Applying Deep-Learning Algorithm Interpreting Kidney, Ureter, and Bladder (KUB) X-Rays to Detect Colon Cancer.

Early screening is crucial in reducing the mortality of colorectal cancer (CRC). Current screening methods, including fecal occult blood tests (FOBT) and colonoscopy, are primarily limited by low patient compliance and the invasive nature of the procedures. Several advanced imaging techniques such as computed tomography (CT) and histological imaging have been integrated with artificial intelligence (AI) to enhance the detection of CRC. There are still limitations because of the challenges associated with image acquisition and the cost. Kidney, ureter, and bladder (KUB) radiograph which is inexpensive and widely used for abdominal assessments in emergency settings and shows potential for detecting CRC when enhanced using advanced techniques. This study aimed to develop a deep learning model (DLM) to detect CRC using KUB radiographs. This retrospective study was conducted using data from the Tri-Service General Hospital (TSGH) between January 2011 and December 2020, including patients with at least one KUB radiograph. Patients were divided into development (n = 28,055), tuning (n = 11,234), and internal validation (n = 16,875) sets. An additional 15,876 patients were collected from a community hospital as the external validation set. A 121-layer DenseNet convolutional network was trained to classify KUB images for CRC detection. The model performance was evaluated using receiver operating characteristic curves, with sensitivity, specificity, and area under the curve (AUC) as metrics. The AUC, sensitivity, and specificity of the DLM in the internal and external validation sets achieved 0.738, 61.3%, and 74.4%, as well as 0.656, 47.7%, and 72.9%, respectively. The model performed better for high-grade CRC, with AUCs of 0.744 and 0.674 in the internal and external sets, respectively. Stratified analysis showed superior performance in females aged 55-64 with high-grade cancers. AI-positive predictions were associated with a higher long-term risk of all-cause mortality in both validation cohorts. AI-enhanced KUB X-ray analysis can enhance CRC screening coverage and effectiveness, providing a cost-effective alternative to traditional methods. Further prospective studies are necessary to validate these findings and fully integrate this technology into clinical practice.

Animal neuropathic pain aroused by conglutinating oxidative regenerative cellulose on dorsal root ganglion.

Neuropathic pain arises as a consequence of injury or disease in the peripheral or central nervous system. Clinical cases have shown that spine postoperative chronic neuropathic pain remains a troublesome issue in medical treatment due to the presence of various degrees of peridural fibrosis and different inflammatory factors after spinal surgery. To address this issue, we developed a new neuropathic mice model that successfully simulates the real clinical situation by applying oxidative regenerative cellulose to L5 DRG (dorsal root ganglion). Behavior tests were done by von Fray and thermal stimuli. ELISA and real-time PCR were employed to detect the expression of genes involved in neuropathic pain. This model not only successfully induces chronic pain but also causes membrane thickening, non-neuronal cell recruitment, and a local increase of TNFα and interleukin-6. Additionally, this model did not cause neuron loss in the affected DRG, which mimics the characteristics of sticky tissue-induced neuropathic pain after clinic surgery. Based on this model, we administrated a TNF inhibitor to mice and successfully reduced mechanical allodynia after DRG surgery. In this study, the developed animal model may be a novel platform for delivering neuropathic pain treatments, such as target-based drug discovery or personalized diagnostic approaches.

