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Sepsis, defined as a life-threatening organ dysfunction arising from a dysregulated host response to infection, often culminates in multiple organ dysfunction syndrome (MODS). The liver, central to metabolism, detoxification, and immune regulation, is particularly vulnerable in this context. Sepsis-induced liver injury (SILI), a frequent and severe complication, markedly worsens clinical outcomes. A growing body of evidence implicates mitochondrial dysfunction as a central pathogenic hub in SILI. During sepsis, mitochondria exhibit profound derangements, including morphological abnormalities, collapse of the membrane potential, respiratory chain failure, excessive reactive oxygen species (ROS) generation, altered dynamics, and defective mitophagy. Beyond intrinsic cellular injury, these dysfunctional organelles can amplify systemic inflammation by releasing damage-associated molecular patterns (DAMPs), which in turn activate innate immune pathways mediated by Toll-like receptors (TLRs), NOD-like receptors (NLRs), and the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) axis. This review provides an integrative overview of the current understanding of mitochondrial dysfunction in SILI. We critically evaluate preclinical advances in mitochondrial-targeted therapies and highlight emerging strategies that hold translational promise for mitigating hepatic injury and improving patient outcomes.

Uterine artery embolization (UAE)-assisted induction of labor is an alternative method of managing pregnant women with complete placenta previa (CPP). Sepsis secondary to UAE, although rare, is a serious complication. We herein present a case of severe sepsis following UAE-assisted termination of a pregnancy at 27 gestational weeks in a woman with CPP. The woman developed a high-grade fever and elevated inflammatory indices following UAE. She did not recover until the infected tissue was removed by emergency cesarean section. This case suggests that the increasing use of UAE for termination of pregnancy in women with CPP requires awareness regarding the possibility of serious sepsis associated with this procedure.

Reducing organic groups on hydrophobic silica aerogels (SA) is worth exploring for lowering their thermal hazard risk. In this work, we used dimethyldichlorosilane (DMDCS) to modify silica alcogels, investigated the effects of DMDCS concentration and focused on the thermal hazard assessment of the DMDCS modified SA (DSA). It was turned out that the DSA had less −CH 3 content in spite of the thermal stability close to the trimethylchlorosilane modified SA (TSA), about 240 °C. The kinetics study suggested the apparent activation energy ( E a ) could be divided into two segments, corresponding to the two processes in the pyrolysis. The positive enthalpy and entropy changes indicated that the thermal oxidation of the DSA was an exothermic reaction, which could not occur without external energy supply. The average E a of the DSA was far larger than that of the TSA and the gross calorific value of the DSA decreased by about 12% compared with that of the TSA. All these results drew a conclusion that the DMDCS modified SA reduced the thermal hazard to some degree, which provided one possible solution to further lower the thermal hazard of hydrophobic SA. Highlights Dimethyldichlorosilane modified silica aerogels (DSA) were prepared at the optimum concentration of 4%. Kinetic and thermodynamic behavior of DSA were studied in detail. DSA has larger apparent activation energy than trimethylchlorosilane modified silica aerogels (TSA). DSA has lower thermal hazard than TSA for a less gross calorific value.

Akkermansia muciniphila is a Gram-negative bacterium that resides within the gut mucus layer, and plays an important role in promoting gut barrier integrity, modulating the immune response and inhibiting gut inflammation. Growth stimulation of A . muciniphila by polyphenols including epigallocatechin-3-gallate (EGCG) from difference sources is well-documented. However, no published in vitro culture data on utilization of polyphenols by A . muciniphila are available, and the mechanism of growth-stimulating prebiotic effect of polyphenols on it remains unclear. Here in vitro culture studies have been carried out on the metabolism of EGCG by A . muciniphila in the presence of either mucin or glucose. We found that A . muciniphila did not metabolize EGCG alone but could co-metabolize it together with both these substrates in the presence of mineral salts and amino acids for mucin and protein sources for glucose. Our metabolomic data show that A . muciniphila converts EGCG to gallic acid, epigallocatechin, and (-)-epicatechin through ester hydrolysis. The (-)-epicatechin formed is then further converted to hydroxyhydroquinone. Co-metabolism of A . muciniphila of EGCG together with either mucin or glucose promoted substantially its growth, which serves as a further demonstration of the growth-promoting effect of polyphenols on A . muciniphila and provides an important addition to the currently available proposed mechanisms of polyphenolic prebiotic effects on A . muciniphila .

