Wiener klinische Wochenschrift. Supplementum最新文献

{"title":"[Effect of various operations for incontinence on the dynamics and topography of the bladder and bladder neck].","authors":"G Ralph","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>245 women who underwent surgery for stress urinary incontinence between 1982 and 1989 were tested urodynamically before and after surgery; lateral colpocystograms were obtained in 118 patients. 116 women underwent colpoperineoplasty, 59 Burch colposuspension, and 70 Stamey/Raz endoscopic suspension of the bladder neck. 72% of the patients were continent after the Burch operation, 70% after the Stamey/Raz procedure, and 54% after colpoperineoplasty. In patients with severe stress incontinence, the Burch and Stamey/Raz procedures were effective significantly more often than colpoperineoplasty (73% and 66% vs 37%). In patients with a hypotonic urethra, the Burch procedure was successful significantly more often than the other two operations (88% v. 62% and 47%). Colpoperineoplasty and the Stamey/Raz procedure both significantly decreased the urethral closure pressure (UCP) at rest while significantly improving the UCP under stress, the depression quotient, the pressure transmission factor. Urodynamic criteria of the urethral stress profiles differed significantly between continent and incontinent women. Colpocystography showed that the Burch and Stamey/Raz operations moved the vesicourethral junction well above the lower margin of the symphysis while colpoperineoplasty moved it to the lower margin. The angle beta was significantly smaller after Burch and Stamey/Raz operations than after colpoperineoplasty. There was no difference in any of the parameters between women with or without micturition complaints.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"185 ","pages":"3-14"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13185640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Diagnostic strategies in exclusion and differentiation of proteinuria, leukocyturia and hematuria].","authors":"W Hofmann","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>New sensitive markers in urine are demonstrated which allow in a strategy concept to exclude and differentiate a proteinuria, leucocyturia and haematuria. The usefulness of the diagnostic strategy is demonstrated in detail by selected clinical cases.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"17-21"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A new kinetic method for measuring beta-N-acetylglucosaminidase activity in urine].","authors":"K Jung,&nbsp;F Priem,&nbsp;G Klein","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A short overview of the biochemical and technical basis for measurement of beta-N-acetylglucosaminidase (beta-NAG, EC 3.2.1.30) is given. Advantages and disadvantages of various methods are discussed and the need has to be well founded to develop a new colorimetric assay. Some technical details of a new colorimetric test for the measurement of beta-NAG in urine are described.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"39-44"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Right heart function and endotoxemia in animals].","authors":"G Redl","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We used a chronic instrumented ovine model to investigate right heart function following an endotoxin bolus. Primary aim of the experiments was to elucidate the influence of the right heart on the cardiopulmonary system. Furthermore, we tried a thromboxane synthetase inhibitor as a therapeutical approach. At least we investigated the IR-ANF release, as the endocrinal function of the right heart, in this model. Following the endotoxin administration we observed a massive increase of the pulmonary arterial pressure. As a result of the increased right ventricular afterload right ventricular ejection fraction decreased and end-systolic volume increased. Impaired right heart function could not be compensated sufficiently using Frank Starling mechanism. Consequently, decreased left ventricular preload, stroke volume and cardiac output followed. Pretreatment with OKY-046, a selective thromboxane synthase inhibitor, attenuated the increase in pulmonary arterial pressure and prevented the early right heart failure including the drop of cardiac output. Furthermore, OKY-046 changed the thromboxane-prostacyclin relationship. Therefore we consider the cardiopulmonary reactions following pretreatment with OKY-046 as a result of the attenuated right ventricular afterload as well as of the increased prostacyclin concentration. Endotoxin induced hypoxaemia could not be prevented by pretreatment with OKY-046 and might be caused by interstitial edema following endothelial leakage. IR-ANF release in our model, accompanied by polyuria and natriuresis, seemed to be independent of right heart dysfunction and increase of right atrial pressure. We suggest endotoxin or a endotoxin induced mediator as a trigger of IR-ANF release.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"188 ","pages":"1-20"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12994675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Excretion of beta-N-acetylglucosaminidase in urine in type I and type II diabetic patients with and without nephropathy].","authors":"E Werle,&nbsp;A Bostedt,&nbsp;W Fiehn,&nbsp;C Hasslacher","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The clinical aspects of the excretion of beta-N-acetylglucosaminidase (beta-NAG, EC 3.2.1.30) in urine of type I and type II diabetics with and without nephropathy are evaluated. Correlation between concentration of albumin and of beta-NAG activity in urine is determined and the circadian rhythm of beta-NAG excretion in urine is examined, the indication of glomerular and tubulointerstitial damage is discussed. Longitudinal studies should demonstrate, whether an increased beta-NAG activity in urine of diabetics with normoalbuminuria is an indicator of nephropathy or a predictor of nephropathy if raised albuminuria is observed.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"59-62"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Microalbuminuria--an early marker of diabetic nephropathy].","authors":"H R Henrichs","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The pathophysiological basis of microalbuminuria is outlined. In a preliminary study (n = 71) and a comprehensive retrospective study over 4 years in type I diabetics (IDDM) (n = 1470) and type II diabetics (NIDDM) (n = 2112), clinical and anamnestic data were compared and the blood pressure, protein excretion, and albumin concentration in the urine were recorded. Early recognition of microalbuminuria in diabetic nephropathy permits successful therapeutic intervention and thus a significant postponement of terminal renal failure.