Exploring the causal links between cigarette smoking, alcohol consumption, and aneurysmal subarachnoid hemorrhage: a two-sample Mendelian randomization analysis.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) represents a critical health concern characterized by elevated mortality and morbidity rates. Although both genetic predisposition and lifestyle choices influence aSAH susceptibility, understanding the causative associations between cigarette smoking, alcohol consumption, and aSAH risk remains imperative. Mendelian randomization (MR) offers a robust methodological framework for dissecting these associations, leveraging genetic variants as instrumental variables. Objective: In this study, a two-sample Mendelian randomization (TSMR) approach was employed to elucidate the causal connections between genetically determined cigarette smoking, alcohol consumption, and aSAH risk. Methods: Genetic instruments associated with cigarette smoking and alcohol consumption were sourced from the genome-wide association study (GWAS) and Sequencing Consortium of Alcohol and Nicotine use (GSCAN). Using a genome-wide association study (GWAS) dataset that encompassed aSAH cases and controls of European ancestry, TSMR, which utilized the inverse variance weighting (IVW) method, was employed to estimate the causal effects. Rigorous criteria were applied for selecting instrumental variables to ensure a robust Mendelian randomization analysis. Results: A significant causal association was found between genetically determined cigarette smoking and an increased risk of aSAH, with a 1-standard deviation (SD) increase in cigarette use genetically linked to a 96% relative risk elevation [OR-IVW = 1.96, 95% confidence interval (CI) = 1.28-3.01, p = 0.0021]. However, genetically determined alcohol consumption did not exhibit a statistically significant association with aSAH risk (OR-IVW = 1.22, 95% CI = 0.61-2.45, p = 0.578). Conclusion: The Mendelian randomization analysis revealed a causal nexus between cigarette smoking and an increased risk of aSAH, advocating for targeted smoking cessation interventions within genetically predisposed cohorts. The results regarding the relationship between alcohol consumption and aSAH were affected by insufficient statistical power. A prudent interpretation of the findings highlights the limitations of Mendelian randomization in elucidating intricate genetic epidemiological relationships. Ongoing research involving larger cohort sizes and advanced methodological approaches is essential for comprehending the genetic underpinnings of aSAH.

Laparoscopic surgery: An effective alternative for managing severe blunt splenic injuries in patients who are ineligible for transcatheter arterial embolization.

BACKGROUND: Transcatheter arterial embolization (TAE) is an effective alternative to nonoperative management (NOM) to improve the spleen salvage rate for patients with blunt splenic injuries (BSIs), but it is not always available at some institutions. Moreover, laparoscopy has also been used to diagnose and treat trauma, including BSIs. METHODS: We present our 11-year experience in performing laparoscopic surgery for spleen salvage in patients with severe BSIs when TAE is infeasible. The outcomes of laparoscopic surgery or TAE for spleen salvage in hemodynamically stable patients with severe BSIs were compared. RESULTS: Fifty-six patients underwent interventions for severe BSIs during this period. Twenty patients underwent laparoscopic surgery, and 36 underwent TAE. There were no significant differences in demographics, preoperative conditions, or clinical characteristics (all p > 0.05). In the laparoscopic surgery group, 15 patients (75 %) underwent laparoscopic splenorrhaphy for spleen salvage surgery, and five (25 %) required splenectomy. No complications requiring intervention were observed in the laparoscopic surgery group, whereas three patients in the TAE group required a late splenectomy for splenic abscess. No significant differences were detected in the splenic preservation rate, complication rate, or length of hospital stay between the groups (all p > 0.05). CONCLUSION: Laparoscopy is feasible and safe for managing hemodynamically stable patients with severe BSIs, and the outcomes are comparable to those of TAE. When TAE is infeasible, laparoscopy can be considered an alternative to increase the spleen salvage rate.

miR-151a-3p regulates the TNIK/PI3K/Akt axis and influences the progression of polycystic ovary syndrome.

