Radical prostatectomy: anatomical predictors of success or failure

A total of 143 patients underwent radical prostatectomy. Surgical specimens were evaluated with respect to local extent of disease, Gleason grade of the primary and relative nuclear roundness of the surgical specimen. The probability of disease control in the total population was 88 per cent at 5 years. Only 8 per cent of the patients who had disease confined to the specimen failed compared to 14 per cent of those who demonstrated extension outside of the surgical margins. The incidence of failure increased as a function of seminal vesicle involvement. Seminal vesicle involvement was greatest among patients with a Gleason grade greater than 7. Postoperative radiation did not offer any apparent advantage in patients with positive margins.     

Ergonomic mode of dental treatment using equipment combination "Ergostar 90 S". Report on clinical experience

Regarding ergonomic principles of work the new dental unit "Ergostar 90 S" was tested during a period of four weeks to estimate its efficiency. In all technical aspects it fulfills international standards. Recommendations for improvement of some ergonomic details are given.     

Localization of a gene for otosclerosis to chromosome 15q25-q26

Among white adults otosclerosis is the single most common cause of hearing impairment. Although the genetics of this disease are controversial, the majority of studies indicate autosomal dominant inheritance with reduced penetrance. We studied a large multi- generational family in which otosclerosis has been inherited in an autosomal dominant pattern. Five of16 affected persons have surgically confirmed otosclerosis; the remaining nine have a conductive hearing loss but have not undergone corrective surgery. To locate the disease- causing gene we completed genetic linkage analysis using short tandem repeat polymorphisms (STRPs) distributed over the entire genome. Multipoint linkage analysis showed that only one genomic region, on chromosome 15q, generated a lod score >2.0. Additional STRPs were typed in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis gene.      

Induced luteolysis in the primate: rapid loss of luteinizing hormone receptors

The molecular mechanisms involved in luteolysis are still unclear in the primate. This study aimed to investigate the effect of induced luteolysis on the ovarian luteinizing hormone (LH) receptor and the steroidogenic enzyme, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the marmoset monkey. Luteolysis was induced in the mid-luteal phase either directly by systemic prostaglandin F2alpha (PGF2alpha), or indirectly by LH withdrawal using systemic gonadotrophin releasing hormone antagonist (GnRHant) treatment. The LH receptor was studied by isotopic mRNA in-situ hybridization and in-situ ligand binding and 3beta-HSD expression was studied using isotopic mRNA in-situ hybridization and immunohistochemistry. Induced luteolysis was associated with a reduction in the expression of LH receptor (P < 0.0001) and 3beta-HSD mRNA, closely followed by a reduction in the LH receptor (P < 0.05) and 3beta-HSD protein concentrations within 24 h. There were no differences in the findings whether luteolysis was induced with PGF2alpha or GnRHant. This study shows that disparate mechanisms to induce luteolysis in the primate result in an identical rapid loss of the LH receptor and 3beta-HSD. In conclusion, induced luteolysis leads to rapid loss of the steroidogenic pathway in luteal cells.      

X-linked liver glycogenosis type II (XLG II) is caused by mutations in PHKA2, the gene encoding the liver alpha subunit of phosphorylase kinase

X-linked liver glycogenosis type II (XLG II) is a recently described X- linked liver glycogen storage disease, mainly characterized by enlarged liver and growth retardation. These clinical symptoms are very similar to those of XLG I. In contrast to XLG I patients, however, XLG II patients do not show an in vitro enzymatic deficiency of phosphorylase kinase (PHK). Recently, mutations were identified in the gene encoding the liver alpha subunit of PHK (PHKA2) in XLG I patients. We have now studied the PHKA2 gene of four unrelated XLG II patients and identified four different mutations in the open reading frame, including a deletion of three nucleotides, an insertion of six nucleotides and two missense mutations. These results indicate that XLG II is due to mutations in PHKA2. In contrast to XLG I, XLG II is caused by mutations that lead to minor structural abnormalities in the primary structure of the liver alpha subunit of PHK. These mutations are found in a conserved RXX(X)T motif, resembling known phosphorylation sites that might be involved in the regulation of PHK. These findings might explain why the in vitro PHK enzymatic activity is not deficient in XLG II, whereas it is in XLG I.      

Die Erythrokinetik bei Osteomyelofibrose

Zusammenfassung Bei 20 Patienten mit Osteomyelofibrose wurden Erythrocytenbildung und Erythrocytenzerstörung mit Hilfe von Cr⁵¹ und Fe⁵⁹ z. T. nach simultaner Verabreichung dieser Isotope untersucht. Die Erythrocytenlebensdauer war oft verkürzt, jedoch meist nicht hochgradig. Nur bei wenigen Kranken war eine aktive Beteiligung der Milz an der vorzeitigen Zerstörung der Erythrocyten nachweisbar. Das Plasmaeisenturnover war fast stets erhöht, die Eiseninkorporation in die Erythrocyten vermindert. Eine extramedulläre Erythropoese war meist, aber nicht ausnahmslos, durch Oberflächenmessung nachzuweisen. Sie fand überwiegend in der Milz statt, doch war die Leber in zwei Fällen der wichtigste Ort der Erythrocytenbildung. Eine Produktion von Erythrocyten im Knochenmark war bei der Hälfte der entsprechend untersuchten Fälle noch in geringem Maße vorhanden. Die komplexe Korrelation dieser Befunde mit den hämatologischen Daten wurde besprochen und die Indikation zur Splenektomie erörtert.

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Summary Production and destruction of erythrocytes were investigated in 20 patients suffering from myelofibrosis. Cr⁵¹ and Fe⁵⁹ were administered simultaneously. The erythrocyte life span was shortened frequently, but only moderately in most instances. In few patients only the spleen played an active part in the accelerated red cell destruction. The plasma iron turnover was increased in most cases, the incorporation of iron into the erythrocytes was decreased. Extramedullary erythropoiesis was demonstrated by means of surface activity measurements in most but not in all patients. It was localised most frequently in the spleen. In two cases, however, the liver was the most important site of erythrocyte production. Some degree of medullary erythropoiesis was seen in 50 percent of our cases. The correlation between these results and the remaining hematological findings as well as the question of when to remove the spleen are discussed.

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Unter technischer Mitarbeit von FräuleinRenate Roesch, FräuleinMargret Philips und FräuleinIngrid Westmattelmann.

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Die Arbeit wurde durchgeführt mit Unterstützung der Deutschen Forschungsgemeinschaft.     

Barriers to Dissemination: Exploring the Criticisms of Behavior Therapy for Tics

The review by Cook and Blacher (2007 ) suggests that behavior therapy for tic disorders is indeed efficacious. Given the empirical support for these treatments, researchers should begin to place effort on examining various strategies for treatment dissemination. The current article addresses possible barriers to dissemination, focusing specifically on various concerns that have been raised by many medical and psychological care providers. The validity of these concerns is examined in the context of existing data. In addition, limitations of the current literature and future directions for research are discussed.