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Abstract Background An intravesical gas explosion is a rare complication of transurethral resection of the prostate (TURP). It was first reported in English literature in 1926, and up to 2022 were only forty-one cases. Injury from an intravesical gas explosion, in the most severe cases appearing as extraperitoneal or intraperitoneal bladder rupture needed emergent repair surgery. Case presentation We present a case of a 75-year-old man who suffered an intravesical gas explosion during TURP. The patient underwent an emergent exploratory laparotomy for bladder repair and was transferred to the intensive care unit for further observation and treatment. Under the medical team’s care for up to sixty days, the patient recovered smoothly without clinical sequelae. Conclusions This case report presents an example of a rare complication of intravesical gas explosion during TURP, utilizing root cause analysis (RCA) to comprehend causal relationships and team strategies and tools to improve performance and patient safety (TeamSTEPPS) method delivers four teamwork skills that can be utilized during surgery and five recommendations to avoid gas explosions during TURP to prevent the recurrence of medical errors. In modern healthcare systems, promoting patient safety is crucial. Once complications appear, RCA and TeamSTEPPS are helpful means to support the healthcare team reflect and improve as a team.

From the perspective of sustainable development and based on literature review, this paper introduces modified Delphi and Decision Making and Trial Evaluation Laboratory (DEMATEL) to explore the critical factors of sustainable development in rural areas and their correlation. Through literature review and modified Delphi analysis, nine key factors of rural sustainable development are first identified, namely industrial activation, working environment, living conditions, infrastructure, public involvement, rural culture, government-related departments, educational resources, and health and welfare. DEMATEL is then adopted to determine the classification of the aforementioned factors, in which four (government-related departments, public involvement, infrastructure, and educational resources) are classified in the cause group and five (health and welfare, living conditions, rural culture, working environment, and industrial activation) are classified in the effect group. According to the centrality and relation of these factors, the causal network diagram is finally drawn before making practical suggestions based on the overall results, with a view to providing a reference for decision-makers in their follow-up rural sustainable development planning.

Thiazolidinediones (TZDs) are PPAR[gamma] agonists with potent insulin-sensitizing effects. However, their use has been curtailed by substantial adverse effects on weight, bone, heart, and hemodynamic balance. TZDs induce the deacetylation of PPAR[gamma] on K268 and K293 to cause the browning of white adipocytes. Here, we show that targeted PPAR[gamma] mutations resulting in constitutive deacetylation (K268R/K293R, 2KR) increased energy expenditure and protected from visceral adiposity and diet-induced obesity by augmenting brown remodeling of white adipose tissues. Strikingly, when 2KR mice were treated with rosiglitazone, they maintained the insulin-sensitizing, glucose-lowering response to TZDs, while displaying little, if any, adverse effects on fat deposition, bone density, fluid retention, and cardiac hypertrophy. Thus, deacetylation appears to fulfill the goal of dissociating the metabolic benefits of PPAR[gamma] activation from its adverse effects. Strategies to leverage PPAR[gamma] deacetylation may lead to the design of safer, more effective agonists of this nuclear receptor in the treatment of metabolic diseases., Introduction The prevalence of metabolic diseases imparts a sense of urgency to research aimed at discovering novel therapeutics for conditions ranging from obesity to diabetes (1). A positive energy balance [...]

Author(s): Omid Tavana [1, 2]; Dawei Li [1, 2]; Chao Dai [1, 2]; Gonzalo Lopez [1, 2, 3, 4]; Debarshi Banerjee [2, 5]; Ning Kon [1, 2]; Chao Chen [6, [...]

Although p53-mediated cell-cycle arrest, senescence and apoptosis serve as critical barriers to cancer development, emerging evidence suggests that the metabolic activities of p53 are also important. Here we show that p53 inhibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repressing expression of SLC7A11, a key component of the cystine/glutamate antiporter. Notably, [p53.sup.3KR], an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced stress. Analysis of mutant mice shows that these non-canonical p53 activities contribute to embryonic development and the lethality associated with loss of Mdm2. Moreover, SLC7A11 is highly expressed in human tumours, and its overexpression inhibits ROS-induced ferroptosis and abrogates [p53.sup.3KR]-mediated tumour growth suppression in xenograft models. Our findings uncover a new mode of tumour suppression based on p53 regulation of cystine metabolism, ROS responses and ferroptosis., Inactivation of the p53 tumour suppression pathway is a pivotal event in the formation of most human cancers (1-5). Traditionally, the tumour suppression activity of p53 was thought to reflect [...]