OBJECTIVES: Polycystic ovarian syndrome (PCOS) is a common reproductive endocrine disease in women of childbearing age, and the incidence of PCOS has increased in recent years. However, the pathogenesis of this disease has not been fully elucidated. METHODS: The expression of miR-151a-3p in ovarian granulosa cells (KGN) was determined using real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8), colony formation and flow cytometric assays were used to investigate the effect of miR-151a-3p on KGN cells. Luciferase reporter analysis and western blotting were used to verify the targeting of miR-151a-3p by Traf and Nck interacting kinase (TNIK). Western blotting (WB) was used to evaluate the protein levels. RESULTS: We found that miR-151a-3p was downregulated and TNIK was upregulated in the serum of PCOS patients. Low expression of miR-151a-3p promoted cell proliferation, colony formation and the G0/G1 transition and reduced apoptosis. Our results showed that low expression of miR-151a-3p promoted the expression of TNIK, which activated the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway. Overexpression of TNIK rescued the effect of miR-151a-3p in ovarian granulosa cells. Finally, our results showed that there was a significant correlation between the expression of miR-151a-3p and the expression of the target TNIK in PCOS patients and that miR-151a-3p promoted disease occurrence by activating the PI3K/AKT signaling pathway. CONCLUSIONS: Low expression of miR-151a-3p promoted KNG cell proliferation by activating the TNIK-mediated PI3K/AKT signaling pathway. The miR-151a-3p/TNIK/PI3K/AKT signaling axis may be a potential therapeutic target for preventing the progression of PCOS.

Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance.

Immune tolerance mechanisms are shared in cancer and pregnancy. Through cross-analyzing single-cell RNA-sequencing data from multiple human cancer types and the maternal-fetal interface, we found B7-H4 (VTCN1) is an onco-fetal immune tolerance checkpoint. We showed that genetic deficiency of B7-H4 resulted in immune activation and fetal resorption in allogeneic pregnancy models. Analogously, B7-H4 contributed to MPA/DMBA-induced breast cancer progression, accompanied by CD8+ T cell exhaustion. Female hormone screening revealed that progesterone stimulated B7-H4 expression in placental and breast cancer cells. Mechanistically, progesterone receptor (PR) bound to a newly identified -58 kb enhancer, thereby mediating B7-H4 transcription via the PR-P300-BRD4 axis. PR antagonist or BRD4 degrader potentiated immunotherapy in a murine B7-H4+ breast cancer model. Thus, our work unravels a mechanistic and biological connection of a female sex hormone (progesterone) to onco-fetal immune tolerance via B7-H4 and suggests that the PR-P300-BRD4 axis is targetable for treating B7-H4+ cancer.

PIKfyve, expressed by CD11c-positive cells, controls tumor immunity.

Cancer treatment continues to shift from utilizing traditional therapies to targeted ones, such as protein kinase inhibitors and immunotherapy. Mobilizing dendritic cells (DC) and other myeloid cells with antigen presenting and cancer cell killing capacities is an attractive but not fully exploited approach. Here, we show that PIKFYVE is a shared gene target of clinically relevant protein kinase inhibitors and high expression of this gene in DCs is associated with poor patient response to immune checkpoint blockade (ICB) therapy. Genetic and pharmacological studies demonstrate that PIKfyve ablation enhances the function of CD11c+ cells (predominantly dendritic cells) via selectively altering the non-canonical NF-κB pathway. Both loss of Pikfyve in CD11c+ cells and treatment with apilimod, a potent and specific PIKfyve inhibitor, restrained tumor growth, enhanced DC-dependent T cell immunity, and potentiated ICB efficacy in tumor-bearing mouse models. Furthermore, the combination of a vaccine adjuvant and apilimod reduced tumor progression in vivo. Thus, PIKfyve negatively regulates the function of CD11c+ cells, and PIKfyve inhibition has promise for cancer immunotherapy and vaccine treatment strategies.

Revisiting the association between vitamin D deficiency and active tuberculosis: A prospective case-control study in Taiwan.

