Superficial bladder cancer in patients under 40 years of age. Efficacy of topical prophylaxis

In patients under the age of 40 years with primary superficial bladder cancer the efficacy of adjuvant topical treatment was the same as in elderly patients (recurrences 23%, progression rate 8%). Patients should therefore be treated on the basis of stage and grade of the tumour regardless of their age.     

Neuroophthalmologic abnormalities and intravascular therapy of traumatic carotid cavernous fistulas

Traumatic fistulas were successfully embolized using various transvascular approaches in 33 of 34 lesions. Complete superselective angiographic demonstration of the exact site of the shunt and possible collaterals was necessary to choose the appropriate embolization techniques. Improvement in the signs of orbital congestion was seen in all cases. Embolization, which directly occludes the fistula, precludes recurrences via collateralization and restores the normal arteriovenous gradient to the eye and optic nerve.     

氯仿重结晶棉酚的质量研究

报道了氯仿重结晶的棉酚的化学性质,样品在不同温度下干燥恒重后,经熔点、薄层层析、紫外光谱、红外光谱、X-射线衍射、热重量分析、元素(C,H,Cl)分析及棉酚合量测定等一系列的分析,确证了在60℃以下棉酚与氯仿成溶剂化物(solvate)。随着干燥温度的升高或在室温长时间的贮存,此现象逐渐消失,100℃真空干燥恒重后成为纯棉酚。     

Dose-escalation study of intravenous nicardipine in patients with aneurysmal subarachnoid hemorrhage

A dose-escalation study of the calcium ion entry blocking drug nicardipine was performed using large dose infusions in 67 patients with recent aneurysmal subarachnoid hemorrhage (SAH). A safe, potentially therapeutic dose of the drug was determined. Patients admitted within 7 days of SAH from a documented cerebral aneurysm were entered into the study if no spasm was present on the initial angiogram. Nicardipine was administered as a continuous intravenous infusion throughout the 14-day period after SAH, regardless of the timing of surgery. To determine the safest possible dose, nicardipine was administered at seven dose levels from 0.01 to 0.15 mg/kg/hr. The total daily doses ranged from 27.7 mg to 375.0 mg. A follow-up angiogram was carried out on all 67 patients 7 to 10 days after SAH. Computerized tomography and neurological examinations were used to determine the presence of cerebral infarction. No major adverse effects, unexpected reactions, or permanent sequelae could be attributed to nicardipine. A decline in blood pressure was noted following administration of the drug. This occurred more frequently among patients given the largest dose but did not produce clinical problems or require discontinuation of the drug. Favorable outcomes were noted in 52 patients (78%). Vasospasm was found by arteriography in 31 patients (46%). A dose-related trend was noted: only eight (24%) of 33 patients treated at the highest dose level (approximately 10 mg/hr) developed arteriographic evidence of vasospasm. Symptomatic vasospasm was diagnosed in only two (6%) of 33 patients treated with this dose. Of the 34 patients receiving the lower dose levels, angiographic spasm was observed in 68% and symptomatic vasospasm in 27%. No deaths due to vasospasm occurred. Nicardipine appears to prevent both vasospasm and cerebral ischemia after SAH. A multicenter randomized double-blind trial to test this hypothesis is planned.     

Transport and storage ofHelicobacter pylori from gastric mucosal biopsies and clinical isolates

Various transport and storage conditions for the recovery ofHelicobacter pylori from gastric biopsies were evaluated. Gastric mucosal biopsies from 16Helicobacter pylori-infected patients were stored in cysteine-Albimi medium containing 20 % glycerol in a refrigerator (4°C) for 1 and 2 weeks and in a –20°C laboratory freezer for 4 and 12 weeks. Two clinical isolates were stored in saline, Stuart's transport media, cysteine-Albimi broth with 20 % glycerol, brucella broth with 20 % glycerol and skim milk with 17 % glycerol at room temperature, 4°C, –20°C and –70°C. Storage at 4°C for 1 and 2 weeks resulted inHelicobacter pylori recovery from 81 % and 19 % of biopsies, respectively. Storage at –20°C yieldedHelicobacter pylori recovery in 100 % and 57 % after 4 and 12 weeks, respectively. At room temperature after 6 h, theHelicobacter pylori titer was reduced. The best storage media for frozen isolates were skim milk/glycerol, brucella broth/glycerol and cysteine-Albimi/glycerol (in descending order). Recovery was better at –70°C than –20°C.     

Human fibroblast tissue factor is inhibited by lipoprotein-associated coagulation inhibitor and placental anticoagulant protein but not by apolipoprotein A-II

Studies of proteins that inhibit tissue factor activity have generally been conducted using either an extracted tissue homogenate ("thromboplastin") or tissue factor protein reconstituted into phospholipid vesicles rather than with tissue factor expressed in cell membranes (its physiological environment). In the present study, a human fibroblast cell strain was used to evaluate the effects of lipoprotein associated coagulation inhibitor (LACI), placental anticoagulant protein (PAP), and apolipoprotein A-II (apo A-II) on human tissue factor in cell membranes. LACI was tested from 7.8 to 500 pmol/L on fibroblasts cultured at cell densities ranging from 3,500 to 9,925 cells/well, and caused a progressive inhibition of tissue factor activity. PAP was tested from 3.9 nmol/L to 1 mumol/L at cell densities ranging from 4,500 to 15,400 cells/well and caused up to 83% inhibition of tissue factor activity. Inhibition by these proteins appeared to be influenced by cell density as well as whether the cells were intact or disrupted. Apo A-II, up to 1 mumol/L, did not inhibit the tissue factor activity of intact or disrupted fibroblasts at any cell density examined even though it did inhibit the activity of tissue factor in phospholipid vesicles. Of these inhibitors of tissue factor-dependent activation of factor X, LACI was the most effective in suppressing the generation of factor Xa activity. The effects obtained with apo A-II are clearly dependent on the nature of the tissue factor preparation with which it is tested. The disparity between the inhibitory effect of apo A-II on the activity of tissue factor reconstituted into lipid vesicles and the absence of effect on the activity of tissue factor remaining in cell membranes serves to reemphasize the necessity of reexamining results obtained with model systems using as nearly physiological reagents as possible.