Hybrid sons between Drosophila melanogaster females and D. simulans males die as 3rd instar larvae. Two genes, D. melanogaster Hybrid male rescue (Hmr) on the X chromosome, and D. simulans Lethal hybrid rescue (Lhr) on chromosome II, interact to cause this lethality. Loss-of-function mutations in either gene suppress lethality, but several pieces of evidence suggest that additional factors are required for hybrid lethality. Here we screen the D. melanogaster autosomal genome by using the Bloomington Stock Center Deficiency kit to search for additional regions that can rescue hybrid male lethality. Our screen is designed to identify putative hybrid incompatibility (HI) genes similar to Hmr and Lhr which, when removed, are dominant suppressors of lethality. After screening 89% of the autosomal genome, we found no regions that rescue males to the adult stage. We did, however, identify several regions that rescue up to 13% of males to the pharate adult stage. This weak rescue suggests the presence of multiple minor-effect HI loci, but we were unable to map these loci to high resolution, presumably because weak rescue can be masked by genetic background effects. We attempted to test one candidate, the dosage compensation gene male specific lethal-3 (msl-3), by using RNA interference with short hairpin microRNA constructs targeted specifically against D. simulans msl-3 but failed to achieve knockdown, in part due to off-target effects. We conclude that the D. melanogaster autosomal genome likely does not contain additional major-effect HI loci. We also show that Hmr is insufficient to fully account for the lethality associated with the D. melanogaster X chromosome, suggesting that additional X-linked genes contribute to hybrid lethality.

Figure 1. Ulcer with visible vessel on initial endoscopy, treated only with hemostatic powder. (2) Four-box model approach to ethical decision making in this case. (3) Same ulcer on repeat endoscopy, now with a pulsatile visible vessel, treated with an over-the-scope clip.

Figure 1. Bifidobacteria relative abundance demonstrates a lasting decline after SARS-CoV-2 mRNA vaccination. [2100] Figure 1. Colonoscopy findings of diffuse edema and pallor of the (a) descending colon (b) sigmoid colon. (c) The infiltrating atypical cells in the lamina propria are strongly and diffusely positive for pancytokeratin confirming the diagnosis of metastatic mammary lobular carcinoma (103).

cannulated with a 15 mm. laparoscopic trochar. An ERCP endoscope is passed through the abdominal wall, through the trochar into the distal stomach. The ampulla is identified and cannulated. A sphincterotomy was performed and the biliary tree is cleared of stones. The endoscope is withdrawn and the gastric cannulation site is surgically closed. Discussion: Laparoscopic assisted ERCP following gastric bypass for morbid obesity is a safe and effective approach for choledocolithiasis. This approach does not sacrifice or disrupt the gastric bypass. This approach is needed. Watch the video at https://tinyurl.com/ACGAbstractS377

Case Description/Methods: A 78-year-old male with a past medical history of hypertension and gastritis presented to clinic for worsening gastroesophageal reflux disease (GERD) over the past six months. The patient reported GERD symptoms for the past twenty years that he had been self-treating with over-the-counter proton pump inhibitors, probiotics, and digestive enzymes without relief. On presentation his vitals, physical exam, and blood work were unremarkable. The patient underwent esophagoduodenoscopy (EGD) which revealed esophagitis, a large paraesophageal hernia, and a single 15-millimeter submucosal nodule in the anterior wall of the gastric body. Cold forceps biopsies obtained from the body and antrum of the stomach were unremarkable and negative for H. pylori. He was referred for endoscopic ultrasound (EUS), where a fine needle biopsy of the benign-appearing gastric body submucosal nodule was performed (figure 1a). Three passes were made with a 22-gauge ultrasound biopsy needle using a transgastric approach. A visible core of tissue was obtained. Final cytology demonstrated superficial gastric mucosa and detached benign liver tissue (figures 1b, 1c). No dysplasia or malignancy was seen. Discussion: ELT has an incidence of 0.24-0.47%. Of the reported cases, ELT is most commonly seen in the gallbladder or pancreas. The etiology of ELT is unknown but is thought to be associated with errors in embryological development. Most ELT is asymptomatic but can develop the same pathologies as the orthotopic liver. It can also cause abdominal pain, bleeding, and compression of neighboring tissues. There is also a strong association between HCC and ELT, necessitating biopsy and endoscopic removal. This case demonstrated ELT incidentally found in the gastric body during EGD and was biopsied by a fine needle using EUS guidance. Histology was without features to suggest malignancy, but to prevent malignant transformation endoscopic resection was recommended.[3716] Figure 1. 1a. Arrow indicating nodule in gastric body, as seen by endoscopic ultrasound. Image 1b. Hematoxylin and eosin stain with 100x magnification. Normal gastric glandular mucosa. Arrow indicating benign unremarkable hepatic tissue found in gastric body. Image 1c. Hematoxylin and eosin stain with 200x magnification. Benign unremarkable hepatic tissue found in gastric body.