Clinical and radiological pictures of hepatocellular carcinoma with intracranial metastasis

Hepatocellular carcinoma (HCC) with extrahepatic spreading is not uncommon. In order to delineate the clinical and radiological pictures of HCC with intracranial metastasis, 33 documented cases were analysed. Eighteen had brain parenchymal metastasis without skull involvement; the other 15 cases disclosed skull metastasis with brain invasion. The underlying HCC are mainly of expanding (13/33, 39.4%) and multifocal (13/33, 39.4%) types. Eighteen cases (18/33, 54.5%) had mental changes not related to hypoglycaemia or hepatic encephalopathy. Eighteen cases (18/20, 90%) disclosed hyperdense mass lesions by non-contrast computed tomography (CT) scans and 17 cases showed homogeneous enhancement (17/22, 77.3%) by post-contrast CT images. In the non-skull involved group, five cases (5/12, 41.7%) disclosed ring-shape enhancement and 14 cases (14/16, 87.5%) had perifocal oedema, which were not seen in the skull involved group. Eight cases (8/33, 24.2%) presented as intracerebral haemorrhage. Twelve (12/33, 36.4%) died of brain herniation. Most (14/18, 77.8%) non-skull involved cases had simultaneous lung metastasis without bony metastasis, while the skull involved group often (10/15, 66.7%) disclosed extracranial bony metastasis without lung metastasis. The difference in extracranial metastasis was statistically significant (P<0.05). The multivariate survival analysis disclosed that lower lactate dehydrogenase level (≤316 U/L, P= 0.029) and treatments (surgery or radiation, P= 0.001) were positively associated with longer survival. In conclusion, HCC with intracranial metastasis is symptomatic and life-threatening. Half the cases may come from pulmonary metastasis and the other half may be from bony metastasis. Brain irradiation or surgery can prolong their survival.     

Role of amino and carboxyl groups of cobrotoxin in the conformational stability and the interaction with acetylcholine receptor

To study the functional involvements of the common interaction of the Leu-1 α-amino group and Asp-58 in cobrotoxin, the lysine ε-amino groups of cobrotoxin were initially guanidinated with o-methylisourea. The α-amino group of Leu-I was then modified with TNBS after the guanidination of cobrotoxin. Both modified derivatives displayed no significant changes in the secondary structure and antigenicity of cobrotoxin, whereas the binding affinity for nicotinic acetylcholine receptor (nAChR) was pronouncedly decreased when Leu-1 was modified. Six out of seven free carboxyl groups and the remaining buried Glu-21 carboxyl group of cobrotoxin were modified with glycine methyl ester in the absence and presence of guanidine HCl, respectively. Alternation in the β-sheet secondary structure of cobrotoxin was observed with the carboxyl-group modified derivatives, which caused a decrease in the binding activity of the toxin molecule to the antibody and nAChR. Moreover, modification of the Glu-21 carboxyl group of cobrotoxin further reduced the nAChR binding activity, while the antigenicity remained unchange. Thus, our results conclude that the Glu-21 residue and the common interaction of the terminal Leu-1 α-amino group and the Asp-58 carboxyl group are related to the nAChR-binding activity of cobrotoxin, and the free carboxyl groups in cobrotoxin are conformation-essential. © Munksgaard 1995.     

Prolonged Ventricular Asystole, Sinus Arrest, and Paroxysmal Atrial Flutter-Fibrillation:

CHOU, H.-H., et al.: Prolonged Ventricular Asystole, Sinus Arrest, and Paroxysmal Atrial Flutter-Fibrillation: An Uncommon Presentation of Vasovagal Syncope. We described a 55-year-old woman with recurrent syncope, complete atrioventricular (AV) block, sparsely scattered idioventricular beats lasting for 56 seconds, and long sinus arrest recorded during the syncopal episode. Paroxysmal atrial flutter-fibrillation was also presented during Holter electrocardiograph (ECG) monitoring without clinical symptom. During tilt test, atrial flutter with variable AV block was induced and the patient suddenly passed out. The vasovagal syncope was successfully treated with a DDD permanent pacemaker with a rate drop response algorithm. Vasovagal syncope with concomitant ventricular asystole and sinus arrest is rare. Aggressive management with permanent pacemaker is strongly advocated in malignant vasovagal syncope. (PACE 2003; 26[Pt. I]:914–917)     