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"63-6"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Interaction between beta-endorphin, steroids and peptide hormones in fibrocystic lesions of the female breast].","authors":"B Schurz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>From preclimacteric women (n = 10, 45-50 years of age) with gross cystic breast disease, levels of beta-endorphin, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, cortisol and prolactin were assayed radiochemically in the breast cyst fluid and in plasma. The beta-endorphin concentration (fmol/ml) was increased more than fourfold in the breast cyst fluid (17.6 +/- 4.6 SEM) than in plasma (4.2 +/- 0.5 SEM). In the breast cyst fluid, estradiol was increased 41-fold (1738.2 +/- 350.5 SEM pg/ml), and progesterone 47-fold (65.47 +/- 8.25 SEM ng/ml) more than in plasma. The significantly increased values of beta-endorphin, estradiol and progesterone in the breast cyst fluid and the identification of beta-endorphin in cyst-lining epithelia demonstrate the local synthesis. Growth factor-like properties of beta-endorphin and estradiol are accountable for the propagation of cystic changes. The autonomic formation and function of beta-endorphin, estradiol and progesterone in cyst compartments can not be related with the levels of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone and cortisol, which were significantly higher in plasma than in the breast cyst fluid. In the breast cyst fluid, prolactin could not detected to be significantly higher than in plasma. In addition the plasma-concentration of testosterone, androstenedione, thyroxin, triiodothyronine, thyroid-binding globulin, sexual-hormone-binding-globulin could be detected within the normal range. In this study we could demonstrate the synergism of beta-endorphin, steroid hormones and peptide hormones which advance the growth of gross cystic disease of preclimacteric women. Beta-endorphin was also examined by immunocytochemical assays (fluorescence, alkaline phosphatase and horseradish peroxidase method), in 11 women with pure fibrocystic disease, in 7 women with fibrocystic disease combined with a carcinoma in situ and in 15 women with fibrocystic disease combined with invasive carcinoma of the breast. Sections of frozen and paraffin embedded tissue of the same patient were reacted with anti-beta-endorphin antiserum. The immunoreactivity of beta-endorphin was intense in normal, proliferative altered and cyst-lining epithelia of fibrocystic disease and decreased in atypical epithelia and carcinoma cells of the breast. The degree of beta-endorphin staining is related to the degree of cell differentiation. In addition, nuclear receptors for estrogen and progesterone were assayed by peroxidase antiperoxidase technique.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"187 ","pages":"3-26"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12814707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Kidney cell damage and liberation of enzymes].","authors":"J E Scherberich","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The pathophysiological and pathobiochemical background of enzymuria in patients with renal involvement in discussed. Selected markers of the human nephron such as angiotensinase-A, aminopeptidase-M, L-gamma-glutamyl-transferase and dipeptidylpeptidase-IV are characterized; inductive as well as ischaemic/toxic events may induce increased shedding of membrane bound marker-enzymes. Pathological enzyme excretion profiles related to defined renal diseases indicate that tissue-proteinuria of renal origin is a potential noninvasive tool for diagnostic purposes.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"5-9"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Electrophysiological studies in acute Guillain-Barré syndrome].","authors":"B Mamoli,&nbsp;M Ackerl","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Based on a synopsis of the literature and our own investigations we discuss the electrophysiological changes in acute Guillain-Barré syndrome. These changes must be viewed in relation to the clinical course of the illness. The SPA evoked by distal stimulation decreases by 50% during the first week of illness, continues decreasing in the second and third weeks and then shows a tendency to normalization. In a similar way, the motor NCV reaches a minimum in the third week and then shows a slow increase again. The motor NCV findings return to normal earlier than SPA. At an early stage we find changes in F-wave and distal latency as well. In connection with the clinical picture, the incidence of changes pointing to a primary demyelinating polyneuropathy can be seen as an electrophysiological sign for the Guillain-Barré syndrome. The relevant criteria are discussed. There are various views concerning the validity of the electrophysiological findings in terms of prognosis of acute Guillain Barré syndrome. Since prognosis is dependent, at first, on the amount of the denervation, the decrease of SPA is of importance. To be able to give a prognosis it is necessary to examine large number of motor nerves electrophysiologically. However, it is very often not possible to make a reliable electrophysiological prognosis in the individual case. The pathophysiological basis for electrophysiological changes in demyelinating PNP's is discussed.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"190 ","pages":"8-12"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12935459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Determination of beta-N-acetylglucosaminidase and albumin in urine: comparison of methods and effect of gel filtration in human and rat urine].","authors":"M Meier,&nbsp;B Wilke,&nbsp;W Junge","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A new kinetic method for determination of beta-N-acetylglucosaminidase (beta-NAG, EC 3.2.1.30) in human and rat urine with chlorophenol red-NAG as substrate is compared to two other methods with 4-nitrophenyl-NAG and 3-cresol-sulfonphthaleinyl-NAG respectively as substrates. The impact of gel filtration of urinary specimens on the determination of beta-NAG-activity and of low albumin concentrations in urine is described.</p>","PeriodicalId":76822,"journal":{"name":"Wiener klinische Wochenschrift. Supplementum","volume":"189 ","pages":"44-7"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13120868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}