Amorphous oxide--a platform for drug delivery.

Usually, a drug is loaded onto the metallic surface of a medical device by applying a polymer layer containing the drug. Unfortunately, polymer coatings on the metallic surface may exhibit numerous problems after implantation, such as late thrombosis, inflammation, and restenosis. Current research was conducted to investigate whether a suitable oxide layer can be used as a polymer-free platform for drug loading, especially for cardiovascular stents. The loading of heparin onto, as well as eluting of heparin from, the amorphous oxide film on the 316LVM stainless steel wire was confirmed by experimental studies using cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), electron spectroscopy for chemical analysis (ESCA), high-performance liquid chromatography (HPLC), and activated clotting time (ACT). Evidence shows that amorphous oxide can be an ideal substitute for the polymer coating of drug-loaded stents to minimize metallic corrosion, inflammation, late-thrombosis, and restenosis.     

起搏器更换时原起搏电极导线参数及更换指标分析

目的:分析74例更换起搏器时电极导线的各项参数的变化并探讨导线更换指标。方法:本组年龄12~87(62.8±18.4)岁,其中病窦综合征45例,房室传导阻滞29例,均为单腔VVI起搏。结果:至测量时原心室起搏电极导线的埋置时间60~148(97.4±22.8)月,首次埋置时起搏阈值为(0.48±0.24)V,更换时为(1.29±0.64)V(P(0.01),增加0.81V,增幅为168%,首次植入时R波幅为(7.8±3.6)mV,更换时为(5.9±3.4)mV(P(0.05)。植入时电极导线阻抗为(664±122)Ω,更换时阻抗为(726±148)Ω,增幅9.3%(P(0.05)。7例因起搏阈值大于2.0 V或阻抗大于1 250Ω而重新植入电极导线。原电极导线使用率为90.5%。结论:埋置起搏电极导线8~9年后,90.5%原电极导线仍在可使用的范围内,能否支持到再次更换需进一步随访。     

Induction of FMLP-mediated calcium mobilization requires crosslinking of surface immunoglobulin in Daudi cells.

We have explored the requirements for the induction of the N-formyl-methionyl-leucyl-phenylalanine (FMLP) response in Daudi cells after anti-immunoglobulin treatment. Our results indicate that (a) induction of responsiveness to FMLP was observed in Daudi only after crosslinking of surface immunoglobulin by anti-immunoglobulin; (b) this induced responsiveness was not observed in Ramos or Wil-2 cells; (c) the F(ab')2 fragment was sufficient for the induction of the FMLP response, but the Fab fragment and the Fc fragment were ineffective; (d) of the many agents active in B lymphocyte regulation which were tested, none were as effective as anti-immunoglobulin in the induction of the FMLP response; and (e) three inhibitors of calcium mobilization (W-7 (N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide), PMA (phorbol 12-myristate 13-acetate), and colchicine), acting on distinct mechanisms, inhibited both the calcium mobilization due to anti-immunoglobulin and the induction of responsiveness to FMLP. Our results suggest important determinants in the induction of a calcium-mobilizing FMLP response in cells of B lymphocyte lineage include (a) the cell type, (b) a selective requirement for activation via surface immunoglobulin, and (c) crosslinking of the surface immunoglobulin.     

Spurious hyperchloremia and decreased anion gap in a patient with dextromethorphan bromide.

Although cold syrup containing dextromethorpan bromide is widely administered, the bromism due to cold syrup has not been reported. We report a patient who had negative anion gap with hyperchloremia and conscious loss because of daily intake of cold complex syrup (containing dextromethorphan bromide 0.4 mg/ml, acetaminophen 8.33 mg/ml) for headache for 4-5 years. The bromide content in cold complex syrup resulted in serum levels of bromide that interfered with the automated analyzers for chloride content. When conscious change is due to bromism, hemodialysis instead of forced hydration and diuresis should be performed immediately. Therefore, patients with a markedly negative anion gap with hyperchloremia should be considered as having halide intoxication.     

Immunohistochemical localization of Na,K-ATPase in the in situ lens, cultured human lens epithelium and lentoid.

The localization of Na,K-ATPase in the lens is quite controversial. We explored this problem through immunoelectron microscopic examination of rat and human lens. Unlike previously reported results, we have found that Na,K-ATPase is localized in the basal plasma membrane, but not in the lateral or apical plasma membrane of both rat and human lens epithelium. The lens fiber lacked immunoreaction. Localization of Na,K-ATPase was also investigated in the cultured human lens epithelium and in lentoid. Immunoreaction was detected in the apical (facing the media) plasma membrane of the lens epithelium cultured on the lens capsule, whereas the reaction was observable in both apical and basal plasma membrane of the lens epithelium cultured on the biopore membrane filters. Immunoreaction in lentoid was observed in the surface plasma membrane. These data indicate that the polarized distribution seen in the in situ lens epithelium changes when these cells are cultured, and that Na,K-ATPase in the cultured lens cells including lentoid is located in the plasma membrane which is in contact with the growth media. This change in polarity of Na,K-ATPase distribution in cultured epithelial cells may be dictated by the need to maintain ion homeostasis by extrusion of sodium ions across the cell membrane facing the media.     

