Search

Background: Federal law requires background checks for firearms purchased from licensed dealers, but states can extend requirements to private sales of handguns and purchases at gun shows (universal background checks for handguns: UBC-HG). Although firearm homicide disproportionately affects African Americans, little is known about how UBG-HG impacts African Americans. We hypothesized that implementation of UBC-HG would reduce rates of firearm homicide of African Americans. Methods: We collected Centers for Disease Control firearm homicide counts for African American and white populations in the 50 states, 1999-2017. Laws were drawn from the State Firearm Laws Database. The exposure and outcome of interest were UBC-HG adoption and firearm homicide. We included non-Hispanic African American and non-Hispanic White populations. We used Poisson regression to perform a differences-in-differences analysis. A categorical variable for state accounted for time-stable state characteristics. We controlled for year to account for trends over time unrelated to policy. We controlled for state-specific, time-variable factors including median household income, population Results: The firearm homicide rate among whites was 1.8 per 100,000 (Interquartile Range [IQR] 1.2-2.7) ranging from 1.4 in 2011 to 1.8 in 2016. The firearm homicide rate was 15.6 per 100,000 (IQR 11.6-21.0) among African Americans, ranging from 14.0 in 2009 to 19.6 in 2017. While no significant difference in firearm homicides among whites (Incidence rate ratio [IRR] 0.93, 95% CI 0.73, 1.20) was appreciated, the passage of UBC-HG was associated with an 19% decrease in African Americans firearm homicides (IRR 0.81, 95% CI 0.70, 0.94; p=0.006). Conclusions: Implementing UBC-HG was associated with decreased firearm homicides among African Americans—the population most at risk. Expanding UBC-HG may be an effective approach to reducing racial disparities in firearm homicides.

Ehyal Shweiki,1 Niels D Martin,2 Alec C Beekley,1 Jay S Jenoff,1 George J Koenig,1 Kris R Kaulback,1 Gary A Lindenbaum,1 Pankaj H Patel,1 Matthew M Rosen,1 Michael S Weinstein,1 Muhammad H Zubair,2 Murray J Cohen1 1Department of Surgery, Thomas Jefferson University Hospital, Philadelphia, PA, USA; 2Department of Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA Abstract: Medical resident education in the United States has been a matter of national priority for decades, exemplified initially through the Liaison Committee for Graduate Medical Education and then superseded by the Accreditation Council for Graduate Medical Education. A recent Special Report in the New England Journal of Medicine, however, has described resident educational programs to date as prescriptive, noting an absence of innovation in education. Current aims of contemporary medical resident education are thus being directed at ensuring quality in learning as well as in patient care. Achievement and work-motivation theories attempt to explain people's choice, performance, and persistence in tasks. Expectancy Theory as one such theory was reviewed in detail, appearing particularly applicable to surgical residency training. Correlations between Expectancy Theory as a work-motivation theory and residency education were explored. Understanding achievement and work-motivation theories affords an opportunity to gain insight into resident motivation in training. The application of Expectancy Theory in particular provides an innovative perspective into residency education. Afforded are opportunities to promote the development of programmatic methods facilitating surgical resident motivation in education. Keywords: learning, education, achievement

Aim: Esophagectomy is the primary surgical treatment for localized malignant neoplasms of the esophagus, and while outcomes have shown that substantial improvement has been made, the ceiling for improvement is still high. Methods: A total of 2506 publications published from January 2002 to March 2012 were identified from PubMed, MEDLINE and the Cochrane Library using the keywords: ‘esophagectomy’, ‘esophagus’, ‘neoplasm’ and ‘cancer’ to identify quality key surgical articles in esophagectomy that were broken down into three groups: preoperative, intraoperative and postoperative care. Discussion: There have been limited preoperative surgical trials, mostly in preoperative antibiotic use, which have led to changes in surgical management. Key and substantial changes have occurred in the intraoperative management for esophageal malignancies around surgical anastomosis technique and anesthesia. Nutritional outcomes still remain a key challenge, and currently there is no established standard of care in the postoperative management of esophagectomy patients. Conclusion: We established quality parameters for leak rates, overall morbidity and mortality, and these form the foundation from which all esophageal surgeons should rank their results. We then utilized the techniques described above to maintain those rates or, better yet, to significantly improve those rates in each surgeons’ practice.

Histoplasmosis, an increasingly important opportunistic infection in immunosuppressed subjects, is characterized by hematogenous dissemination of the yeast from the lung. The mechanism of this dissemination is not fully understood. Laminin, the major glycoprotein of the extracellular matrix, is known to mediate the attachment of various invasive pathogens to host tissues. In the current study, laminin is demonstrated to bind to Histoplasma capsulatum in a rapid, specific, and saturable manner. Scatchard analysis with 125I-labeled laminin revealed an estimated 3.0 x 10(4) binding sites per yeast with an apparent Kd for laminin binding of 1.6 x 10(-9) M. Laminin binding to H. capsulatum was decreased from 62 +/- 1 to 17 +/- 1 ng (P < 0.001) in the presence of 3,000 nM of Ile-Lys-Val-Ala-Val, a pentapeptide within one major cell attachment site of laminin. A 50-kD H. capsulatum laminin-binding protein was demonstrated using an 125I-Ln blot of H. capsulatum cell wall proteins. The 50-kD protein is also recognized by antibodies directed at the 67-kD laminin receptor, suggesting they are related. This study proposes a possible mechanism for H. capsulatum attachment to laminin, an important first step required for the yeast to recognize and traverse the basement membrane.

