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Purpose This study aims to analyze the number of suicide deaths in women, trends in suicide mortality, characteristics of suicide by age, and outcomes of suicide means over the past decade (2011–2021) in South Korea. Methods Using cause of death data from Statistics Korea, an in-depth analysis of Korean women’s suicide trends was conducted for the period of 2011–2021. Results In 2021, women’s suicide death in Korea was 4,159, a rate of 16.2 per 100,000 population. The rate increased by 1.4% from the previous year. Since 2011, women’s suicide rate has been on a steady downward trend, but since 2018, it has been on the rise again. Suicide rates among women in their 20s and 30s have increased, especially since the coronavirus disease 2019 pandemic, and suicide rates among women over 70 years remain high. As compared to 2011, pesticide poisoning and hanging among the means of suicide have decreased significantly, while drug and carbon monoxide continue to increase. Conclusion Suicide rates for Korean women in their 20s and 30s have increased significantly in recent years, and those for women over 70 years remain high. Therefore, it is necessary to investigate the causes and establish national policies for targeted management of these age groups, which contributes significantly to the rising suicide rate among Korean women.

Exosomes derived from mesenchymal stem cells have shown promise in treating metabolic disorders, yet their specific mechanisms remain largely unclear. This study investigates the protective effects of exosomes from human umbilical cord Wharton’s jelly mesenchymal stem cells (hWJMSCs) against adiposity and insulin resistance in high-fat diet (HFD)-induced obese mice. HFD-fed mice treated with hWJMSC-derived exosomes demonstrated improved gut barrier integrity, which restored immune balance in the liver and adipose tissues by reducing macrophage infiltration and pro-inflammatory cytokine expression. Furthermore, these exosomes normalized lipid metabolism including lipid oxidation and lipogenesis, which alleviate lipotoxicity-induced endoplasmic reticulum (ER) stress, thereby decreasing fat accumulation and chronic tissue inflammation in hepatic and adipose tissues. Notably, hWJMSC-derived exosomes also promoted browning and thermogenic capacity of adipose tissues, which was linked to reduced fibroblast growth factor 21 (FGF21) resistance and increased adiponectin production. This process activated the AMPK-SIRT1-PGC-1α pathway, highlighting the role of the FGF21–adiponectin axis. Our findings elucidate the molecular mechanisms through which hWJMSC-derived exosomes counteract HFD-induced metabolic dysfunctions, supporting their potential as therapeutic agents for metabolic disorders.

Abstract Mucosal tissues serve as the first defense line and their commensal microbiota play a role in sustaining of host health. This study aimed to isolate and evaluate a putative probiotic strain on various mucosal regions. Lactobacillus sakei HEM 224 was isolated from traditional Korean kimchi and identified. In the safety assessment L. sakei HEM 224 showed negative results for hemolysis, biogenic amine production and transferable antibiotic resistance. The probiotic potential of strain HEM 224 in diverse mucosal areas was shown in two different models, viz. a murine model with colitis induced by dextran sulfate sodium (DSS) and an allergic airway inflammation model induced by ovalbumin (OVA). In the colitis model, oral administration of L. sakei HEM 224 improved colitis physiology with immunomodulation, enhancing barrier components and gut microbiota alteration. In the allergic airway inflammation model, the intranasal administration of the strain decreased type 2 inflammation and enhanced epithelial barrier integrity from the airways. These results demonstrate that L. sakei HEM 224 can ameliorate inflammatory conditions in both the gastrointestinal and respiratory tracts through the reinforcement of the epithelial barrier and immunomodulation.