BACKGROUND: To revisit the association between vitamin D deficiency (VDD, defined as serum 25(OH)D < 20 ng/ml) and incident active tuberculosis (TB), after two potentially underpowered randomized trials showed statistically non-significant 13%-22% decrease in TB incidence in vitamin D supplementation groups. METHODS: We prospectively conducted an age/sex-matched case-control study that accounting for body-mass index (BMI), smoking, and other confounding factors to examine the association between VDD and active TB among non-HIV people in Taiwan (latitude 24°N), a high-income society which continues to have moderate TB burden. RESULTS: We enrolled 62 people with incident active TB and 248 people in control group. The TB case patients had a significantly higher proportion of VDD compared to the control group (51.6% vs 29.8%, p = 0.001). The 25(OH)D level was also significantly lower in TB patients compared to control group (21.25 ± 8.93 ng/ml vs 24.45 ± 8.36 ng/ml, p = 0.008). In multivariable analysis, VDD (adjusted odds ratio [aOR]: 3.03, p = 0.002), lower BMI (aOR: 0.81, p < 0.001), liver cirrhosis (aOR: 8.99, p = 0.042), and smoking (aOR: 4.52, p = 0.001) were independent risk factors for incident active TB. CONCLUSIONS: VDD is an independent risk factor for incident active TB. Future randomized trials examining the effect of vitamin D supplementation on TB incidence should focus on people with a low BMI or other risk factors to maximize the statistical power.

PAD4 controls tumor immunity via restraining the MHC class II machinery in macrophages.

Tumor-associated macrophages (TAMs) shape tumor immunity and therapeutic efficacy. However, it is poorly understood whether and how post-translational modifications (PTMs) intrinsically affect the phenotype and function of TAMs. Here, we reveal that peptidylarginine deiminase 4 (PAD4) exhibits the highest expression among common PTM enzymes in TAMs and negatively correlates with the clinical response to immune checkpoint blockade. Genetic and pharmacological inhibition of PAD4 in macrophages prevents tumor progression in tumor-bearing mouse models, accompanied by an increase in macrophage major histocompatibility complex (MHC) class II expression and T cell effector function. Mechanistically, PAD4 citrullinates STAT1 at arginine 121, thereby promoting the interaction between STAT1 and protein inhibitor of activated STAT1 (PIAS1), and the loss of PAD4 abolishes this interaction, ablating the inhibitory role of PIAS1 in the expression of MHC class II machinery in macrophages and enhancing T cell activation. Thus, the PAD4-STAT1-PIAS1 axis is an immune restriction mechanism in macrophages and may serve as a cancer immunotherapy target.

PIKfyve controls dendritic cell function and tumor immunity.

The modern armamentarium for cancer treatment includes immunotherapy and targeted therapy, such as protein kinase inhibitors. However, the mechanisms that allow cancer-targeting drugs to effectively mobilize dendritic cells (DCs) and affect immunotherapy are poorly understood. Here, we report that among shared gene targets of clinically relevant protein kinase inhibitors, high PIKFYVE expression was least predictive of complete response in patients who received immune checkpoint blockade (ICB). In immune cells, high PIKFYVE expression in DCs was associated with worse response to ICB. Genetic and pharmacological studies demonstrated that PIKfyve ablation enhanced DC function via selectively altering the alternate/non-canonical NF-κB pathway. Both loss of Pikfyve in DCs and treatment with apilimod, a potent and specific PIKfyve inhibitor, restrained tumor growth, enhanced DC-dependent T cell immunity, and potentiated ICB efficacy in tumor-bearing mouse models. Furthermore, the combination of a vaccine adjuvant and apilimod reduced tumor progression in vivo. Thus, PIKfyve negatively controls DCs, and PIKfyve inhibition has promise for cancer immunotherapy and vaccine treatment strategies.

Cellulose nanofibers embedded chitosan/tannin hydrogel with high antibacterial activity and hemostatic ability for drug-resistant bacterial infected wound healing.

