[Functional diagnostics of mobility control, mobility stabilization and hypermobility. Reliability of clinical tests - results of a multicenter study]. / Funktionelle Diagnostik der Bewegungssteuerung, Bewegungsstabilisation und Hypermobilität. Reliabilität klinischer Tests - Ergebnisse einer Multicenterstudie.

BACKGROUND: Complex forms of musculoskeletal dysfunction are thought to be risk factors for the development of chronic pain syndromes of the locomotor system. Unfortunately there are insufficient data on the reliability and validity of clinical tests for musculoskeletal dysfunctions. METHOD: The intrarater and interrater reliability of clinical tests for hypermobility and for the stabilisation system were examined in a multicentre trial. A total of 68 patients in 6 centres were functionally examined by 2 examiners once (intrarater reliability) and by 1 examiner twice (interrater reliability). RESULTS: The tests for hypermobility showed good to very good reliability. The results for the stabilisation system were more variable whereby 23 tests showed a kappa-coefficient greater than 0.5 and 15 tests good to very good reliability. DISCUSSION: All tests for hypermobility and 23 tests for the stabilisation system are suitable for further evaluation. The broad range in test reliability might be explained by the differences in examiner skills demanded by each test. Therefore, dependent on their validity, some tests will be useful in specialized centres while others might be used in primary care.

Comparative analysis of biofeedback and physical therapy for treatment of urinary stress incontinence in women.

OBJECTIVE: To compare the effectiveness of an intensive group physical therapy program with individual biofeedback training for female patients with urinary stress incontinence. DESIGN: Randomized study of two therapeutic interventions consisting of a specific physical therapy program (PT) or biofeedback training (BF) daily for 4 wk, followed by a 2-mo, unsupervised home exercise program in both groups in an outpatient clinic of a large university hospital. Forty women, referred by gynecologists for nonoperative treatment of genuine stress incontinence of mild-to-moderate severity, were included. Measurements of daytime/nocturnal urinary frequency and subjective improvement of incontinence were the main outcome measures at initial presentation, after completion of the therapy program, and at follow-up after 3 mo. Standardized examinations of digital contraction strength, speculum tests, and manometric measurements were documented as secondary outcome measures. RESULTS: In the PT group, the daytime urination frequency decreased 22% after 4 wk of therapy and 19% after 3 mo (P < 0.05) from baseline. The nocturnal urination frequency was reduced by 66% after 4 wk of therapy and 62% after 3 mo (P < 0.001). In the BF group, the daily urination frequency decreased 10% after 4 wk of therapy and 5% after 3 mo (P > 0.05). The nocturnal urination frequency declined 36% after 4 wk of therapy and 66% after 3 months (P < 0.05). Subjective assessment after 3 mo showed that in the PT group, 28% of patients were free of incontinence episodes, 68% reported improved symptoms (incontinence episodes improved by >50%), and 4% were unchanged. In the BF group, 62% were free of incontinence episodes, and 38% were improved. Results of the digital contraction strength assessments, speculum tests, and manometric measurements showed statistically significant improvement in all variables in both groups after 3 months. CONCLUSION: Four weeks of both intensive group physical therapy or individual biofeedback training followed by an unsupervised home exercise program for 2 mo are effective therapies for female urinary stress incontinence and result in a significantly reduced nocturnal urinary frequency and improved subjective outcome. Only group physical therapy resulted in reduced daytime urinary frequency. BF therapy resulted in a better subjective outcome and higher contraction pressures of the pelvic floor muscles.

DNA fragments in the blood plasma of cancer patients: quantitations and evidence for their origin from apoptotic and necrotic cells.

Increased levels of DNA fragments have frequently been found in the blood plasma of cancer patients. Published data suggest that only a fraction of the DNA in blood plasma is derived from cancer cells. However, it is not known how much of the circulating DNA is from cancer or from noncancer cells. By quantitative methylation-specific PCR of the promoter region of the CDKN2A tumor suppressor gene, we were able to quantify the fraction of plasma DNA derived from tumor cells. In the plasma samples of 30 unselected cancer patients, we detected quantities of tumor DNA from only 3% to as much as 93% of total circulating DNA. We investigated possible origins of nontumor DNA in the plasma and demonstrate here a contribution of T-cell DNA in a few cases only. To investigate the possibility that plasma DNA originates from apoptotic or necrotic cells, we performed studies with apoptotic (staurosporine) and necrotic (staurosporine plus oligomycin) cells in vitro and with mice after induction of apoptotic (anti-CD95) or necrotic (acetaminophen) liver injury. Increasing amounts of DNA were found to be released in the supernatants of cells and in the blood plasma samples of treated animals. A clear discrimination of apoptotic and necrotic plasma DNA was possible by gel electrophoresis. The same characteristic patterns of DNA fragments could be identified in plasma derived from different cancer patients. The data are consistent with the possibility that apoptotic and necrotic cells are a major source for plasma DNA in cancer patients.

[QT syndrome: new diagnostic possibilities]. / QT-Syndrome: Neue diagnostische Möglichkeiten.

Electrocardiographic and clinical characteristics are currently used as diagnostic criteria for the long QT-syndrome. In borderline electrocardiographic findings associated with unclear syncope, it is often difficult to ensure or exclude long QT-syndrome. Schwartz and coworkers therefore created a point system as a guide in clinical decision making. In recent years genetic diagnostics have entered the arena of long-QT assessment. Aside from new insights into the pathophysiology of the long QT-disorder, it is expected that genetic diagnostics will offer substantial help to ascertain long QT-syndrome in patients with borderline electrocardiographic and clinical findings and improve risk stratification in long-QT family members. Performing linkage analysis, coupling of autosomal-dominant congenital long QT-syndrome (Romano-Ward Syndrome) to chromosomes 11 (LQT1/11p15.5), 3 (LQT3/3p21), 7 (LQT2/7q35), and 4 (LQT4/4q25-27) was demonstrated. More recently, the disease genes in long QT-syndrome 1, 2, and 3 could be identified. Analysis of the base-pair sequence allowed detection of several different mutations in different families illustrating genetic heterogeneity. Aside from diagnostic aspects, molecular genetics may also guide pharmacological therapy by identifying the specific ion-channel disorder leading to QT-prolongation and sudden death.