Hospital privileges for family physicians. Patterns of recent residency graduates, residency director perceptions, and resident expectations

A national mail survey was performed that examined reports of recent residency graduates about hospital privileges for family physicians, perceptions of residency program directors about the percentage of their graduates who obtain privileges, and plans of third-year residents for seeking privileges. Privileges in medicine, pediatrics, surgery, obstetrics, and coronary care/intensive care units (CCU/ICU) were examined. Questionnaires were mailed to a random sample of 308 residency graduates aged 30 to 35 years, all 383 family practice residency directors, and a random sample of 319 third-year residents. Two mailings produced an 82 percent response rate. Most recent graduates had privileges in medicine (97 percent), pediatrics (95 percent), and CCU/ICU (87 percent). A majority (64 percent) had obstetric privileges, and a minority (36 percent) had surgical privileges. Directors were accurate in their perceptions of privileges attained by graduates in medicine, pediatrics, and CCU/ICU, but underestimated the percentage who had privileges in surgery and overestimated the percentage who had privileges in obstetrics. Residents planned on seeking privileges in medicine, pediatrics, and obstetrics at a rate similar to recent graduates, with lower percentages planning on seeking them in surgery and CCU/ICU. Privileges in surgery and obstetrics were more prevalent in the Midwest and West.     

Squamous metaplasia of the peritoneum.

The capacity of the peritoneal serosa to undergo metaplasia to müllerian-type epithelium is well recognized. We report a case of squamous metaplasia of the peritoneum that was studied by light microscopy. Immunohistochemical techniques, and electron microscopy. The pathogenesis of peritoneal squamous metaplasia is obscure, but may be a response to chronic irritation.     

Comparison of hemoglobins Wood (alpha 2 beta 2 97 leu) and Malm? (alpha 2 beta 2 97 gln). Diagnostic value of citrate agar electrophoresis.

Diagnostic value of citrate agar electrophoresis. Am J Clin Pathol 71:668-671, 1979. Of approximately three dozen hemoglobin variants that have greater than usual oxygen affinity, nearly half are inseparable from hemoglobin A by electrophoresis at pH 8.6. A comparison of hemoglobins Wood (alpha2beta297leu) and Malm? (alpha2beta297gln) is of interest from several standpoints. They represent similar substitutions at the identical locus in the beta chain. They result in identical clinical and hematologic manifestations. Oxygen affinities of these variants are identical. Both are poorly resolved from hemoglobin A by electrophoresis at pH 8.6. The position of each is identical when studied by isoelectric focusing in polyacrylamide gel. Finally, they are easily distinguished by citrate agar electrophoresis at pH 6.2. The excellent resolution of hemoglobins Malm? and Wood from each other results neither from difference in charge, nor size, nor in quaternary structure. This technic provides a simple but effective means for identifying and differentiating these hemoglobin variants. Comparison with the results of citrate agar electrophoresis of other high oxygen-affinity hemoglobins indicates that the findings for hemoglobins Malm? and Wood are unique and unambiguous.     

Locality commissioning. The long and winding road

It is unlikely that locality commissioning, as it stands, could respond to any future government policy that identifies it as the way forward. The size of localities should remain flexible. The government has indicated that it wishes to support pilots where localities have delegated budgetary responsibility, but it is unclear whether this will emerge as a preferred model.     

Immunolocalization of CD1d in human intestinal epithelial cells and identification of a beta2-microglobulin-associated form

In order to better understand the role of intestinal CD1d, we sought to define the cellular localization and further characterize the biochemical structure of CD1d in human intestinal epithelial cells (IEC). Using a CD1d-specific rabbit anti-gst-CD1d antibody, immunoprecipitation of radiolabeled cell surface proteins detected a previously identified 37 kDa protein as well as a 48-50 kDa protein which were confirmed by Western blotting with a CD1d-specific mAb, D5. Immunoprecipitation of protein lysates with the CD1d-specific mAb, D5 and 51.1.3, and the beta2-microglobulin (beta2m)-specific mAb, BBM.1, followed by N-glycanase digestion and Western blotting with the D5 mAb showed that the 48-50 kDa protein was a beta2m-associated, CD1d glycoprotein. CD1d was immunolocalized to the apical and lateral regions of native small and large intestinal IEC as defined by confocal laser microscopy using the D5 mAb and the rabbit anti-gst-CD1d antibody. In addition, a large apical intracellular pool of CD1d was identified. Identical observations were made with polarized T84 cells. Selective biotin labeling of apical and basolateral cell surfaces followed by immunoprecipitation with the D5 mAb, N-glycanase digestion and avidin blotting confirmed the presence of glycosylated CD1d on both cell surfaces and immunolocalization of the 37 kDa non-glycosylated form of CD1d to the apical cell surface. These studies show that CD1d is located in an ideal position for luminal antigen sampling and presentation to subjacent intraepithelial lymphocytes.     

Hypoxia enhances stimulus-dependent induction of E-selectin on aortic endothelial cells.

In many diseases, tissue hypoxia occurs in conjunction with other inflammatory processes. Since previous studies have demonstrated a role for leukocytes in ischemia/reperfusion injury, we hypothesized that endothelial hypoxia may "superinduce" expression of an important leukocyte adhesion molecule, E-selectin (ELAM-1, CD62E). Bovine aortic endothelial monolayers were exposed to hypoxia in the presence or absence of tumor-necrosis factor alpha (TNF-alpha) or lipopolysaccharide (LPS). Cell surface E-selectin was quantitated by whole cell ELISA or by immunoprecipitation using polyclonal anti-E-selectin sera. Endothelial mRNA levels were assessed using ribonuclease protection assays. Hypoxia alone did not induce endothelial E-selectin expression. However, enhanced induction of E-selectin was observed with the combination of hypoxia and TNF-alpha (270% increase over normoxia and TNF-alpha) or hypoxia and LPS (190% increase over normoxia and LPS). These studies revealed that a mechanism for such enhancement may be hypoxia-elicited decrements in endothelial intracellular levels of cAMP (<50% compared with normoxia). Addition of forskolin and isobutyl-methyl-xanthine during hypoxia resulted in reversal of cAMP decreases and a loss of enhanced E-selectin surface expression with the combination of TNF-alpha and hypoxia. We conclude that endothelial hypoxia may provide a novel signal for superinduction of E-selectin during states of inflammation.