Depletion of stratum corneum intercellular lipid lamellae and barrier function abnormalities after long-term topical corticosteroids

The intercellular lipid lamellae of the stratum corneum (SC) is believed to provide the permeability barrier of the epidermis. Previous functional studies have demonstrated an increase in the transepidermal water loss (TEWL) after long-term use of topical corticosteroids (TCS); however, direct morphological confirmation of this barrier abnormality is still lacking. The aim of this study was to determine whether any abnormality could be detected in the structure of the SC intercellular lipid lamellae in patients after long-term TCS. Atrophic skin and untreated normal skin of 10 patients after long-term TCS were examined by transmission electron microscopy using ruthenium tetroxide- fixed tissue for the multilamellar lipid sheets of SC, and oil red O stain for neutral lipids of the SC. Layers of the SC were evaluated by 0·1% methylene blue stain after alkaline expansion, and TEWL was measured by Evaporimeter EPI. The TCS-treated atrophic skin had fewer layers of horny cells, mean 9–4 layers, than the normal control skin, 18 layers (P<0·001) and increased TEWL of 21·3g/m² compared with the control skin TEWL of 6·7 g/m²(P<0·01). The mean neutral lipid content of the SC was also significantly lower (P<0·001). Moreover, ultrastructural studies revealed a marked decrease in both the numbers of intercellular lipid lamellae of SC and membrane-coating granules of stratum granulosum in the atrophic skin. These results suggest that the diminution in the SC intercellular lipid lamellae and SC cell layers play an important part in the pathogenesis of barrier dysfunction after long-term use of TCS.     

桃核承气汤改善四氯化碳诱导的大鼠肝损伤

目的：探讨桃核承气汤对四氯化碳诱导的大鼠肝损伤的保护作用。方法：30只大鼠分为正常对照组,模型组,大、小剂量桃核承气汤组和水飞蓟素组。桃核承气汤组灌胃桃核承气汤（0．3g／kg或0．5g／kg）,水飞蓟素组灌胃水飞蓟素25mg／kg。灌胃后1h腹腔注射四氯化碳1．5mL／kg。注射24h后将大鼠处死,检测肝组织病理学改变,血液中天门冬氨酸氨基转移酶（aspartate amino transferase,AST）、丙氨酸氨基转移酶（alanine aminotransferase,ALT）活性及脂质过氧化程度。结果：桃核承气汤不仅明显降低血液中AST及ALT活性,抑制四氯化碳引起的肝脏脂质过氧化,并且增加肝脏中谷胱甘肽含量;组织病理分析发现桃核承气汤可抑制脂质堆积,肝细胞坏死及淋巴细胞浸润。结论：桃核承气汤具有类抗氧化物之作用,对肝损伤有保护作用,甚至功能优于水飞蓟素。     

锑剂治疗家兔血吸虫病有效方法的探求

1.本文报告锑钾治疗家兔血吸虫病的剂量与疗程的探求。首先探求促使成虫大量向肝转移时所需有效剂量,继则探求控制成虫不能向肠复位时所需有效剂量与日程。2.锑钾每日按体重每公斤8毫克,分别注射1,2,3天,停药1天后肝内成虫检出率分别74.1%,93.5%,与98.0%。3.在锑钾每日按体重每公斤8毫克连续二日后,继以第2天锑排泄量(相当于锑钾1.62毫克/每公斤体重)的1,2,3倍,分别维持3,5,7天。结果成虫残余率与维持的剂量大小及日程长短成反比。4.根据这次动物实验结果,以锑钾每日按体重每公斤8毫克注射两天,继以维持第2天锑排泄量的三倍,连续3-5天治疗家兔血吸虫病,可以获得比较满意的结果。