Transurethral collagen injection for treatment of stress urinary incontinence

Summary Minimally invasive treatment of urinary incontinence has become a subject of major interest in recent years. We examined the use of transurethral collagen injection for incontinence treatment. A total of 48 patients were selectet for this procedure from April 1993 to February 1997 – 26 male patients (19 post-RPX incontinence and 7 post-TUR incontinence) and 22 female patients (all after previous incontinence surgery) were treated by injection of collagen into the continence region. The whole group underwent an average of 1.8 sessions, and a mean collagen injection volume of 14.5 ml was delivered per session. Mean follow-up was 9.2 months. Of the female population, 68.2 % were cured or greatly improved. In the male population only 47.3 % of the post-RPX patients and 6/7 of the post-TUR patients benefited from the procedure. In males, treatment outcome depends on the degree of pretreatment incontinence, because all grade III incontinence patients did worse. Therefore we conclude: transurethral collagen injection is an interesting method in the treatment of urinary incontinence if proper patient selection is assured.      

Extraction of an artery in rectal biopsy]

A biopsy of a rectal carcinoma has led to the extraction of a 2.5 cm arterial specimen, followed by an arterial bleeding. The cause of this exceptional complication was the presence of atypical vessels reaching the rectal lumen due to tumor ulceration.     

Isolated polyarteritis nodosa of the male reproductive system associated with a germ cell tumor of the testis: a case report

Polyarteritis nodosa (PAN) presents mostly as a systemic disease with poor prognosis, rarely in an isolated form with a usually favorable outcome. Both forms may affect the male reproductive system and both forms have been associated with malignancies. We describe for the first time the occurrence of isolated PAN in the reproductive system combined with a mixed germ cell tumor of the testis in a 21-year-old man presenting with symptoms of chronic epididymitis. Two years after surgery he is without evidence of recurrence of either the tumor or PAN.     

Ethanol-Induced Enhancement of Cocaine Bioactivation and Irreversible Protein Binding: Evidence Against a Role of Cytochrome P-450IIE1

Chronic ethanol consumption potentiates cocaine-induced liver injury in rodents. Since cocaine has to be bioactivated by a cytochrome P-450-dependent N-oxidative pathway to exert its hepatotoxic effects, we studied the role of the ethanol-inducible P-450IIE1 for cocaine metabolism. Male Sprague-Dawley rats were pretreated with either a liquid diet containing ethanol (30% of calories) for 4 weeks or injected with pyrazole (200 mg/kg/day, ip, for 3 days). Both agents induced microsomal p-nitrophenol hydroxylation which is a probe for the catalytic activity of P-450IIE1. However, only ethanol, but not pyrazole, increased both microsomal cocaine N-demethylase activity (by 47%) and the extent of irreversible binding of [3H]-cocaine to microsomal proteins (by 100%), which was taken as a quantitative endpoint for the formation of a reactive metabolite. Cocaine N-demethylation and irreversible protein binding of cocaine were not inhibited by P-450IIE1 isozyme-selective substrates, nor was the rate of cocaine metabolism and binding decreased by functionally active polyclonal anti-rat P-450IIE1 antibodies. Furthermore, pyrazole pretreatment sensitized cultured hepatocytes to the glutathione-dependent cytotoxic effects of nontoxic concentrations of cocaine. These results indicate that (a) cocaine is not a major substrate for the ethanol-inducible P-450IIE1, (b) the enhancing effects of ethanol on cocaine bioactivation may be due to induction of other P-450 isoforms, and (c) induction of P-450IIE1 may potentiate cocaine-induced hepatocellular toxicity in vitro independently of cocaine metabolism, e.g., by P-450IIE1-dependent oxidative stress.     

Pharmacokinetics of intravenously administered 125I-labelled human alpha 1-acid glycoprotein

The volumes of distribution of many acidic drugs have been shown to be close to that of their binding protein, i.e. serum albumin. The distribution of basic drugs mainly bound to alpha 1-acid glycoprotein (AAG) can be questioned with respect to its dependency upon the distribution of this plasma protein. So, a pharmacokinetic study was performed in 7 subjects with human 125I-labelled alpha 1-acid glycoprotein. The steady-state volume of distribution was found to be 5.37 +/- 0.82L. The central volume was 3.23 +/- 0.33L, close to that of plasma volume and the peripheral volume was 2.14 +/- 0.63L. These data allowed the establishment of an equation giving access to the volume of distribution of a basic drug by relating its unbound fraction to physiological distribution of alpha 1-acid glycoprotein. The values yielded by this equation show that the actual and calculated volumes of distribution of basic drugs mainly bound to AAG are discrepant. This protein is thus not the main factor controlling the distribution of basic drugs within the body.     