The human endometrium is a highly regenerative tissue capable of undergoing scarless repair during the menstruation and postpartum phases. This process is mediated by endometrial adult stem/progenitor cells. During the healing of endometrial injuries, swift reepithelization results in the rapid covering of the wound surface and facilitates subsequent endometrial restoration. The involvement of endogenous endometrial epithelial stem cells, stromal cells, and bone marrow-derived cells in the regeneration of the endometrial epithelium has been a subject of prolonged debate. Increasing evidence suggests that the regeneration of the endometrial epithelium mainly relies on epithelial stem cells rather than stromal cells and bone marrow-derived cells. Currently, no consensus has been established on the identity of epithelial stem cells in the epithelial compartment. Several markers, including stage-specific embryonic antigen-1 (SSEA-1), sex-determining region Y-box 9 (SOX9), neural-cadherin (N-cadherin), leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5), CD44, axis inhibition protein 2 (Axin2), and aldehyde dehydrogenase 1A1 (ALDH1A1), have been suggested as potential candidate markers for endometrial epithelial stem cells. The identification of endometrial epithelial stem cells contributes to our understanding of endometrial regeneration and offers new therapeutic insights into diseases characterized by regenerative defects in the endometrium, such as intrauterine adhesion. This review explores different perspectives on the origins of human and mouse endometrial epithelial cells. It summarizes the potential markers, locations, and hierarchies of epithelial stem cells in both human and mouse endometrium. It also discusses epithelial cell-based treatments for intrauterine adhesion, hoping to inspire further research and clinical application of endometrial epithelial stem cells. Graphical abstract

The application of chemodynamic therapy (CDT) for cancer is a serious challenge owing to the low efficiency of the Fenton catalyst and insufficient H 2 O 2 expression in cells. Herein, we fabricated a PDGFB targeting, biodegradable FePt alloy assembly for magnetic resonance imaging (MRI)-guided chemotherapy and starving-enhanced chemodynamic therapy for cancer using PDGFB targeting, pH-sensitive liposome-coated FePt alloys, and GOx (pLFePt-GOx). We found that the Fenton-catalytic activity of FePt alloys was far stronger than that of traditional ultrasmall iron oxide nanoparticle (UION). Upon entry into cancer cells, pLFePt-GOx nanoliposomes degraded into many tiny FePt alloys and released GOx owing to the weakly acidic nature of the tumor microenvironment (TME). The released GOx-mediated glucose consumption not only caused a starvation status but also increased the level of cellular H 2 O 2 and acidity, promoting Fenton reaction by FePt alloys and resulting in an increase in reactive oxygen species (ROS) accumulation in cells, which ultimately realized starving-enhanced chemodynamic process for killing tumor cells. The anticancer mechanism of pLFePt-GOx involved ROS-mediated apoptosis and ferroptosis, and glucose depletion-mediated starvation death. In the in vivo assay, the systemic delivery of pLFePt-GOx showed excellent antitumor activity with low biological toxicity and significantly enhanced T 2 -weighted magnetic resonance imaging (MRI) signal of the tumor, indicating that pLFePt-GOx can serve as a highly efficient theranostic tool for cancer. This work thus describes an effective, novel multi-modal cancer theranostic system.

Objective This study was performed to assess whether prophylactic uterine artery embolization (UAE) is beneficial for second-trimester abortion with complete placenta previa (CPP). Methods Patients with CPP who underwent second-trimester pregnancy termination by labor induction with or without UAE from January 2010 to January 2018 were retrospectively reviewed. In total, 25 patients were eligible for analysis. The primary outcomes were the abortion success rate and bleeding volume, and the secondary outcomes were the induction-to-abortion time, length of hospital stay, and complications. Results CPP occurred in all 25 patients. Fifteen patients underwent prophylactic UAE (UAE group) and 10 did not (control group). Abortion was successful in 13 of 15 (86.7%) women in the UAE group and in 9 of 10 (90.0%) women in the control group. There was no significant difference in the bleeding volume or induction-to-abortion time between the two groups. The hospital stay was longer and pyrexia was more common in the UAE than control group. Conclusion Prophylactic UAE did not markedly improve the outcomes of second-trimester abortion in patients with CPP. Conversely, it may increase the risk of complications and prolong the hospital stay.

