缺氧缺血性脑病新生鼠补钙前后脑细胞,红细胞内外钙的变化

为了观察一般剂量补钙对缺氧缺血性脑病（ＨＩＥ）脑细胞和红细胞内外钙变化的影响，以探讨ＨＩＥ时补钙是否增加脑细胞钙超载，用ＨＩＥ新生动物模型进行了实验研究，结果表明：（１）缺氧缺血时红细胞、脑细胞及脑组织出现钙积聚；（２）补钙后，血浆总钙浓度明显升高，而脑细胞、脑组织及红细胞钙积聚并未加重；（３）血浆总钙浓度与脑细胞或红细胞胞浆游离钙离子浓度无相关关系。提示：（１）ＨＩＥ时钙内流可能是全身性的；（２）对ＨＩＥ并低钙血症患儿吸氧后一般剂量补钙可能是安全的。     

Family relationships and the development of social competence in adolescence

Abstract Resilient adolescents are notable for their social competence, which enables them to form and maintain close relationships. The evidence is that adolescents' social competence is derived from their experience of close relationships within their family. On the basis of structured interviews, adolescents' working models of attachments can be categorized into secure, dismissive, or pre-occupied. These attachment styles are associated with very divergent beliefs about the self and others, with differing patterns of emotion regulation and with differing risk profiles for maladjustment. Parenting styles and family relationships appear to have considerable influence on attachment behaviour. Further evidence for the importance of the family comes from research on ego development. Family level behavioural patterns have been discerned from family research interviews which are associated with stagnation or advancement in ego development during adolescence. Though the results suggest causal connections, the direction of effects is far from clear. Longitudinal research underpins the importance of childhood temperament as a contributing factor to the quality of the family environment that the child and then adolescent experiences.     

DNA-Methylierung von monohalogenierten Methanen in F-344 Ratten

Monohalogenated methanes (methyl chloride, methyl bromide and methyl iodide) are mutagenic and carcinogenic. The possible mechanism of these effects, DNA methylation, was studied. DNA adducts from orgnas of F344 rats exposed to these chemicals were separated and identified with high performance liquid chromatography (HPLC) and gaschro-matography/massspectrometry (GC/ MS). DNA adducts, 7-methylguanine (7-MeG) and O⁶-Methylguanine(0⁸-MeG), incorporation of¹⁴C into de novo synthesis of nucleobases could be observed in enzymatic DNA hydrolysates by HPLC and determination of the radioactivity in the fractions. The formation of DNA add,ue,ts in the studied organs was only quantitatively different. The formation of O⁶-MeG was further pioved by analysing the acidic hydrolysates using HPLC with non-radioactive O⁶MeG as internal standard. 7-MeG and 3-MeA were identified with GC/MS analysis.     

Pharmacokinetics and pharmacodynamics of benazepril hydrochloride in patients with major proteinuria

Summary We have investigated whether the pharmacokinetics and pharmacodynamics of the ACE inhibitor benazepril hydrochloride are altered with proteinuria by studying 8 patients with major proteinuria of different causes who were given a single dose of 10 mg p.o.The maximum plasma concentration of benazepril was found between 0.5 and 2 h after dosing (median 1 h). Its elimination was almost complete within 6 h. Peak plasma levels of benazeprilat, the active metabolite of benazepril, were observed between 1 and 6 h (median 2.5 h). The elimination of benazeprilat from plasma was biphasic, with mean initial and terminal half-lives of 3.0 and 17.3 h, respectively. On average, the pharmacokinetic parameters of benazepril and benazeprilat in the patients did not differ from those in a historical control group of healthy volunteers, but intersubject variability in the AUC and half-lives of benazeprilat was greater in the patients.Plasma ACE was completely inhibited from 1.5 to 6 h after dosing, and at 48 h the mean inhibition was still 42 %. Plasma renin showed substantial intersubject variation. Mean supine blood pressure (systolic/diastolic) was reduced from baseline by a maximum of 18/13 mm Hg at 6 h. Proteinuria was diminished after benazepril in 7 patients.In conclusion, the results of this study suggest that proteinuria in the nephrotic range does not require a change in benazepril dosage.     

The consequences of H2 receptor antagonist — piroxicam coadministration in patients with joint disorders

Summary A randomised crossover study was performed in subjects with rheumatoid arthritis (or other arthropathies) to investigate if any alteration in the steady pharmacokinetics of the NSAID piroxicam (a drug which is extensively metabolised via cytochrome P450) or its major metabolites occurred as a result of coadministering either cimetidine or nizatidine.Twelve females and 2 males with mean age, weight, and albumin concentrations of 58 years, 61 kg, and 40 g·L^–1 respectively, completed the study. Comparisons were made between the following parameters: plasma piroxicam AUCs [AUC_0-24(P)], plasma 5-hydroxypiroxicam AUCs [AUC_0-24(5-OHP)], the ratio of these i.e. AUC_0-24(5-OHP):AUC_0-24(p), the % piroxicam daily dose excreted in urine as 5-hydroxypiroxicam (before and after glucuronidase incubation); and the mean of the steady state trough piroxicam, and 5-hydroxypiroxicam concentrations (obtained during each study phase in addition to the wash-out period).A statistically significant difference as a result of initiating either cimetidine or nizatidine was obtained only for the ratio AUC_0-23(5-OHP):AUC_0-24(P). This was indicative of a weak potential to inhibit piroxicam hydroxylation.No clinically significant alteration in the steady state pharmacokinetics of piroxicam occurred in these subjects as a result of cimetidine or nizatidine coadministration. Consequently it is unlikely that any adverse events would arise from these combinations.     

Phase II trial of piroxantrone in patients with recurrent and metastatic squamous cell carcinoma of the head and neck

Summary Twenty-two patients with recurrent or metastatic squamous cell carcinoma of the head and neck were treated with piroxantrone 150 mg/m² intravenously every 21 days. There were no objective responses. The 95% upper confidence bound for response is 15%. Primary toxicity was hematologic.