Ueber die entzündlichen Veränderungen der Glomeruli und die acute Nephritis

Ohne Zusammenfassung Hierzu Taf. V.     

Ueber Riesenzellen mit wandständigen Kernen in Tuberkeln und die fibröse Form des Tuberkels

Ohne ZusammenfassungHierzu Taf. VII–VIII.     

Weitere Mitteilungen über die epitheliale Struma

Ohne ZusammenfassungHierzu eine Textfigur.     

Anatomische Beiträge zur Kenntniss der Cretinen

Ohne Zusammenfassung     

Zur Frage der Ascaridenintoxikation

Ohne Zusammenfassung     

Aminoguanidine prevents arterial stiffening in a new rat model of type 2 diabetes

BACKGROUND: Formation of advanced glycation end-products (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study focused on investigating the role of aminoguanidine (AG), an inhibitor of AGE formation, in the prevention of noninsulin-dependent diabetes mellitus (NIDDM)-derived arterial stiffening and cardiac hypertrophy in rats. MATERIALS AND METHODS: The NIDDM was induced in male Wistar rats, which were administered intraperitoneally with 180 mg kg(-1) nicotinamide (NA) 30 min before an intravenous injection of 50 mg kg(-1) streptozotocin (STZ). After induction of diabetes mellitus type 2, animals receiving daily peritoneal injections with 50 mg kg(-1) AG for 8 weeks were compared with the age-matched, untreated, diabetic controls. RESULTS: After exposure to AG, the STZ-NA diabetic rats had improved aortic distensibility, as evidenced by 18.8% reduction of aortic characteristic impedance (P < 0.05). Treatment of the experimental syndrome with AG also resulted in a significant increase in wave transit time (+23.7%, P < 0.05) and a decrease in wave reflection factor (-26.6%, P < 0.05), suggesting that AG may prevent the NIDDM-induced augmentation in systolic load of the left ventricle. Also, the glycation-derived modification on aortic collagen was found to be retarded by AG. The diminished ratio of left ventricular weight to body weight suggested that prevention of the diabetes-related cardiac hypertrophy by AG may correspond to the drug-induced decline in aortic stiffening. CONCLUSIONS: Long-term administration of AG to the STZ-NA diabetic rats imparts significant protection against the NIDDM-derived impairment in vascular dynamics, at least partly through inhibition of the AGE accumulation on collagen in the arterial wall.     

Qualitative urinary organic acid analysis: Methodological approaches and performance

Summary  A programme for proficiency testing of biochemical genetics laboratories undertaking urinary qualitative organic acid analysis and its results for 50 samples examined for factors contributing to poor performance are described. Urine samples from patients in whom inherited metabolic disorders have been confirmed as well as control urines were circulated to participants and the results from 94 laboratories were evaluated. Laboratories showed variability both in terms of their individual performance and on a disease-specific basis. In general, conditions including methylmalonic aciduria, propionic aciduria, isovaleric aciduria, mevalonic aciduria, Canavan disease and 3-methylcrotonyl-CoA carboxylase were readily identified. Detection was poorer for other diseases such as glutaric aciduria type II, glyceric aciduria and, in one sample, 3-methylcrotonyl-CoA carboxylase deficiency. To identify the factors that allow some laboratories to perform well on a consistent basis while others perform badly, we devised a questionnaire and compared the responses with the results for performance in the scheme. A trend towards better performance could be demonstrated for those laboratories that regularly use internal quality control (QC) samples in their sample preparation (p = 0.079) and those that participate in further external quality assurance (EQA) schemes (p = 0,040). Clinicians who depend upon these diagnostic services to identify patients with these defects and the laboratories that provide them should be aware of the potential for missed diagnoses and the factors that may lead to improved performance. Electronic supplementary material  The online version of this article (doi: ) contains supplementary material, which is available to authorized users. Competing interests: None declared