治疗血吸虫病药—盐酸奎宁锑的毒性及口服后锑在大鼠体内的吸收、分布及排洩

大白鼠口服盐酸奎宁锑后,锑自胃肠道消失得很慢,八小时后;仍有约90%的锑在胃肠道存留.如先将胃与小肠间以线结扎,再使动物口服本品,肠道的锑含量仍逐渐增加.大鼠口服盐酸奎宁锑后,锑很快进入胆汁中,锑的排洩以粪为主,自尿排出者,为量极微.大白鼠口服盐酸奎宁锑24小时后,各脏器均合有锑.除胃肠外,锑的浓度以肝脏为最高,肾和脾的浓度约为肝脏的一半,而肺、心、脑和血中的锑浓度极小.可见,口服盐酸奎宁锑后锑之所以自胃肠道消失得很少,并不一定由于锑的吸收很少,部分已吸收的锑经胆管又排洩至肠道.     

Health Related Quality of Life (HRQoL) among Breast Cancer Patients Receiving Chemotherapy in Hospital Melaka: Single Centre Experience

Objective: To investigate the impact of chemotherapy on quality of life (QoL) among breast cancer patients and to evaluate the relationship with age, cancer stage and presence of any comorbidity. Methods: A prospective study was conducted among breast cancer patients receiving chemotherapy in Hospital Melaka from 1st January 2014 to 31st July 2014. The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30) was given to patients to fill in prior chemotherapy (baseline) and after the third cycle of chemotherapy. Socio-demographic and clinical data were collected and analyzed using SPSS version 20. Result: Respondents were 32 female patients [mean age (SD): 49.7(9.93) years]. They reported a significant lower global health status (P < 0.01) and significant higher symptoms of nausea and vomiting (P < 0.01), loss of appetite (P = 0.028) and diarrhea (P = 0.026) after the third cycle of chemotherapy as compared to baseline. Compare to, this study showed significant better emotional functioning (P < 0.01) and social functioning (P < 0.01) than the EORTC QLQ-C30 Reference Values 2008 for breast cancer cases. Under symptom scales higher scores were noted for appetite loss (P = 0.017), nausea and vomiting (P < 0.01). Age, stage and comorbidity had no clear associations with global health status in our patients (P > 0.05). Conclusion: Chemotherapy did reduce the QoL of breast cancer patients. Management of chemotherapy-induced loss of appetite, diarrhea, nausea and vomiting should be improved for a better outcome.     

Review article: Endothelial progenitor cells in renal disease

This brief overview is intended to provide basic information about endothelial progenitors, their definition and consensus markers used for their detection, describe the pathways of their mobilization and homing and highlight the mechanisms and manifestations of their incompetence that occurs in some chronic kidney diseases. Discussion is geared towards the potential role of endothelial progenitor cells in organ regeneration, in particular, in kidney regeneration. The concept we attempted to promote attributes to the incompetence of endothelial progenitor cells in failed regeneration and ensuing progression of chronic kidney disease. This field of inquiry remains insufficiently explored, especially in renal diseases. Promising areas for future exploration are emphasized.     

Initial evaluation of an intracorporeal oxygenation device

We describe a recently developed intracorporeal gas transfer device, its potential applications and hazards. To date, patients with potentially reversible respiratory failure have been treated with controlled oxygen therapy and positive pressure ventilation, but this treatment may itself contribute to lung parenchymal damage from barotrauma and oxygen toxicity. Total or partial extracorporeal gas exchange can be used to reduce these risks, but this treatment is complex and has significant morbidity and mortality. This gas exchange device has been designed to provide partial gas transfer with simplicity of insertion and use. The oxygenator lies in the vena cava to provide prepulmonary gas exchange. In preliminary studies with three calves we have shown that the device increases both mean mixed venous and arterial oxygen content and reduces mean arterial carbon dioxide tension.     

