A study of fibrin clot structure under various ionic conditions using stereoscopic IVEM images

Fibrin clots are formed by the conversion of fibrinogen into fibrin monomers which assemble to produce two-stranded protofibrils that aggregate to form fibers. These fibers may also aggregate laterally with other fibers to form larger fiber bundles. Investigations of fibrin clot structures under various ionic conditions using SEM showed dramatic differences in fiber morphology and clot structure. Fibrin clots formed under various ionic conditions were investigated by the examination of stereoscopic IVEM images. This technique provides greater depth discrimination and higher resolution images of clot ultrastructure. Details of fiber association and branching are of particular interest.Purified human fibrinogen was prepared at a concentration of 0.5 mg/ml in 0.4M, 0.2M, and 0.05M buffers (0.05M Tris-HCI, pH 7.4, with 2mM CaCl2). Fibrinogen solutions were mixed with thrombin to a final concentration of 0.3U/ml and aiiquots placed onto Formvar and carbon coated grids. After clotting for 1 hr. at room temperature, clots were fixed with 3% glutaraldehyde in 0.1 M Na-cacodylate buffer, pH 7.2, for 5 min. Grids were kept constantly moist to avoid collapse or syneresis.</jats:p

Methicillin-resistant Staphylococcus aureus strains in New York City hospitals: inter-hospital spread of resistant strains of type 88

A survey of methicillin-resistant strains of Staphylococcus aureus received for phage typing indicated a marked increase of resistant strains received in 1982 and 1983. Of 62 hospitals in New York City which sent strains for phage typing, 35 had methicillin-resistant isolates. A significant development was the presence of strains of the same phage type at several hospitals, indicating a possible inter-hospital spread of these strains. Among strains present at several hospitals, the largest group was of experimental phage type 88. Strains of type 88 were received from 23 hospitals, representing 56% of all methicillin-resistant strains received from New York City hospitals. Strains of type 88 were resistant to all antistaphylococcal antibiotics, with the exception of vancomycin, and represented a major source of nosocomial infections at 13 hospitals. As experimental phage 88 is not routinely used for typing in U.S. laboratories, the nationwide distribution of strains of type 88 is difficult to assess.</jats:p

Expression of parafibromin in major renal cell tumors

Parafibromin, encoded by HRPT2 gene, is a recently identified tumor suppressor. Complete and partial loss of its expression have been observed in hyperparathyroidism-jaw tumor (HPT-JT), parathyroid carcinoma, breast carcinoma, lung carcinoma, gastric and colorectal carcinoma. However, little has been known about its expression in renal tumors. In order to study the expression of parafibromin in a series of the 4 major renal cell tumors - clear cell renal cell carcinoma (ccRCC), papillary renal cell carcinoma (pRCC), chromophobe renal cell carcinoma (chRCC) and oncocytoma, one hundred thirty nine renal tumors including 61 ccRCCs, 37 pRCCs, 22 chRCCs and 19 oncocytomas were retrieved and used for the construction of renal tissue microarrays (TMAs). The expression of parafibromin was detected by immunohistochemical method on the constructed TMAs. Positive parafibromin stains are seen in 4 out of 61 ccRCCs (7%), 7 out of 37 pRCCs (19%), 12 out of 23 chRCCs (52%) and all 19 oncocytomas (100%). Parafibromin expression varies significantly (P<8.8×10(−16)) among the four major renal cell tumors and were correlated closely with tumor types. No correlation of parafibromin expression with tumor staging in ccRCCs, pRCCs and chRCCs, and Fuhrman nuclear grading in ccRCCs and pRCCs was seen. In summary, parafibromin expression was strongly correlated with tumor types, which may suggest that it plays a role in the tumorigenesis in renal cell tumors

Expression of parafibromin in major renal cell tumors.

Parafibromin, encoded by HRPT2 gene, is a recently identified tumor suppressor. Complete and partial loss of its expression have been observed in hyperparathyroidism-jaw tumor (HPT-JT), parathyroid carcinoma, breast carcinoma, lung carcinoma, gastric and colorectal carcinoma. However, little has been known about its expression in renal tumors. In order to study the expression of parafibromin in a series of the 4 major renal cell tumors - clear cell renal cell carcinoma (ccRCC), papillary renal cell carcinoma (pRCC), chromophobe renal cell carcinoma (chRCC) and oncocytoma. One hundred thirty nine renal tumors including 61 ccRCCs, 37 pRCCs, 22 chRCCs and 19 oncocytomas were retrieved and used for the construction of renal tissue microarrays (TMAs). The expression of parafibromin was detected by immunohistochemical method on the constructed TMAs. Positive parafibromin stains are seen in 4 out of 61 ccRCCs (7%), 7 out of 37 pRCCs (19%), 12 out of 23 chRCCs (52%) and all 19 oncocytomas (100%). Parafibromin expression varies significantly (P\u3c 8.8 x10-16) among the four major renal cell tumors and were correlated closely with tumor types. No correlation of parafibromin expression with tumor staging in ccRCCs, pRCCs and chRCCs, and Fuhrman nuclear grading in ccRCCs and pRCCs. In summary, parafibromin expression was strongly correlated with tumor types, which may suggest that it plays a role in the tumorigenesis in renal cell tumors

Emergence of gentamicin- and methicillin-resistant Staphylococcus aureus strains in New York City hospitals

Gentamicin- and methicillin-resistant strains of Staphylococcus aureus have been isolated from Spring 1979 to the present from many hospitals in New York City. A large proportion of the strains were resistant to the majority of antistaphylococcal antibiotics. The ratio of multiply resistant strains was highest among tetracycline-resistant strains. There were significant differences in phage susceptibility patterns and the resistance spectrum of strains isolated at different hospitals, whereas strains isolated at the same hospital often showed a marked degree of similarity. This suggests multiple origins of gentamicin- and methicillin-resistant strains isolated in New York City.</jats:p