Plummer-Vinson Syndrome

A 37-year-old African American woman with no past medical history presented to the Emergency Department with a chief complaint of abdominal pain. She also reported associated fatigue and dysphagia. Over the past two months, she reported 40 Lbs. unintentional weight loss and decrease appetite. Her dysphagia primarily to solids, which also had been worsening over the past few weeks. She had no history of similar symptoms in the past. She was not on any medications. On admission, vital signs were stable. In the Emergency Department,. Hemoglobin on admission was 3.3 g/dL [11.9–15.1 g/dL] with a mean corpuscular volume of 61.1. Her serum iron on admission was 10 ug/dL [60–140 ug/dL], iron saturation was 2% [15–50%], and ferritin was 1.0 ng/mL [11.0–307 ng/mL]. Upon further questioning, the patient stated that she did not describe menorrhagia. She denied hematemesis, hematochezia, or melena. She was transfused with 3 units of packed red blood cells and was started on 1000 mg of IV iron dextran complex infusions. Gastroenterology was consulted, and the patient underwent esophagogastroduodenoscopy (EGD) and colonoscopy. Colonoscopy showed erythematous and edematous mucosa in the terminal ileum which was Biopsied. The EGD revealed a few intrinsic stenoses in the upper esophagus which were successfully dilated with savary. A pathology exam of the terminal ileum showed well differentiated neuroendocrine tumor. Given the clinical, laboratory, and endoscopic (as shown below) Esophageal web located in the upper esophagus. a diagnosis of Plummer-Vinson syndrome was made. Her dysphagia improved over the three days in the hospital after iron infusions and blood transfusions, and she was able to tolerate a regular diet. Approximately 2 months after her discharge, a follow-up phone call was made to the patient. She stated that she had been compliant with all her medications and her dysphagia had resolved. At the time of the phone call, she was tolerating a regular diet without any dietary restrictions.https://scholarlycommons.henryford.com/merf2020caserpt/1132/thumbnail.jp

TCT-126 Outcomes of Chronic Total Occlusion Percutaneous Coronary Intervention of the Left Anterior Descending Artery

Background: Improvement of left ventricular ejection fraction (LVEF) after chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has been modest in prior studies. Methods: Our cohort included patients who underwent LAD CTO PCI at a single center (Henry Ford Hospital) from 2014 to 2021. We evaluate the change in LVEF after LAD CTO PCI using the paired t test in all patients, those with ischemic cardiomyopathy (CM), and those who underwent a viability test. Results: From December 2014 to February 2022, a total of 237 LAD CTO PCI procedures were performed at Henry Ford Hospital (proximal LAD: 56.6%). In-hospital MACE occurred in 13 patients (5.5%; death: 1.3%). Landmark analysis after discharge showed an overall survival of the cohort was 92.7% and MACE-free survival of 85.0% over a median follow-up of 2 years. The median baseline EF was 50% (IQR 35%-55%). Only 51 patients had reduced baseline LVEF (40% or less). After a median follow-up of 9.2 months (IQR 3-28.6 months), there was a significant improvement in LVEF after LAD CTO PCI (mean 10.9%, 95% CI 7.1%-14.8%, P \u3c 0.001). When limiting the analysis to patients who had ischemic cardiomyopathy, proximal LAD CTO PCI, and were on optimal medical therapy (n = 29), LVEF was significantly improved (mean increase of 14%, 95% CI 9.5-18.5%, P \u3c 0.001) after a median follow-up period of 6.2 months (3-29.5 months). Conclusion: LAD CTO PCI was associated with a significant 10% improvement in LVEF in ICM patients and was more pronounced (14% improvement) in those who had proximal LAD treated and were on optimal medical therapy. Categories: CORONARY: Complex and Higher Risk Procedures for Indicated Patients (CHIP

The αGal Epitope of the Histo-Blood Group Antigen Family Is a Ligand for Bovine Norovirus Newbury2 Expected to Prevent Cross-Species Transmission

Among Caliciviridae, the norovirus genus encompasses enteric viruses that infect humans as well as several animal species, causing gastroenteritis. Porcine strains are classified together with human strains within genogroup II, whilst bovine norovirus strains represent genogroup III. Various GI and GII human strains bind to carbohydrates of the histo-blood group family which may be shared among mammalian species. Genetic relatedness of human and animal strains as well as the presence of potentially shared ligands raises the possibility of norovirus cross-species transmission. In the present study, we identified a carbohydrate ligand for the prototype bovine norovirus strain Bo/Newbury2/76/UK (NB2). Attachment of virus-like particles (VLPs) of the NB2 strain to bovine gut tissue sections showed a complete match with the staining by reagents recognizing the Galα1,3 motif. Alpha-galactosidase treatment confirmed involvement of a terminal alpha-linked galactose. Specific binding of VLPs to the αGal epitope (Galα3Galβ4GlcNAcβ-R) was observed. The binding of Galα3GalαOMe to rNB2 VLPs was characterized at atomic resolution employing saturation transfer difference (STD) NMR experiments. Transfection of human cells with an α1,3galactosyltransferase cDNA allowed binding of NB2 VLPs, whilst inversely, attachment to porcine vascular endothelial cells was lost when the cells originated from an α1,3galactosyltransferase KO animal. The αGal epitope is expressed in all mammalian species with the exception of the Hominidaea family due to the inactivation of the α1,3galactosyltransferase gene (GGTA1). Accordingly, the NB2 carbohydrate ligand is absent from human tissues. Although expressed on porcine vascular endothelial cells, we observed that unlike in cows, it is not present on gut epithelial cells, suggesting that neither man nor pig could be infected by the NB2 bovine strain

Cyclin E as a potential therapeutic target in high grade serous ovarian cancer.

Cyclin E1 (CCNE1) gene amplification occurs in approximately 20% of ovarian high grade serous carcinoma (HGSC) and is associated with chemotherapy resistance and, in some studies, overall poor prognosis. The role of cyclin E1 in inducing S phase entry relies upon its interactions with cyclin dependent kinases (CDK), specifically CDK2. Therapies to target cyclin E1-related functions have centered on CDK inhibitors and proteasome inhibitors. While many studies have helped elucidate the functions and regulatory mechanisms of cyclin E1, further research utilizing cyclin E1 as a therapeutic target in ovarian cancer is warranted. This review serves to present the scientific background describing the role and function of cyclin E1 in cancer development and progression, to distinguish cyclin E1-amplified HGSC as a unique subset of ovarian cancer deserving of further therapeutic investigation, and to provide an updated overview on the studies which have utilized cyclin E1 as a target for therapy in ovarian cancer