Publications by authors named "J Buchwald"

Purpose: Chronic traumatic encephalopathy (CTE) has been diagnosed in 91.7% of retired United States National Football League (NFL) players at postmortem. There is no treatment or cure for CTE.

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Introduction: Uncomplicated surgical approaches that minimize anastomotic complications while improving revisional metabolic/bariatric surgical (MBS) outcomes are needed.

Methods: This prospective single-center study assessed the feasibility, safety, and efficacy of the novel linear magnetic anastomosis system (LMAS [3 cm]) in performing a side-to-side duodeno-ileostomy (MagDI) bipartition to revise clinically suboptimal primary sleeve gastrectomy (SG). Patients with severe obesity with/without type 2 diabetes (T2D) with suboptimal weight loss, regain, and/or T2D recurrence post SG underwent revisional MagDI.

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Background: Means of addressing technical challenges in forming gastrojejunostomy (GJ) anastomoses and maintaining their patency are sought.

Objectives: Evaluation of preclinical feasibility and healing efficacy of a novel linear magnetic compression anastomosis (MCA) device to form a patent GJ versus sutured jejunal enterotomy (JE) sites in swine.

Setting: Single-center veterinary testing facility.

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HIV-1 gp120 glycan binding to C-type lectin adhesion receptor L-selectin/CD62L on CD4 T cells facilitates viral attachment and entry. Paradoxically, the adhesion receptor impedes HIV-1 budding from infected T cells and the viral release requires the shedding of CD62L. To systematically investigate CD62L-shedding mediated viral release and its potential inhibition, we screened compounds specific for serine-, cysteine-, aspartyl-, and Zn-dependent proteases for CD62L shedding inhibition and found that a subclass of Zn-metalloproteinase inhibitors, including BB-94, TAPI, prinomastat, GM6001, and GI25423X, suppressed CD62L shedding.

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Introduction: The most significant genetic risk factor for late-onset Alzheimer's disease (AD) is APOE4, with evidence for gain- and loss-of-function mechanisms. A clinical need remains for therapeutically relevant tools that potently modulate APOE expression.

Methods: We optimized small interfering RNAs (di-siRNA, GalNAc) to potently silence brain or liver Apoe and evaluated the impact of each pool of Apoe on pathology.

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