Upper abdominal trauma: pitfalls in CT diagnosis

Medical records and computed tomographic (CT) scans of 83 patients with upper abdominal trauma were retrospectively reviewed to determine errors in diagnosis using CT. Patients with possible pancreatic injury, small bowel perforation, or injury to an occult malignancy represented the most difficult diagnostic cases. A false-positive diagnosis of pancreatic injury occurred in seven of 77 patients (9%) and represented the most frequent error in the series. In three patients with subsequently surgically proved small bowel perforation, one duodenal and two proximal jejunal, the injuries were not correctly diagnosed on CT scans. In retrospect, positive CT findings were present in the case of duodenal rupture. Additionally, in two patients, duodenal rupture was suspected based on CT findings of extraluminal gas and fluid near the duodenum, but both cases were proved normal at surgery. The series included three patients with trauma involving unsuspected tumors in the liver, kidney, and stomach.     

Gaucher disease: sonographic appearance of the spleen

Ultrasonographic (US) examinations of the upper abdomen were performed in 80 patients with Gaucher disease. Of the 49 patients that had not undergone splenectomy, 47 had splenic enlargement. Sixteen patients had multiple lesions in the spleen. Most patients had discrete hypoechoic lesions that corresponded pathologically to focal homogeneous clusters of Gaucher cells. Several patients had similar lesions that were hyperechoic and were composed of Gaucher cells and fibrosis or infarction. A few patients had a geographic pattern of irregular areas of involvement of Gaucher cells among normal splenic parenchyma. The liver was often enlarged but otherwise sonographically unremarkable. Patients with Gaucher disease often have US examinations of the left upper quadrant for abdominal pain. A variety of US findings in the spleen typical for Gaucher disease should be recognized and not interpreted as acute changes.     

Decarboxylated-S-adenosylmethionine excretion: a biochemical marker of ornithine decarboxylase inhibition by alpha-difluoromethylornithine

In an attempt to define a biochemical marker of ornithine decarboxylase inhibition in humans, alpha-difluoromethylornithine hydrochloride (DFMO), an irreversible ornithine decarboxylase inhibitor, was infused i.v. in seven cancer patients over 10-day courses at doses of 10-90 g/day and 24-h urinary excretion of polyamines and decarboxylated-S-adenosylmethionine was determined before, during, and after treatment. DFMO produces marked increases in urinary decarboxylated-S-adenosylmethionine excretion, up to 84 times pretreatment values. This response appears to be time dependent, requiring several days to reach a maximum and lasting at least 4-5 days after stopping DFMO. In contrast, urinary excretion of the polyamines putrescine, cadaverine, spermidine, N1-monoacetylspermidine, N8-monoacetylspermidine, and spermine, were not consistently altered by DFMO. We conclude that urinary excretion of decarboxylated-S-adenosylmethionine represents a valid biochemical indicator of ornithine decarboxylase inhibition in humans, whereas urinary polyamines are of no value.     

Echographic differentiation of histological types of intraocular melanoma

The aim of this study was to assess the differentiation of histologically different types of choroidal melanomas by means of clinical and quantitative acoustic/texture parameters of echograms. Clinical parameters were graded by morphological, kinetic and quantitative statements about the A- and B-mode echograms by a skilled diagnostician. Acoustic/texture parameters were obtained by processing and analysing radio frequency, AM-demodulated and FM-demodulated echograms. The data were preprocessed to remove influences induced by beam diffraction and focusing. The correlations between the clinical parameters were lower than 0.5 but significant in a few cases. The best set of four clinical echographic parameters enabled a retrospective classification of spindle type melanomas vs. mixed + epithelioid type melanomas with an accuracy of 77% (area under the ROC-curve of 86%). These figures do not enable, however, a prospective diagnosis. The correlations of the clinical parameters with the acoustic/texture parameters were investigated. The mutual correlations between the latter parameters were also assessed, the most significant (0.70) being between the speckle size and the slope of the linearized backscattering spectrum. The discriminant analysis performed with the best four acoustic/texture parameters (n = 30) yielded a sensitivity of 89%, a specificity of 92% and an area under the ROC-curve corresponding to a probability of correct classification of 96.6%. When using these data prospectively to classify tumours of unknown cell type (n = 21), this classification could be performed in 86% of cases.     

