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Median operative time was 192 minutes (95-250). Length of hospital stay was 2 days (2-6). Conclusions Robotic resection of gastric GIST's appears oncologically safe, and may expand the benefits of MIS to a greater cohort of complex cases.Atherosclerosis is characterized, as an inflammatory disorder in the circulatory system, with increasing tendency toward mortality and morbidity. Thus, developing novel therapeutic targeting inflammation is necessary. Here, we investigated the effects of interleukin-36 receptor antagonist (IL-36RN), a newly identified anti-inflammatory factor, on atherosclerosis. The regulation of NLRP3 inflammasome by IL-36RN was determined in vitro in macrophage cells after oxidized low-density lipoprotein (ox-LDL) stimulation. The IL-1β and caspase-1 p10 secretion were assessed by enzyme-linked immunosorbent assay and western blot analysis. Finally, the IL-36RN/NLRP3 inflammasome pathway was confirmed in apolipoprotein E-deficient mice. IL-36RN suppressed the expression of NLRP3, the secretion of IL-1β, and caspase-1 p10 in vitro, while IL-36 pathway stimulation activated the NLRP3 inflammasome, which was inhibited by IL-36RN. In the mouse model of atherosclerosis, IL-36RN delivered by the lentivirus vector inhibited the development of atherosclerosis, and the atheroprotective effects of IL-36RN were attenuated by IL-36 pathway stimulation. Furthermore, the regulation of NLRP3 inflammasome by IL-36RN was also confirmed in vivo. We demonstrated here that IL-36RN exerted atheroprotective functions through IL-36RN/NLRP3 inflammasome pathway.Electrical stimulation (ES) has been shown to improve some of impairments after spinal cord injury (SCI), but the underlying mechanisms remain unclear. The Wnt signaling pathways and the endocannabinoid system appear to be modulated in response to SCI. This study aimed to investigate the effect of ES therapy on the activity of canonical/noncanonical Wnt signaling pathways, brain-derived neurotrophic factor (BDNF), and fatty-acid amide hydrolase (FAAH), which regulate endocannabinoids levels. Forty male Wistar rats were randomly divided into four groups (a) Sham, (b) laminectomy + epidural subthreshold ES, (c) SCI, and (d) SCI + epidural subthreshold ES. A moderate contusion SCI was performed at the thoracic level (T10). Epidural subthreshold ES was delivered to upper the level of T10 segment every day (1 hr/rat) for 2 weeks. Then, animals were killed and immunoblotting was used to assess spinal cord parameters. Results revealed that ES intervention for 14 days could significantly increase wingless-type3 (Wnt3), Wnt7, β-catenin, Nestin, and cyclin D1 levels, as well as phosphorylation of glycogen synthase kinase 3β and Jun N-terminal kinase. Additionally, SCI reduced BDNF and FAAH levels, and ES increased BDNF and FAAH levels in the injury site. We propose that ES therapy may improve some of impairments after SCI through Wnt signaling pathways. Outcomes also suggest that BDNF and FAAH are important players in the beneficial impacts of ES therapy. However, the precise mechanism of BDNF, FAAH, and Wnt signaling pathways on SCI requires further investigation.While studies in humans suggest a role for psychosocial factors as well as biological and genetic processes in the development of eating disorders, the specific etiologic mechanisms remain largely unknown. In this virtual issue, we present a collection of 14 archived articles from the International Journal of Eating Disorders to highlight the utility of animal studies of eating disorders to advance our understanding of eating disorder etiology. Selected articles establish animal studies as valid tools to study disordered eating behavior, offer insight into potential neurobiological mechanisms, and highlight novel targets for future pharmacological treatments. Clinical implications of each article's findings are included to demonstrate the translational value of animal studies for the eating disorders field. We hope that the exciting concepts and findings in this issue inspire future animal studies of eating disorders.Penile cancer is an under-studied disease that occurs more commonly in developing countries and 30-50% of cases show high-risk human papillomavirus (HPV) infection. Therapeutic advances are slow, largely due to the absence of animal models for translational research. Here, we report the first mouse model for HPV-related penile cancer. Ten-week-old mice expressing all the HPV16 early genes under control of the cytokeratin 14 (Krt14) gene promoter and matched wild-type controls were exposed topically to dimethylbenz(o)anthracene (DMBA) or vehicle for 16 weeks. At 30 weeks of age mice were sacrificed for histological analysis. Expression of Ki67, cytokeratin 14 and of the HPV16 oncogenes E6 and E7 was confirmed using immunohistochemistry and quantitative PCR, respectively. HPV16-transgenic mice developed intraepithelial lesions including condylomas and penile intraepithelial neoplasia (PeIN). Lesions expressed cytokeratin 14 and the HPV16 oncogenes E6 and E7 and showed deregulated cell proliferation, demonstrated by Ki67-positive supra-basal cells. HPV16-transgenic mice exposed to DMBA showed increased penile intraepithelial neoplasia (PeIN) incidence and squamous cell carcinoma. Malignant lesions showed varied histological features closely resembling those of HPV-associated human penile cancers. Wild-type mice showed no malignant or pre-malignant lesions even when exposed to DMBA. These observations provide the first experimental evidence to support the etiological role of HPV16 in penile carcinogenesis. Importantly, this is the first mouse model to recapitulate key steps of HPV-related penile carcinogenesis and to reproduce morphological and molecular features of human penile cancer, providing a unique in vivo tool for studying its biology and advancing basic and translational research. This article is protected by copyright. All rights reserved.Introduction Covid-19 has ushered in drastic changes to the healthcare system in order to "flatten the curve"; in particular, surgical operations that can consume vital, limited resources, not to mention the risk to staff, anesthesiologists, and surgeons. However, under unique circumstances with diligent preparation, vital oncologic operations can be performed safely. Methods Prospective comparison of surgical cases during the pandemic from December 2019 to May 2020 to the correlating time frame from December 2018 to May 2019. Results A significant decline in case volume was not appreciated until the United States declared a national state of emergency, allowing patients with cancer to continue to undergo curative tumor resection until then (428.3 ± 51.5 vs 166.6 ± 59.8 cases/week; P less then .001). The decrease was consistent with the mean case volume during the holidays (213.8 ± 76.8 vs 166.6 ± 59.8 case/week; P = .648). C-176 cost Evaluation of surgical subspecialties demonstrated a significant decrease for all subspecialties with the greatest decline in sarcoma (P = .