Relationship between gastric cancer and precancerous lesions

ＲｅｌａｔｉｏｎｓｈｉｐｂｅｔｗｅｅｎｇａｓｔｒｉｃｃａｎｃｅｒａｎｄｐｒｅｃａｎｃｅｒｏｕｓｌｅｓｉｏｎｓＭＡＪｕｎＬｉｎｇ１，ＬＩＵＷｅｉＤｏｎｇ２，ＺＨＡＮＧＺａｉＺｈｅｎ１，ＺＨＡＮＧＬｉａｎ３，ＹＯＵＷｅｉＣｈｅｎｇ３ａｎｄＣＨＡＮ...     

糖尿病及其血管并发症的介入治疗

糖尿病(diabetes mellitus,DM)根据发病机制的不同,可分为1型和2型．糖尿病介入治疗主要是针对1型DM由于胰岛β细胞缺乏造成胰岛素分泌绝对不足进行胰岛β细胞或者干细胞移植,从而增加胰岛素分泌的绝对量达到治疗DM的目的．DM的血管并发症介入治疗,最常见的是糖尿病足的治疗,使用经皮经腔血管成形术(percutaneous transluminal angioplasty,PTA)和血管内支架为糖尿病足及其他周围血管病变提供了一个新的治疗途径．     

氨噻肟类青霉素衍生物的研究

本文报道了几个氨噻肟类青霉素衍生物的合成及抗菌活性,其中一个化合物的抗菌活性与氨苄青霉素相似,表明此类化合物具有进一步研究价值。     

Clinical experience with docetaxel for Chinese breast cancer patients: Hematological toxicity profiles

BACKGROUND: Asians are generally regarded to tolerate cytotoxic drugs less well than their Caucasian counterpart. A substantial proportion of patients receive suboptimal doses of chemotherapy for fear of severe toxicity. This retrospective study aims to evaluate the adverse events, especially hematological, of docetaxel in Chinese patients with breast cancer. PATIENTS AND METHODS: Fifty-nine patients, age ranged from 33 to 70 (median=47) years, were assigned to receive 3 to 6 (median=4) cycles of Docetaxel 100 mg/m2 every 21 days as neoadjuvant (n=3), adjuvant (n=26), neoadjuvant plus adjuvant (n=3), or active therapy for metastatic or relapsed breast cancer (n=27). RESULTS: A total of 56 (95%) patients completed the assigned whole regimen and only 3 (5%) patients discontinued due to either poor tolerance to the drug's side effects or worsening of disease leading to death. On average, the received dose intensity (RDI) was 0.86 for docetaxel 100 mg/m2 in this study. Among all the clinical adverse events, hematological toxicities were not excessively higher. Of the total 59 patients, major adverse events of all grades were leukopenia (22%), neutropenia (20%), fever (19%), and febrile neutropenia (14%). Only 12% and 14% of patients experienced grade 3 or 4 leukopenia and neutropenia, respectively. CONCLUSION: In view of the increasing breast cancer incidence and the acceptable toxicity profile of docetaxel among Chinese patients, a dosage of 100 mg/m2 can be recommended for use among Asians.     

Administration of dexamethasone induces proteinuria of glomerular origin in mice

The administration of glucocorticoids has been reported to exacerbate proteinuria in a few patients with glomerulonephritis. This effect has not been well recognized, and the pathogenetic mechanism responsible for this phenomenon remains to be clarified. In this study, we observed that a high daily oral dose (0.5 mg/kg body weight) of dexamethasone was capable of inducing overt proteinuria in mice, beginning on day 5 and persisting for a 19-day duration. One fourth of mice also intermittently presented with slight hematuria beginning on day 12. Renal lesions in the dexamethasone-treated mice, which were killed on day 23, were characterized by mild mesangial expansion, segmental or global hyalinosis/sclerosis in deep cortical glomeruli, and focal tubular changes. No glomerular inflammatory cell infiltration or proliferative lesion was noted in any of the mice. Ultrastructural features of glomeruli included mesangial widening characterized by either an increase of mesangial matrix, dilated mesangial channels filled with slightly electron-dense material or mesangial lysis-like appearance showing intracytoplasmic microcysts filled with electron-lucent material, and evidence to support injury of endothelial cells, erythrocytes, and podocytes. An immunofluorescence study revealed enhanced glomerular deposition of IgG, IgA, IgM, and fibrinogen (P < 0.001, compared with normal control mice), but no glomerular C3 deposition was identified in any of the dexamethasone-treated mice. Charge analysis showed no impairment in anionic property of glomerular tufts in the dexamethasone-treated mice. In addition, the dexamethasone-induced proteinuria was greatly attenuated by treatment with a low molecular weight heparin, although it was not reduced by an angiotensin-converting enzyme inhibitor. Data from these experiments suggest that a large dose of glucocorticoids is potentially nephrotoxic. Alteration of a size-dependent permeability may predominantly contribute to the dexamethasone-induced proteinuria. However, the effect of glomerular hyperfiltration may be only partially involved in the pathogenesis of this dexamethasone-induced glomerulopathy in mice.     

肾移植术后妊娠4例

1病例资料本组4例患者来自我院(1994/2004)468例肾移植术后患者,妊娠时年龄(27.5±2.3)岁,妊娠距肾移植时间(30.2±10.5)mo,原发病3例为慢性肾小球肾炎,1例为1型糖尿病.均为首次移植患者,供肾热缺血时间(6.0±2.1)min,冷缺血时间(8.4±1.2)h,供、受者ABO血型相容,淋巴细胞毒性试验阴性.     

Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function

Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report). A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC- gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC- delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function.