Millions of patients annually suffer life-threatening illnesses caused by bacterial infections of skin wounds. However, the treatment of wounds infected with bacteria is a thorny issue in clinical medicine, especially with drug-resistant bacteria infections. Therefore, there is an increasing interest in developing wound dressings that can efficiently fight against drug-resistant bacterial infections and promote wound healing. In this work, an anti-drug-resistant bacterial chitosan/cellulose nanofiber/tannic acid (CS/CNF/TA) hydrogel with excellent wound management ability was developed by electrospinning and fiber breakage-recombination. The hydrogel exhibited an outstanding antibacterial property exceeding 99.9 %, even for drug-resistant bacteria. This hydrogel could adhere to the tissue surface due to its abundant catechol groups, which avoided the shedding of hydrogel during the movement. Besides, it exhibited extraordinary hemostatic ability during the bleeding phase of the wound and then regulated the wound microenvironment by absorbing water and moisturizing. Moreover, the CS/CNF/TA also promoted the regrowth of vessels and follicles, accelerating the healing of infected wound tissue, with a healing rate exceeding 95 % within a 14-day timeframe. Therefore, the CS/CNF/TA hydrogel opens a new approach for the healing of drug-resistant bacterial infected wounds.

MSCs overexpressing GDNF restores brain structure and neurological function in rats with intracerebral hemorrhage.

Mesenchymal stem cells (MSCs) have been applied in transplantation to treat intracerebral hemorrhage (ICH) but with limited efficacy. Accumulated evidence has shown that glial cell-derived neurotrophic factor (GDNF) plays a crucial part in neuronal protection and functional recovery of the brain after ICH; however, GDNF has difficulty crossing the blood-brain barrier, which limits its application. In this study, we investigated the influences of MSCs overexpressing GDNF (MSCs/GDNF) on the brain structure as well as gait of rats after ICH and explored the possible mechanisms. We found that cell transplantation could reverse the neurological dysfunction and brain damage caused by ICH to a certain extent, and MSCs/GDNF transplantation was superior to MSCs transplantation. Moreover, Transplantation of MSCs overexpressing GDNF effectively reduced the volume of bleeding foci and increased the level of glucose uptake in rats with ICH, which could be related to improving mitochondrial quality. Furthermore, GDNF produced by transplanted MSCs/GDNF further inhibited neuroinflammation, improved mitochondrial quality and function, promoted angiogenesis and the survival of neurons and oligodendrocytes, and enhanced synaptic plasticity in ICH rats when compared with simple MSC transplantation. Overall, our data indicate that GDNF overexpression heightens the curative effect of MSC implantation in treating rats following ICH.

Role of laparoscopy in management of patients with anterior abdominal stab wounds.

BACKGROUND: In this retrospective cohort study, we assessed the utility of laparoscopic surgery for diagnostic and therapeutic purposes in patients with anterior abdominal stab wounds (AASWs). We also investigated patient characteristics that might suggest a greater suitability of laparoscopic interventions. METHODS: Over a 25-year span, we analyzed AASW patients who had operations, categorizing them based on the presence of significant intra-abdominal injuries and whether they received laparoscopic surgery or laparotomy. We compared variables such as preoperative conditions, surgical details, and postoperative outcomes. We further evaluated the criteria indicating the necessity of direct laparotomies and traits linked to overlooked injuries in laparoscopic surgeries. RESULTS: Of 142 AASWs surgical patients, laparoscopic surgery was conducted on 89 (62.7%) patients. Only 2 (2.2%) had overlooked injuries after the procedure. Among patients without significant injuries, those receiving laparoscopic surgery had less blood loss than those receiving laparotomy (30.0 vs. 150.0 ml, p = 0.004). Patients who underwent laparoscopic surgery also had shorter hospital stays (significant injuries: 6.0 vs. 11.0 days, p < 0.001; no significant injuries: 5.0 vs. 6.5 days, p = 0.014). Surgical complications and overlooked injury rates were comparable between both surgical methods. Bowel evisceration correlated with higher laparotomy odds (odds ratio = 16.224, p < 0.001), while omental evisceration did not (p = 0.107). CONCLUSIONS: Laparoscopy is a safe and effective method for patients with AASWs, fulfilling both diagnostic and therapeutic needs. For stable AASW patients, laparoscopy could be the preferred method, reducing superfluous nontherapeutic laparotomies.

Allyl Isothiocyanate Suppresses the Proliferation in Oral Squamous Cell Carcinoma via Mediating the KDM8/CCNA1 Axis.

