Deltoid flap combined with fascia lata autograft for rotator cuff defects: a histologic study

The purpose of this study was to compare the histological characteristics of an autogenous fascia lata graft alone and a fascia lata graft combined with a deltoid flap in the reconstruction of rotator cuff tears. Ten New Zealand white rabbits were divided into two groups. Infraspinatus tendon defects (1 × 1 cm) were created in each animal. Reconstruction consisted of either a fascia lata graft alone or a fascia lata graft combined with a distally based deltoid flap. At 3 months, tissue harvest and histological analysis was performed. Compared to the fascia lata graft alone, there was significantly increased remodeling activity and neovascularization in the group that included a deltoid flap. Also, there was pronounced interdigitation at the graft/flap interface in the latter group. A mutually beneficial relationship may exist when an autogenous fascial graft is combined with a functional deltoid flap for reconstructing large rotator cuff defects.     

Sinonasal hemangiopericytoma. A reassessment with electron microscopy, immunohistochemistry, and long-term follow-up

Sinonasal hemangiopericytomas are rare, occasionally misdiagnosed neoplasms that have often been considered distinct from hemangiopericytomas of other sites. Eleven cases were studied. Nine arose from the nasal cavity and two from the paranasal sinuses. The patients' mean age was 58 years. In nine cases there were no appreciable mitoses; in two, mitoses were frequent. Of 10 cases studied by immunostaining, all were positive for vimentin; two had faint focal staining for actin; one focally expressed S-100 protein; all were negative for cytokeratins, desmin, and Factor VIII-related antigen; and none bound Ulex europaeus agglutinin 1. Five cases were studied by electron microscopy. The most consistent features were basal lamina-like material partly surrounding tumor cells and completely separating them from endothelium, tapered cytoplasmic extensions, and orderly bundles of filaments. Intercellular junctions and pinocytotic vesicles were present in some tumors. Of nine cases with adequate follow-up, tumors recurred in four cases (44%) after a mean of 6.5 years, and none metastasized. A review of the literature showed that high local recurrence rates, late recurrences, and low rates of metastasis were features of tumors in this location. This might be a reflection of early presentation, small tumor bulk, and difficulty of complete resection, rather than evidence for a biologically distinct neoplasm.     

Alcohollike liver disease in nonalcoholics. A clinical and histologic comparison with alcohol-induced liver injury

Individuals who deny alcohol consumption may develop liver injury that histologically resembles the liver injury found in alcoholic patients. To determine whether any clinical or histologic features distinguish alcoholic and nonalcoholic subjects with "alcohollike" liver injury, the clinical records and liver biopsy specimens of 68 alcoholic and 39 nonalcoholic patients with alcohollike injury on liver biopsy were compared. The clinical and biochemical features of the two groups differed significantly. Alcoholism was associated with more severe clinical and biochemical manifestations of liver disease. However, there was considerable overlap among histologic features of the two clinically defined groups. Based on histology alone, alcoholic and nonalcoholic patients were often indistinguishable. The observations suggest that the clinical differences between the alcoholic and non-alcoholic patients cannot be attributed to qualitative or quantitative differences in liver histology. On the other hand, histologic similarities between the two groups raise the possibility that a shared condition, perhaps nutritional or hormonal, is responsible for the histologic expression of alcohollike injury in both groups.     

A Comparison of DEF X-Ray Film and a Photodiode Array (Reticon) as Detectors for an X-Ray Crystal Spectrometer

A crystal spectrometer with a photodiode array (PDA) detector was tested for a range of x-ray energies between 1 and 2 keV. A laser-produced plasma has been used as an x-ray source and was generated by the high-power (Vulcan) glass laser system at the SERC Rutherford Appleton Laboratory, UK. The performance of the array was directly compared with the response of Kodak DEF x-ray film. In order to compare quantitatively the performances of the PDA and the film, detective quantum efficiency (DQE) considerations are presented for both devices. It is demonstrated that the PDA has a useful dynamic range which is approximately seven times greater than that of film, a peak DQE of approximately six times that of film, and a greatly superior low-signal performance. The operational characteristics of the PDA are discussed.     

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.