Abnormal prothrombin in the plasma of rats carrying hepatic tumors

Vitamin K is required for the posttranslational formation of gamma- carboxyglutamyl residues in a number of plasma clotting factors. Interference with vitamin K action results in the appearance of abnormal (des-gamma-carboxy) forms of prothrombin in human plasma. Vitamin K-sufficient patients with primary hepatocellular carcinoma also secrete significant quantities of abnormal prothrombin; this response has now been studied in a rat model. Normal Buffalo strain rats had 9 micrograms/mL of circulating plasma abnormal prothrombin, whereas Buffalo strain rats carrying the transplantable Morris hepatoma tumor no. 7777 had 33 micrograms/mL at 3 weeks after transplant. Vitamin K-dependent carboxylase activity was normal in the liver of these rats, but very low in the tumor tissue. Rats carrying Morris hepatoma tumors no. 9618A and 5123D did not secrete significant amounts of abnormal prothrombin. Carboxylase activity in these tumors was 15 times that of the 7777 tumor. The data suggest that the secretion of abnormal prothrombin by hepatocellular tumors is the result of normal expression of the prothrombin gene by those tumors and a failure of the tumor to express the carboxylase gene.     

噻芬太尼的主要药效和致依赖性潜力的实验研究

本文研究噻芬太尼的镇痛药效和制动作用,评价其致身体依赖性潜力。小鼠热板法测得噻芬太尼的镇痛作用强度分别为吗啡、芬太尼和埃托啡的3260,22和1.5倍。以瘫痪作为制动指标测得噻芬太尼对大鼠、家兔、狗和猴制动作用强度为埃托啡的2～3倍。小鼠跳跃实验和大鼠饮药液自然戒断实验表明该药具有一定致身体依赖性潜力。大鼠ⅳ快速成瘾实验及长达20周的猴身体依赖性实验则未出现依赖性戒断症状。     

Permanent increase of the GAD67/synaptophysin ratio in rat cerebral cortex nerve endings as a result of hypoxic ischemic encephalopathy sustained in early postnatal life: a confocal laser scanning microscopic study

The aim of this study was to investigate whether perinatal hypoxia-ischemia preferentially destroys GABAergic nerve endings in rat cerebral cortex tissue which, in its turn, could then account for the reported higher risk of developing epilepsy later in life. To that end rat pups, with an age of 12–13 days postnatally, were unilaterally to hypoxic-ischemic conditions. After a survival period of to 2 to 6 months, the animals were sacrificed by perfusion fixation and their brains were used for cutting transversal vibratome and frozen sections. These sections were double-stained with primary antibodies against one of the two GABA synthesizing enzymes, glutamic acid decarboxylase with a mol. wt. of 66,600 (GAD₆₇) and one of the intrinsic membrane proteins synaptic vesicles, synaptophysin, followed by fluorophore-conjugated second antibodies. By using the confocal laser scanning microscope, we determined the ratio between the amount of GAD₆₇/synaptophysin immunofluorescence in nerve endings per unit volume of tissue in the hypoxia-damaged neocortex. It turned out that this ratio, contrary to expectations, was significantly higher in the hypoxia-damaged cortical areas than in matched areas on the contralateral side. It appeared, moreover, that this effect was directly proportional to the severity of the incurred damage. The conclusion was drawn that these observations do not support the hypothesis that perinatal hypoxia-ischemia ultimately leads to a preferential loss of GABAergic nerve endings in the damaged neocortex and, as such, to a shortage of inhibition.