Background CycloZ, a combination of cyclo-His-Pro and zinc, has anti-diabetic activity. However, its exact mode of action remains to be elucidated. Methods KK-Ay mice, a type 2 diabetes mellitus (T2DM) model, were administered CycloZ either as a preventive intervention, or as a therapy. Glycemic control was evaluated using the oral glucose tolerance test (OGTT), and glycosylated hemoglobin (HbA1c) levels. Liver and visceral adipose tissues (VATs) were used for histological evaluation, gene expression analysis, and protein expression analysis. Results CycloZ administration improved glycemic control in KK-Ay mice in both prophylactic and therapeutic studies. Lysine acetylation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha, liver kinase B1, and nuclear factor-κB p65 was decreased in the liver and VATs in CycloZ-treated mice. In addition, CycloZ treatment improved mitochondrial function, lipid oxidation, and inflammation in the liver and VATs of mice. CycloZ treatment also increased the level of β-nicotinamide adenine dinucleotide (NAD+), which affected the activity of deacetylases, such as sirtuin 1 (Sirt1). Conclusion Our findings suggest that the beneficial effects of CycloZ on diabetes and obesity occur through increased NAD+ synthesis, which modulates Sirt1 deacetylase activity in the liver and VATs. Given that the mode of action of an NAD+ booster or Sirt1 deacetylase activator is different from that of traditional T2DM drugs, CycloZ would be considered a novel therapeutic option for the treatment of T2DM.

Clinically, prostate cancer is infamous for its histological and molecular heterogeneity, which causes great challenges to pinpoint therapy and pharmaceutical development. To overcome these difficulties, researchers are focusing on modulating tumor microenvironment and immune responses in addition to genetic alteration and epigenetic regulation. Here, we aimed to identify potential biomarkers or modulators of prostate cancer by investigating genes specifically altered in prostate cancer cells treated with established anti-cancer agents. Glycerol kinase 1 (GK1) is phosphotransferase encoded on the X chromosome, is associated with the synthesis of triglycerides and glycerophospholipids, and has been mainly studied for X-linked metabolic disorder GK deficiency (GKD). Interestingly, our DNA microarray analysis showed that several anti-cancer agents highly induced the expression of GK1, especially GK1a and GK1b isoforms, in human prostate cancer PC-3 cells. To elucidate the relationship between GK1 and cancer cell death, a human GK1b-specific expression vector was constructed and transfected into the PC-3 cells. Surprisingly, GK1b overexpression dramatically reduced cell viability and significantly accelerated apoptotic cell death. These findings suggest that GK1b may serve as a promising modulator and biomarker of cell death in prostate cancer, offering potential avenues for therapeutic intervention.

The beneficial effects of probiotics for the improvement of metabolic disorders have been studied intensively; however, these effects are evident in a probiotic strain-specific and disease-specific manner. Thus, it is still essential to evaluate the efficacy of each strain against a target disease. Here, we present an anti-obese and anti-diabetic probiotic strain, Lactiplantibacillus plantarum APsulloc331261 (GTB1™), which was isolated from green tea and tested for safety previously. In high-fat-diet-induced obese mice, GTB1™ exerted multiple beneficial effects, including significant reductions in adiposity, glucose intolerance, and dyslipidemia, which were further supported by improvements in levels of circulating hormones and adipokines. Lipid metabolism in adipose tissues was restored through the activation of PPAR/PGC1α signaling by GTB1™ treatment, which was facilitated by intestinal microbiota composition changes and short-chain fatty acid production. Our findings provide evidence to suggest that GTB1™ is a potential candidate for probiotic supplementation for comprehensive improvement in metabolic disorders.

Abstract RET (REarranged during Transfection) is a receptor tyrosine kinase that transduces various external stimuli into biological functions, such as survival and differentiation, in neurons. In the current study, we developed an optogenetic tool for modulating RET signaling, termed optoRET, combining the cytosolic region of human RET with a blue-light–inducible homo-oligomerizing protein. By varying the duration of photoactivation, we were able to dynamically modulate RET signaling. Activation of optoRET recruited Grb2 (growth factor receptor-bound protein 2) and stimulated AKT and ERK (extracellular signal-regulated kinase) in cultured neurons, evoking robust and efficient ERK activation. By locally activating the distal part of the neuron, we were able to retrogradely transduce the AKT and ERK signal to the soma and trigger formation of filopodia-like F-actin structures at stimulated regions through Cdc42 (cell division control 42) activation. Importantly, we successfully modulated RET signaling in dopaminergic neurons of the substantia nigra in the mouse brain. Collectively, optoRET has the potential to be developed as a future therapeutic intervention, modulating RET downstream signaling with light.