Author(s): Donglai Wang [1]; Ning Kon [1]; Gorka Lasso [2]; Le Jiang [1]; Wenchuan Leng [3]; Wei-Guo Zhu [4]; Jun Qin [3, 5]; Barry Honig [2]; Wei Gu (corresponding author) [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.03.037 Byline: Delin Chen (1), Ning Kon (1), Muyang Li (1), Wenzhu Zhang (1), Jun Qin (2), Wei Gu Abstract: Although the importance of the ARF tumor suppressor in p53 regulation is well established, numerous studies indicate that ARF also suppresses cell growth in a p53/Mdm2-independent manner. To understand the mechanism of ARF-mediated tumor suppression, we identified a ubiquitin ligase, ARF-BP1, as a key factor associated with ARF in vivo. ARF-BP1 harbors a signature HECT motif, and its ubiquitin ligase activity is inhibited by ARF. Notably, inactivation of ARF-BP1, but not Mdm2, suppresses the growth of p53 null cells in a manner reminiscent of ARF induction. Surprisingly, in p53 wild-type cells, ARF-BP1 directly binds and ubiquitinates p53, and inactivation of endogenous ARF-BP1 is crucial for ARF-mediated p53 stabilization. Thus, our study modifies the current view of ARF-mediated p53 activation and reveals that ARF-BP1 is a critical mediator of both the p53-independent and p53-dependent tumor suppressor functions of ARF. As such, ARF-BP1 may serve as a potential target for therapeutic intervention in tumors regardless of p53 status. Author Affiliation: (1) Institute for Cancer Genetics, Department of Pathology, College of Physicians and Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, New York 10032 (2) Departments of Biochemistry and Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030 Article History: Received 13 September 2004; Revised 24 February 2005; Accepted 30 March 2005 Article Note: (miscellaneous) Published: June 30, 2005

Homologous recombination hotspots increase the frequency of recombination in nearby DNA. The M26 hotspot in the ade6 gene of Schizosaccharomyces pombe is a meiotic hotspot with a discrete, cis-acting nucleotide sequence (5[prime]-ATGACGT-3[prime]) defined by extensive mutagenesis. A heterodimeric M26 DNA binding protein, composed of subunits Mts1 and Mts2, has been identified and purified 40,000-fold. Cloning, disruption, and genetic analyses of the mts genes demonstrate that the Mts1/Mts2 heterodimer is essential for hotspot activity. This provides direct evidence that a specific trans-acting factor, binding to a els-acting site with a unique nucleotide sequence, is required to activate this meiotic hotspot. Intriguingly, the Mts1/Mts2 protein subunits are identical to the recently described transcription factors Atf1 (Gad7) and Pcr1, which are required for a variety of stress responses. However, we report differential dependence on the Mts proteins for hotspot activation and stress response, suggesting that these proteins are multifunctional and have distinct activities. Furthermore, ade6 mRNA levels are equivalent in hotspot and nonhotspot meioses and do not change in mrs mutants, indicating that hotspot activation is not a consequence of elevated transcription levels. These findings suggest an intimate but separable link between the regulation of transcription and meiotic recombination. Other studies have recently shown that the Mts1/Mts2 protein and M26 sites are involved in meiotic recombination elsewhere in the S. pombe genome, suggesting that these factors help regulate the timing and distribution of homologous recombination.

Hypothalamic neurons expressing agouti-related peptide (AgRP) regulate eating and glucose metabolism. Ablation of FOXO1 in AgRP neurons of mice results in reduced food intake, leanness, improved glucose homeostasis, and increased sensitivity to insulin and leptin. We tentatively identified G-protein-coupled receptor Gpr17 as an effector of FOXO1 orexigenic signals in AgRP neurons. In this study, we generated and characterized AgRP neuron-specific Gpr17 knockout mice (Agrp-Gpr17(-/-)) to test the hypothesis that Gpr17 regulates appetite, energy expenditure, and metabolism. Agrp-Gpr17(-/-) mice show reduced food intake, increased relative energy expenditure, and increased satiety, resulting in leanness and reduced body fat. They also show increased central nervous system sensitivity to insulin and leptin and reduced plasma glucose excursions following the administration of glucose or pyruvate. In summary, AgRP neuron-specific Gpr17 knockouts phenocopy FOXO1 knockouts in the same cell type, thus supporting our original hypothesis and providing further impetus to develop Gpr17 antagonists for the treatment of obesity. [ABSTRACT FROM AUTHOR]