The dysregulated expression of cyclin genes can lead to the uncontrolled proliferation of cancer cells. Histone demethylase Jumonji-C domain-containing protein 5 (KDM8, JMJD5) and cyclin A1 (CCNA1) are pivotal in cell cycle progression. A promising candidate for augmenting cancer treatment is Allyl isothiocyanate (AITC), a natural dietary chemotherapeutic and epigenetic modulator. This study aimed to investigate AITC's impact on the KDM8/CCNA1 axis to elucidate its role in oral squamous cell carcinoma (OSCC) tumorigenesis. The expression of KDM8 and CCNA1 was assessed using a tissue microarray (TMA) immunohistochemistry (IHC) assay. In vitro experiments with OSCC cell lines and in vivo experiments with patient-derived tumor xenograft (PDTX) and SAS subcutaneous xenograft tumor models were conducted to explore AITC's effects on their expression and cell proliferation. The results showed elevated KDM8 and CCNA1 levels in the OSCC patient samples. AITC exhibited inhibitory effects on OSCC tumor growth in vitro and in vivo. Additionally, AITC downregulated KDM8 and CCNA1 expression while inducing histone H3K36me2 expression in oral cancer cells. These findings underscore AITC's remarkable anticancer properties against oral cancer, highlighting its potential as a therapeutic option for oral cancer treatment by disrupting the cell cycle by targeting the KDM8/CCNA1 axis.

Anti-angiogenic agents combined with immunotherapy for advanced non-small cell lung cancer: a systematic review and meta-analysis.

BACKGROUND: Anti-angiogenic agents could enhance tumor immunity response, and anti-angiogenesis plus immunotherapy has become a novel treatment option for advanced non-small cell lung cancer (NSCLC). The efficacy of this combination therapy remains controversial and obscure. AIM: We conducted a meta-analysis to evaluate the clinical efficacy and safety of this therapeutic strategy in patients with advanced NSCLC and provide more guidance for treating NSCLC clinically. METHODS: A systematic literature search was performed in PubMed, Embase, Web of Science, CNKI, and Wanfang databases to identify relevant studies published up to December 2021. The primary endpoint was the objective response rate (ORR). Second endpoints were progression-free survival (PFS), overall survival (OS), and grade ≥3 AEs adverse events (AEs). The sensitivity analysis was conducted to confirm the stability of the results. STATA 15.0 was utilized for all pooled analyses. RESULTS: Eleven studies were eventually included in the meta-analysis, involving 533 patients with advanced NSCLC. The pooled ORR rate was 27% (95% CI 18% to 35%; I2 =84.2%; p<0.001), while the pooled median PFS and OS was 5.84 months (95% CI 4.66 to 7.03 months; I2=78.4%; p<0.001) and 14.20 months (95% CI 11.08 to 17.32 months; I2=82.2%; p=0.001), respectively. Most common grade ≥3 AEs included hypertension, hand-foot syndrome, diarrhea, adrenal insufficiency, hyponatremia, proteinuria, rash, thrombocytopenia, and fatigue. CONCLUSION: Anti-angiogenesis combined with immunotherapy demonstrated satisfactory antitumor activity and an acceptable toxicity profile in patients with advanced NSCLC. The pooled results of our meta-analysis provided further evidence supporting the favorable efficacy and safety of this therapeutic strategy.

Comparative effects of hepatocyte growth factor and tacrolimus on acute liver allograft early tolerance.