Background A ureterocele is a cystic dilatation of the terminal ureter that can be located entirely within the bladder or extend into the urethra. In rare cases, female patients may present with a vaginal mass due to prolapse of an ectopic ureterocele and experience urinary incontinence due to laxity of the external urinary sphincter. Case presentation A 37-year-old female presented with a one-year history of recurrent urinary symptoms, including frequent urination, urgency, and dysuria. Over the past two months, she noticed a prolapsed vulvar mass accompanied by urinary incontinence. Three weeks prior to admission, she underwent tension-free vaginal tape–obturator (TVT-O) surgery at another hospital for presumed stress urinary incontinence (SUI). Three days ago, the vulvar mass increased to the size of an egg and could not be manually reduced, accompanied by straining during voiding. Ultrasound and MRI revealed bilateral ureteroceles, with the left ureterocele prolapsed from the bladder to the urethral opening. A diagnosis of ureterocele prolapse with incarceration was made, and the patient underwent manual reduction followed by cystoscopic resection of the left ureterocele. Two days postoperatively, she developed acute pyelonephritis, which was successfully treated with antibiotics. Discussion and Conclusions Prolapsed ureteroceles are a rare condition, and their symptoms can mimic those of SUI, which is typically treated with midurethral sling procedures. However, this treatment approach may inadvertently result in an incarcerated prolapsed ureterocele, requiring urgent medical intervention. This case emphasizes the critical importance of accurate diagnosis of ureteroceles to avoid inappropriate application of midurethral slings and highlights the need for vigilance regarding the potential development of acute pyelonephritis following ureterocele resection.

Analyzing the tail quantiles of a response distribution is sometimes more important than analyzing the mean in biomarker studies. Inferences in a quantile regression are complicated when there exist a large number of candidate markers, together with some prespecified controlled covariates. In this study, we develop a new and simple testing procedure to detect the effects of biomarkers in a high-dimensional quantile regression in the presence of protected covariates. The test is based on the maximum-score-type statistic obtained from a conditional marginal regression. We establish the asymptotic properties of the proposed test statistic under both null and alternative hypotheses and propose an alternative multiplier bootstrap method, with theoretical justifications. We use numerical studies to show that the proposed method provides adequate controls of the family-wise error rate with competitive power, and that it can also be used as a stopping rule in a forward regression. The proposed method is applied to a motivating genome-wide association study to detect single nucleotide polymorphisms associated with low glomerular filtration rates in type 1 diabetes patients.

Lipids are high energy, complex biomolecular compounds essential for cellular and organellar membrane formation. Accumulation of circulatory lipids is however associated with pathophysiological conditions including cardiometabolic disorders, diabetic dyslipidemia and obesity. Epidemiological studies have correlated heavy-metal exposure with dyslipidemias and metabolic syndrome. Here, we review the role of cadmium, lead, mercury and arsenic on inducing dyslipidemias through lipid metabolism dysregulation, with focus on metal effects on lipogenic genes, gut microbiome and endocrine secretion. The main gene transcription factors impaired by heavy metals are CCAAT-enhancer binding protein, peroxisome proliferative-activated receptor, sterol regulatory element binding protein, carbohydrate responsive element binding protein and liver × receptor. These factors regulate genes responsible for β-oxidation, de novo lipogenesis, and the synthesis and transport of fatty acids, cholesterol, phospholipids and triglycerides. Dysregulated lipid profiles in organisms exposed to metals show higher cholesterol and triglycerides, very low-density lipoprotein and non-high density lipoprotein cholesterol levels, with a corresponding low high-density lipoprotein cholesterol. Hormones and gut microbiome are also impaired by heavy-metal exposure.