International statistical classification of diseases and related health problems. Tenth revision

The International Classification of Diseases has, under various names, been for many decades the essential tool for national and international comparability in public health. This statistical tool has been customarily revised every 10 years in order to keep up with the advances of medicine. At first intended primarily for the classification of causes of death, its scope has been progressively widening to include coding and tabulation of causes of morbidity as well as medical record indexing and retrieval. The ability to exchange comparable data from region to region and from country to country, to allow comparison from one population to another and to permit study of diseases over long periods, is one of the strengths of the International Statistical Classification of Diseases, Injuries, and Causes of Death (ICD). WHO has been responsible for the organization, coordination and execution of activities related to ICD since 1948 (Sixth Revision of the ICD) and is now proceeding with the Tenth Revision. For the first time in its history the ICD will be based on an alphanumeric coding scheme and will have to function as a core classification from which a series of modules can be derived, each reaching a different degree of specificity and adapted to a particular specialty or type of user. It is proposed that the chapters on external causes of injury and poisoning, and factors influencing health status and contact with health services, which were supplementary classifications in ICD-9, should form an integral part of ICD-10. The title of ICD has been amended to "International Statistical Classification of Diseases and Related Health Problems"', but the abbreviation "ICD" will be retained.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of the immunomodulator diacetyl-splenopentin on antigen-induced arthritis in rabbits

Long-term treatment with the immunomodulator diacetyl-splenopentin reduces the severity of chronic joint inflammation and cartilage destruction in rabbits with antigen-induced arthritis. The level of specific antibodies as well as specific and non-specific cell-mediated immune reactivities including the proliferative response of spleen lymphocytes to cartilage proteoglycans in treated animals are lower than in untreated arthritic rabbits. Moreover, suppressor cell activity, which normally decreases during the early phase of inflammation, is enhanced and hyperreactive helper cell potential is reduced. These findings suggest that treatment with diacetyl-splenopentin normalizes the immune regulation, which is disturbed in the early phase of inflammation. This might result in a depression of the hyperreactive immune system including the autoimmunity developed against cartilage. Lowered immune reactivity in the joint in turn reduces the severity of chronic joint inflammation.Preliminary results were presented at the 6th Halle Summer Colloquium on Modulation, Mediation and Inhibition of Inflammation (H. Bekemeier and R. Hirschelmann, eds.). Wiss. Beitr. Martin-Luther-Universität Halle-Wittenberg 1987/7. Halle (Saale) 1987.     

A Saccharomyces cerevisiae mutant defective in the kinesin-like protein Kar3 is sensitive to NaCl-stress

Several mutants of Saccharomyces cerevisiae showing poor growth in the presence of elevated concentrations of NaCl were isolated to identify genes involved in the osmo-stress response. One of these mutants (WAY.5-4A-11; osr11) which showed a clear 2:2 segregation of the salt-stress phenotype upon tetrad analysis when crossed to a wild-type strain has been characterised. The mutation responsible for poor growth under salt-stress was recessive. The corresponding gene was cloned by complementation of the mutant phenotype and a 3.5-kb fragment was isolated. The sequence of this fragment matched that of KAR3, a gene previously identified to be involved in karyogamy and mitosis. Allelism of OSR11 to KAR3 was confirmed by tetrad analysis, and disruption mutants showed the same NaCl-phenotype as the original osr11 mutation. The disruption mutant was more sensitive to high sucrose concentrations than the original mutant was to high glucose concentrations. In a different genetic background (W303-1A), the kar3 disruptants were less sensitive to osmo-stress than the WAY.5-4A strain. Heat-stress, nitrogen-starvation and cultivation on ethanol failed to affect the growth of osr11 and kar3 mutants, pointing to a possible specific involvement of KAR3 in the osmotic-stress response. Microscopic studies showed that cell division of the kar3 mutants was impaired and NaCl-stress conditions aggravated the phenotype. Received: 7 April / 21 July 1997     

Combination of WAGR and Potocki-Shaffer contiguous deletion syndromes in a patient with an 11p11.2-p14 deletion

Aniridia, Wilms tumor, genitourinary abnormalities, growth and mental retardation are the cardinal features of the WAGR 11p13 deletion syndrome. The Potocki-Schaffer syndrome or proximal 11p deletion syndrome (previously DEFECT11 syndrome) is a contiguous gene syndrome associated with deletions in 11p11.2, principal features of which are multiple exostoses and enlarged parietal foramina. Mental handicap, facial dysmorphism and craniosynostosis may also be associated. We report a patient with combined WAGR and Potocki-Shaffer syndromes, and obesity. She presented with aniridia, cataract, nystagmus, corneal ulcers and bilateral congenital ptosis. A left nephroblastoma was detected at 15 months. Other features included moderate developmental delay, growth deficiency, facial dysmorphism, multiple exostoses and cranial lacunae. High-resolution and molecular cytogenetics confirmed a del(11)(p11.2p14.1) deletion with a proximal breakpoint between the cosmid DO8153 and the BAC RP11-104M24 to a distal breakpoint between cosmids CO8160 (D11S151) and F1238 (D11S1446). The deletion therefore includes EXT2, ALX4, WT1 and PAX6. This case appears to be the second patient reported with this combined deletion syndrome and confirms the association of obesity in the WAGR spectrum, a feature previously reported in four cases, and for which the acronym WAGRO has been suggested. Molecular and follow-up data on the original WAGRO case are briefly presented.