IntroductionAllergic airway diseases are one of the serious health problems in worldwide and allergic airway inflammation is a prerequisite led to the exacerbated situation such as mucus hypersecretion, epithelial barrier damage and microbiota dysbiosis. Because of side effects and low efficiencies of current therapeutics, the need for novel alternatives has been urged. Probiotics in which have diverse and beneficial modulatory effects have been applied to the airway inflammation model and the underlying mechanism needs to be investigated.MethodsWe aimed to evaluate whether our target strain, Lactiplantibacillus plantarum APsulloc331261 (GTB1TM) isolated from green tea, can ameliorate allergic airway inflammation in mice and to figure out the mechanism. We induced allergic airway inflammation to mice by ovalbumin (OVA) and administered GTB1 orally and the immune and epithelial barrier markers were assessed. The gut metabolite and microbiota were also analysed, and the in vitro cell-line experiment was introduced to confirm the hypothesis of the study.ResultsGTB1 ameliorated type 2 inflammation and suppressed mucin hypersecretion with the inhibition of MUC5AC in inflamed mice. Moreover, GTB1 increased the butyrate production and the relative abundance of butyrate producer, Clostridium cluster IV. We assumed that butyrate may have a potential role and investigated the effect of butyrate in mucin regulation via human airway epithelial cell line, A549. Butyrate significantly reduced the gene expression of MUC5AC in A549 cells suggesting its regulatory role in mucus production.ConclusionTherefore, our study demonstrates that the oral administration of GTB1 can ameliorate allergic airway inflammation and mucin hypersecretion by butyrate production.

The role of 3D genome organization is not well understood in the transcriptional regulation of dendritic cells. Here the authors show that activation of dendritic cells in vitro induces dynamic reprogramming of the chromatin looping and enhancer activity linked to changes in gene expression and implicates a role for the chromatin architecture protein CTCF in the inflammatory response of dendritic cells.

Post-transplant lymphoproliferative disorders (PTLDs) are lymphoid or plasmacytic proliferations ranging from polyclonal reactive proliferations to overt lymphomas that develop as consequence of immunosuppression in recipients of solid organ transplantation (SOT) or allogeneic bone marrow/hematopoietic stem cell transplantation. Immunosuppression and Epstein-Barr virus (EBV) infection are known risk factors for PTLD. Patients with documented histopathologic diagnosis of primary PTLD at our institution between January 2000 and October 2019 were studied. Sixty-six patients with PTLD following SOT were followed for a median of 9.0 years. The overall median time from transplant to PTLD diagnosis was 5.5 years, with infant transplants showing the longest time to diagnosis at 12.0 years, compared to pediatric and adolescent transplants at 4.0 years and adult transplants at 4.5 years. The median overall survival (OS) was 19.0 years. In the monomorphic diffuse large B-cell (M-DLBCL-PTLD) subtype, median OS was 10.7 years, while median OS for polymorphic subtype was not yet reached. There was no significant difference in OS in patients with M-DLBCL-PTLD stratified by quantitative EBV viral load over and under 100,000 copies/mL at time of diagnosis, although there was a trend towards worse prognosis in those with higher copies.

Abstract Polymer electrolyte membrane water electrolysis (PEMWE) is an attractive hydrogen energy production technology that offers various advantages such as compact design, high operating pressure, high current densities, and high hydrogen gas purity. However, PEMWE still faces several critical challenges, particularly with respect to the oxygen evolution reaction (OER) at the anode. Highly active, corrosion‐resistant electrocatalytic materials are required for the acidic OER owing to its sluggish kinetics involving four‐electron transfer under harsh anodic potentials. To date, IrO2‐ or RuO2‐based noble metal electrocatalysts have been employed as commercial acidic OER electrocatalysts for PEMWE. However, they remain inadequate in terms of satisfying the industrial activity/stability‐related requirements. Above all, the two noble metals are too rare and expensive, which significantly inhibits widespread commercialization of PEMWE. Therefore, low‐cost, highly active, and highly stable OER electrocatalysts that can operate in acidic media must be urgently developed. This review paper presents various state‐of‐the‐art strategies employed to address the aforementioned issues by classifying them according to objectives such as improving activity, enhancing stability, and reducing cost. Then, finally, we summarize major tasks and strategies to overcome them and put forward a few issues in this field.