Begg正畸技术的临床应用（51例报告）

５１例应用Ｂｅｇｇ正畸技术矫治错畸形，各种类型的牙性及轻度骨性错畸形，均取得满意的效果。对牙轴唇倾并伴有深覆的安氏Ⅱ类错打开咬合、内收前牙的效果尤佳。     

Immunohistochemical study of lymph nodes in patients with cat scratch disease.

BACKGROUND/PURPOSE: Bartonella henselaeis the causative agent of cat scratch disease (CSD), manifesting as fever and acute regional lymphadenopathy. Although serologic testing is the reference method for diagnosis, successful use of immunohistochemical (IHC) stain of regional lymph nodes for the diagnosis of CSD has been reported. To determine the characterization and diagnostic potential of IHC in lymphadenopathy of CSD, lymph nodes were excised from patients with suspected CSD for further evaluation. METHODS: Polyclonal antibody-based IHC studies were performed for the detection of B. henselae. Between January 2001 and December 2004, the reference laboratory of the Center for Disease Control, Taiwan, received a total of 377 sera from 352 reported suspected CSD cases. Twenty-three formalin-fixed paraffin-embedded lymph nodes from 16 patients and two skin biopsies from two patients suspected of having CSD were included in this study. Nine of them were serologically confirmed to have CSD and the others were seronegative but suspected to have CSD by the attending physicians. Seven lymph node specimens were obtained from tuberculosis patients for comparison. RESULTS: We demonstrated that the microorganisms existed in the cytoplasm of histiocytes within the granulomatous lesions in nine lymph nodes and one skin biopsy. Among the nine lymph nodes with IHC (+) stains, three were seronegative. On the other hand, three cases were IHC (+) and six cases were IHC (-) among nine seronegative patients. In addition, two seronegative patients with skin biopsy showed one IHC (+) and one IHC (-). CONCLUSION: IHC can contribute to the etiologic diagnosis of B. henselaelymphadenopathy when serology and molecular techniques are not available.     

高血压合并阻塞性睡眠呼吸暂停的短期血压变异性研究

目的 比较高血压合并阻塞性睡眠呼吸暂停患者的短期血压变异性。方法 将155例分为对照组、高血压组、高血压合并轻度或中重度阻塞性睡眠呼吸暂停组，EE较患者不同活动状态的短期血压变异性。结果 高血压合并中重度阻塞性睡眠呼吸暂停组患者睡眠期间和早晨血压变异系数分别为：收缩压18．69、21．32；舒张压19．41、23．61，明显高于其他各组。结论 夜间睡眠期间和早晨短期血压变异性增加，是高血压合并中重度阻塞性睡眠呼吸暂停患者夜间和早晨心血管事件发生率增加的重要危险因素。     

Risk factors associated with venous thromboembolic events in patients with malignancy.

Malignancy is a major risk factor for venous thromboembolic events, but not all patients with malignancy develop such events. This study attempts to identify risk factors in patients with malignancy who develop venous thromboembolic events. In the current study, 566 consecutive patients without venous thromboembolic events and 416 patients with, admitted to University of Michigan with malignancy between 1992 and 2000, were identified using International Classification of Diseases-9 Clinical Modification codes. Data on potential risk factors was obtained from the University of Michigan Cancer Registry and the medical record. Univariate and multivariate analysis was used to identify factors associated with venous thromboembolic events and mortality. The mean patient age was 45.6 years with a mean survival of 7.8 years from cancer diagnosis. Venous thromboembolic events were associated with solid tumors (odds ratio 5.0; 95% confidence interval 1.7-14.9; P = 0.004), infection (4.9; 1.2-19.8; P = 0.03), and increasing age (1.05; 1.03-1.08; P < 0.001). While leukopenia (4.2; 1.2-14.6; P = 0.02) was associated with an increased incidence of venous thromboembolic events, neutropenia was not. Sex, type of therapy, and cancer stage were not independently associated with venous thromboembolic events. Survival was decreased in patients with venous thromboembolic events (5.9 versus 9.2 years, P < 0.0001). Solid tumors (3.9; 1.8-8.4; P = 0.001), infection (3.3; 1.1-9.9; P = 0.03), advanced stage (1.6; 1.2-2.1; P = 0.001), and increasing age (1.02; 1.0-1.04; P = 0.01) were associated with decreased survival. Patients with malignancy who have solid tumors, advanced age, infection, and leukopenia have a significantly increased risk of venous thromboembolic events.