorocarbon compounds (PFCs) at low field (0.14 T) is presented. The pO₂ measurement method is based on the paramagnetic effect of dissolved molecular oxygen (O₂) which reduces the PFC ¹⁹F T_1? Specific objectives related to imaging of PFCs through use of the protocol include improved image signal-to-noise characteristics and elimination of ¹⁹F chemical shift artifacts. A parametric Wiener deconvolution filtering algorithm is used for suppression of ¹⁹F chemical shift artifacts. Application of the protocol is illustrated in a series of calculated pO₂ maps of a gas equilibrated, multi-chamber phantom containing perfluorotributylamine (FC-43). The utility of the protocol is demonstrated in vivo through images of a commercially available perfluorocarbon based blood substitute emulsion containing FC-43 sequestered in the liver and spleen of a rat.     

血清CA125检测对子宫内膜异位症的临床诊断价值

目的 :探讨血清CA12 5测定对术前子宫内膜异位症的诊断价值。方法 :99例子宫内膜异位症经腹手术前测定CA12 5水平 ,并与 90例作对照比较。结果 :子宫内膜异位症CA12 5阳性率 >3 5U /ml,为 5 7.5 7% ,对照组为 8.88% (P <0 .0 1)。内膜异位囊肿高于卵巢囊肿 (P <0 .0 1) ,子宫腺肌病高于子宫肌瘤 (P <0 .0 5 )。结论 :血清CA12 5测定对子宫内膜异位症有较理想的诊断价值 ,对异位囊肿与卵巢囊肿 ,子宫腺肌病与子宫肌瘤有鉴别意义