Effect of Amiodarone on Electric Induction, Morphology, and Rate of Ventricular Tachycardia and its Relation to Clinical Efficacy

Using His bundle electrograms and programmed ventricular stimulation, the effects of chronic amiodarone treatment on induction, morphology, and the rate of ventricular tachycardia (VT) were studied in 17 consecutive patients treated with amiodarone for control of recurrent sustained VT or ventricular fibrilation. Studies were done before and after treatment with amiodarone for an average duration of 5.3 (range 2 to 18) months. During the control study, sustained VT could be induced in 16 patients. VT was initiated by single or double right ventricular (RV) extrastimuli in 14 patients, by double left ventricular (LV) extrastimuli in 1 patient, and by RV burst pacing in 1 patient. Only one pattern (morphology) of VT similar to that of spontaneous VT was induced in 12 patients and two patterns of VT in 4 patients. The average cycle length (CL) (mean ± SD) of induced VT was 325.8 ± 61.2 ms. After amiodarone, VT could be induced in 7 of 17 patients and was initiated by single RV extrastimuli in 5 patients, double RV extrastimuli in 1 patient, and RV burst pacing in 1 patient. In 3 of 5 patients in whom VT could be initiated by single RV extrastimuli, initiation of VT required double RV or double LV extrastimuli in the control study; in 1 of 5 patients VT could not be induced in the control study. Amiodarone induced nonclinical, polymorphic VT in 4 patients in whom only clinical VT could be induced during the control study. Compared to control, the CL of induced VT was significantly longer (322 ± 65.7 vs 416 ± 41.5 ms; P < 0.001). During a follow-up period ranging from 4 to 53 (mean ± SD; 18.6 ± 11.4) months, VT did not recur in 8 patients with no inducible VT and in 6 patients with persistence of inducible VT. One patient without inducible VT died suddenly; VT recurred in 2 patients, one without inducible VT and one with inducible VT. The results show that programmed stimulation studies late in the course of treatment do not accurately reflect the clinical efficacy of amiodarone in VT.     

意识障碍患者发生鼻蝇蛆病1例及文献复习

鼻蝇蛆病是一种较为罕见的寄生虫病,蝇蛆在鼻腔内生长对鼻腔、鼻窦造成损伤,一旦移行,会导致眼、颅腔等周围结构受损,妥善治疗和积极防控才能减少和避免严重并发症的出现.2020年5月14日中南大学湘雅医院收治的1例脑梗死昏迷患者发生了鼻蝇蛆病.该患者在治疗原发病的过程中,发现感染了蝇蛆.给予脱水降颅压、护脑、控制血糖和血压、...     

Dyslipidemia and coronary artery disease

Genetically determined and metabolically induced disturbances in lipid metabolism, as manifested in several types of dyslipidemia, have been shown to be causally related to the development of coronary artery disease (CAD). A diversity of clinical and angiographic studies has been made to evaluate the linkage between plasma lipid-control therapy in the development of initial and recurrent cardiovascular events. The plan of treatment invariably begins with a low-fat, low-cholesterol diet before initiation of drug therapy. However, many patients have difficulty in adhering to the low-fat diet. Fortunately, metabolic studies show that foods which contain fats rich in stearic (saturated) and oleic (monounsaturated) fatty acids may be given in limited amounts to boost patients' compliance to a low-fat diet and to prevent their blood lipids from rising to abnormal levels. A bile acid sequestrant (cholestyramine or colestipol) is the first-line drug for control of hypercholesterolemia. Either gemfibrozil or gemfibrozil plus niacin is prescribed to raise high-density lipoprotein (HDL) levels of CAD patients. Approval of two HMG CoA reductase inhibitors, pravastatin and simvastatin, by the FDA gives physicians the additional flexibility of employing a single or a combination drug therapy for optimal control of dyslipidemia. The association of low serum cholesterol level (< 160mg/dl) with increase in noncardiac mortality has prompted health professionals to consider modifying the universal screening and treatment of serum cholesterol in children and young women and to use hypolipidemic drugs in patients judiciously.