We describe a sibship of three males, including monozygous twins, with cerebral and cerebellar malformations and congenital lymphedema. The parents of these children are related, being half second cousins. The clinical, radiologic and histopathologic features do not fit a previously recognized pattern. We feel this sibship represents a syndrome that has not been previously described, though it closely resembles the Walker Warburg syndrome.

Pneumocystis carinii is an extracellular organism which is thought to require attachment to alveolar epithelial cells for its growth and replication in humans. Fibronectin (Fn) binding to P. carinii is essential for optimal P. carinii attachment. This study demonstrates that gp120, a 110-120-kD membrane glycoprotein on P. carinii, mediates attachment of the organism to cultured lung cells and is the site of Fn binding to P. carinii. A 51Cr-labeled P. carinii binding assay was used to quantify attachment of the organism to the alveolar epithelial cell line A549. Addition of free gp120, purified from whole P. carinii organisms, caused a significant decrease in attachment of P. carinii to A549 cells from 44.2 +/- 5.5% to 22.4 +/- 4.2% (P less than 0.01). Preincubation of the P. carinii organisms with a polyclonal antibody to gp120 also resulted in a marked decrease in P. carinii attachment to A549 cells from 46.8% +/- 5.2% to 21.3 +/- 4.8% (P less than 0.01). Furthermore, addition of free gp120 to P. carinii organisms caused a significant reduction in specific binding of 125I-Fn to P. carinii (from 83.3 +/- 8.5 ng to 47.1 +/- 5.9 ng, P less than 0.01). Similarly, anti-gp 120 antibody decreased specific Fn binding to P. carinii from 74.3 +/- 8.4 ng to 25.5 +/- 5.3 ng (P less than 0.001). Solubilized P. carinii organisms separated by gel electrophoresis and blotted with 125I-Fn demonstrated specific binding of the 125I-Fn to gp120. In addition, a specific anti-beta 1-integrin antiserum reacted with gp120 by Western blot, suggesting structural homology between gp120 and the beta-subunit of integrins. Thus, the data suggest that the P. carinii membrane glycoprotein gp120 functions as a Fn binding protein and is required for optimal P. carinii attachment to alveolar epithelial cells.

A dental health programme which employed group self prophylaxis by school children aged 5-9 years is described. The group used 10 per cent SnF2-ZrSiO4 paste and was supervised within the school by an auxiliary of parents under the direction of a dentist. There was a 36 per cent reduction in DMFT increment at the end of two years in the children aged 7-9 years.

Hyperoxia and paraquat ingestion are two clinical examples of lung injury thought to be mediated by oxidant mechanisms. An in vitro cytotoxicity assay using freshly explanted 51Cr-labeled lung tissue as the target was used to quantify the ability of hyperoxia and paraquat to directly injure lung parenchymal cells in an environment where indirect mechanisms such as recruitment of inflammatory cells were not possible. There are clear species differences in the susceptibility of lung parenchyma to direct injury by hyperoxia (95% O2) and paraquat (10 microM--10 mM) for 18 h at 37 degrees C, with human and rat lung being more sensitive than rabbit lung. Oxygen radical inhibitors, particularly catalase (1,100 U/ml) and alpha-tocopherol (10 micrograms/ml), reduced hyperoxia and paraquat-induced lung injury, although their ability to do so depended on the oxidant and the species. The simultaneous use of hyperoxia and paraquat accelerated the in vitro lung parenchymal cell injury in each species tested. These studies demonstrate that both oxygen and paraquat can directly injure the cells of the lower respiratory tract without enlisting the aid of additional blood-derived inflammatory cells. In addition, the 51Cr-labeled lung explant assay used for these studies allows for the quantitative assessment of direct lung cell injury and thus may prove useful as an in vitro model by which to investigate lung injury of other etiologies.

Cigarette smoking increases the numbers and oxidative metabolism of alveolar macrophages. Increased production of superoxide (O2-) and H2O2 by alveolar macrophages may contribute to the pathogenesis of cigarette-induced lung diseases. The cytotoxicity mediated by alveolar macrophages from smokers (n = 11) and nonsmokers (n = 13) was compared in an in vitro assay in which the target cells were chromium 51-labeled lung explants. The spontaneous cellular cytotoxicity mediated by smoker macrophages was significantly greater than that of nonsmoker macrophages (cytotoxic index 20.3% +/- 1.9% compared with 5.5% +/- 0.9%, P less than 0.001). Phorbol myristate acetate significantly increased the cytotoxic index of nonsmoker macrophages but did not cause further increases in smoker macrophage killing. The antioxidants superoxide dismutase and catalase produced partial inhibition of smoker macrophage cytotoxicity, suggesting that target cell killing was mediated in part by oxidant mechanisms. Supplementation of smokers' diets with high-dose oral vitamin E failed to decrease smoker alveolar macrophage cytotoxicity. These findings demonstrate that smoker alveolar macrophages possess enhanced cytotoxic potential for normal lung parenchymal cells.