John Blair Deaver, M.D., and his marvelous retractor.

John Blair Deaver was born near Buck, Pennsylvania, in Lancaster County on July 25, 1855, to Dr. Joshua Montgomery Deaver and Elizabeth Clair Moore. The elder Deaver was a reputable country physician, educated at the University of Maryland, who fathered three physicians and a college president. John Blair Deaver (Fig. 1) went to boarding school at West Nottingham Academy in Maryland. After boarding school he taught in Lancaster County country schools to raise funds to attend the nation’s first medical school, the University of Pennsylvania. On receiving his M.D. degree in 1878, Dr. Deaver completed 1-year internships at both Germantown Hospital and Philadelphia Children’s Hospital, after which he embarked into clinical practice. Alongside his brother, Dr. Harry Clay Deaver, he made home visits to patients to perform surgeries as well as managed a busy 16th Street and Vine Street Philadelphia office

Foxp3 Represses Retroviral Transcription by Targeting Both NF-κB and CREB Pathways

Forkhead box (Fox)/winged-helix transcription factors regulate multiple aspects of immune responsiveness and Foxp3 is recognized as an essential functional marker of regulatory T cells. Herein we describe downstream signaling pathways targeted by Foxp3 that may negatively impact retroviral pathogenesis. Overexpression of Foxp3 in HEK 293T and purified CD4(+) T cells resulted in a dose-dependent and time-dependent decrease in basal levels of nuclear factor-κB (NF-κB) activation. Deletion of the carboxyl-terminal forkhead (FKH) domain, critical for nuclear localization and DNA-binding activity, abrogated the ability of Foxp3 to suppress NF-κB activity in HEK 293T cells, but not in Jurkat or primary human CD4(+) T cells. We further demonstrate that Foxp3 suppressed the transcription of two human retroviral promoters (HIV-1 and human T cell lymphotropic virus type I [HTLV-I]) utilizing NF-κB-dependent and NF-κB-independent mechanisms. Examination of the latter identified the cAMP-responsive element binding protein (CREB) pathway as a target of Foxp3. Finally, comparison of the percent Foxp3(+)CD4(+)CD25(+) T cells to the HTLV-I proviral load in HTLV-I-infected asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis suggested that high Foxp3 expression is associated with low proviral load and absence of disease. These results suggest an expanded role for Foxp3 in regulating NF-κB- and CREB-dependent cellular and viral gene expression

Optimal technical management of stump closure following distal pancreatectomy: a retrospective review of 215 cases.

BACKGROUND: Pancreatic fistula (PF) is a major source of morbidity following distal pancreatectomy (DP). Our aim was to identify risk factors related to PF following DP and to determine the impact of technique of transection and stump closure. METHODS: We performed a retrospective review of 215 consecutive patients who underwent DP. Perioperative and postoperative data were collected and analyzed with attention to PF as defined by the International Study Group of Pancreatic Fistula. RESULTS: PF developed in 36 patients (16.7%); fistulas were classified as Grade A (44.4%), B (44.4%), or C (11.1%). The pancreas was transected with stapler (n = 139), cautery (n = 70), and scalpel (n = 3). PF developed in 19.8% of remnants which were stapled/oversewn and 27.7% that were stapled alone (p = 0.4). Of the 69 pancreatic remnants transected with cautery and oversewn, a fistula developed in 4.3% (p = 0.004 compared to stapled/oversewn; p = 0.006 compared to stapled/not sewn). The median length of postoperative hospital stay was significantly increased in patients who developed PF (10 vs. 6 days, p = 0.002) CONCLUSION: The method of transection and management of the pancreatic remnant plays a critical role in the formation of PF following DP. This series suggests that transection using electrocautery followed by oversewing of the pancreatic remnant has the lowest risk of PF