Allostimulated CD8+ T cells (aCD8+ T cells), as the main mediators of acute liver rejection (ARJ), are hyposensitive to apoptosis due to the inactivation of death receptor FAS-mediated pathways and fail to allow tolerance induction, eventually leading to acute graft rejection. Although tacrolimus (FK506), the most commonly used immunosuppressant (IS) in the clinic, allows tolerance induction, its use is limited because its target immune cells are unknown and it is associated with increased incidences of malignancy, infection, and nephrotoxicity, which substantially impact long-term liver transplantation (LTx) outcomes. The dark agouti (DA)-to-Lewis rat LTx model is a well-known ARJ model and was hence chosen for the present study. We show that both hepatocyte growth factor (HGF) (cHGF, containing the main form of promoting HGF production) and recombinant HGF (h-rHGF) exert immunoregulatory effects mainly on allogeneic aCD8+ T cell suppression through FAS-mediated apoptotic pathways by inhibiting cMet to FAS antagonism and Fas trimerization, leading to acute tolerance induction. We also showed that such inhibition can be abrogated by treatment with neutralizing antibodies against cMet (HGF-only receptor). In contrast, we did not observe these effects in rats treated with FK506. However, we observed that the effect of anti-rejection by FK506 was mainly on allostimulated CD4+ T cell (aCD4+ T cell) suppression and regulatory T cell (Treg) promotion, in contrast to the mechanism of HGF. In addition, the protective mechanism of HGF in FK506-mediated nephrotoxicity was addressed. Therefore, HGF as a tolerance inducer, whether used in combination with FK506 or as monotherapy, may have good clinical value. Additional roles of these T-cell subpopulations in other biological systems and studies in these fields will also be meaningful.

New Synthesized Activating Transcription Factor 3 Inducer SW20.1 Suppresses Resistin-Induced Metabolic Syndrome.

Obesity is an emerging concern globally with increasing prevalence. Obesity is associated with many diseases, such as cardiovascular disease, dyslipidemia, and cancer. Thus, effective new antiobesity drugs should be urgently developed. We synthesized SW20.1, a compound that induces activating transcription factor 3 (ATF3) expression. The results of Oil Red O staining and quantitative real-time polymerase chain reaction revealed that SW20.1 was more effective in reducing lipid accumulation in 3T3-L1 preadipocytes than the previously synthesized ST32db, and that it inhibited the expression of the genes involved in adipogenesis and lipogenesis. A chromatin immunoprecipitation assay indicated that SW20.1 inhibited adipogenesis and lipogenesis by binding to the upstream promoter region of resistin at two sites (-2861/-2854 and -241/-234). In mice, the intraperitoneal administration of SW20.1 reduced body weight, white adipocyte weight in different regions, serum cholesterol levels, adipogenesis-related gene expression, hepatic steatosis, and serum resistin levels. Overall, SW20.1 exerts antiobesity effects by inhibiting resistin through the ATF3 pathway. Our study results indicate that SW20.1 is a promising therapeutic drug for diet-induced obesity.

Yeast biomass ornamented macro-hierarchical chitin nanofiber aerogel for enhanced adsorption of cadmium(II) ions.

There is an urgent need to develop sustainable, renewable, and environment-friendly adsorbents to rectify heavy metals from water. In the current study, a green hybrid aerogel was prepared by immobilizing yeast on chitin nanofibers in the presence of a chitosan interacting substrate. A cryo-freezing technique was employed to construct a 3D honeycomb architecture comprising the hybrid aerogel with excellent reversible compressibility and abundant water transportation pathways for the accelerated diffusion of Cadmium(II) (Cd(II)) solution. This 3D hybrid aerogel structure offered copious binding sites to accelerate the Cd(II) adsorption. Moreover, the addition of yeast biomass amplified the adsorption capacity and reversible wet compression of hybrid aerogel. The monolayer chemisorption mechanism explored by Langmuir and pseudo-second-order kinetic exhibited a maximum adsorption capacity of 127.5 mg/g. The hybrid aerogel demonstrated higher compatibility for Cd(II) ions as compared to the other coexisted ions in wastewater and manifested a better regeneration potential following four consecutive sorption-desorption cycles. Complexation, electrostatic attraction, ion-exchange and pore entrapment were perhaps major mechanisms involved in the removal of Cd(II) revealed by XPS and FT-IR. This study unveiled a novel avenue for efficient green-synthesized hybrid aerogel that may be sustainably used as an excellent purifying agent for Cd(II) removal from wastewater.