Purpose This study aimed to identify maternal, infant, and perinatal mortality using the national population data of South Korea between 2018 and 2020, and to analyze mortality rates according to characteristics such as age, date of death, and cause of death in each group. This study updates the most recent study using 2009 to 2017 data. Methods Analyses of maternal, infant, and perinatal mortality were done with data identified through the supplementary investigation system for cases of death from the Census of Population Dynamics data provided by Statistics Korea from 2018 to 2020. Results Between 2018 and 2020, a total of 99 maternal deaths, 2,427 infant deaths, and 2,408 perinatal deaths were identified from 901,835 live births. The maternal mortality ratio was 11.3 deaths per 100,000 live births in 2018; it decreased to 9.9 in 2019 but increased again to 11.8 in 2020. The maternal mortality ratio increased steeply in women over the age of 40 years. An increasing trend in the maternal mortality ratio was found for complications related to the puerperium and hypertensive disorders. Both infant and perinatal mortality continued to decrease, from 2.8 deaths per 1,000 live births in 2018 to 2.5 in 2020 and from 2.8 in 2018 to 2.5 in 2020, respectively. Conclusion Overall, the maternal, infant, and perinatal mortality statistics showed improvements. However, more attention should be paid to women over 40 years of age and specific causes of maternal deaths, which should be taken into account in Korea’s maternal and child health policies.

Purpose Korea has implemented an early screening for colorectal cancer since 2004. However, it is not known whether this has translated into improved survival over the years. Methods We acquired colorectal cancer mortality data from the Cause of Death Statistics in Korea from 2000 to 2020. We characterized the data into year of death, cancer-specific loci, and age group. We analyzed age-standardized mortality rates (ASMR) according to year of death, age group, and primary location to find trends in colorectal cancer mortality over a 20-year period. Results The crude mortality rate of colorectal cancer increased from 8.78 per 100,000 in 2000 to 17.27 per 100,000 in 2020. The second decade was slower in increments compared to the first decade. ASMR showed a decrease over the second decade after an initial increase in the first decade. The decrease was primarily from the lowering of ASMR for rectosigmoid cancers. Age group analysis showed a lowering of ASMR mainly in the 45–59-year, 60–74-year, and ≥ 75-year age groups; however, 0–29-year and 30–44-year age groups showed generally unchanged ASMR over the total period. Conclusion After a brief incline of age-specific mortality of colorectal cancers during the early 2000s, colorectal cancer mortality has gradually been decreasing in the past decade. This was mainly due to decreased mortalities in rectosigmoid colon cancers especially in the age groups that were the target of early screening.

As it has become clear that the gut microbiota play a critical role in brain function, probiotics have recently been spotlighted as therapeutic agents for various psychiatric disorders including major depressive disorder. Despite much interest, however, our understanding of the efficacy of probiotics for treating depression is still limited due to the complexity of the gut-brain axis. The present study aimed to evaluate the anti-depressive effect of Lactiplantibacillus plantarum APsulloc 331,261 in vivo and to elucidate the possible mechanism of action of this strain. The consumption of the strain APsulloc 331,261 could significantly reduce depressive-like behaviors and downregulate hippocampal inflammation. Interestingly, administration of the strain shifted the gut microbial community towards increasing acetate and propionate production. This modulation might stimulate increased serotonin synthesis in the colon and increase the serotonin level and neurogenesis in the brain. These results may serve to support the proposal of a new probiotic candidate strain for ameliorating depression.

Purpose The purpose of this study was to investigate how pediatric intensive care unit (PICU) nurses and the mothers of hospitalized children perceived their partnership and identify the detailed differences in the common domains of partnership between them. Methods A qualitative descriptive design with semi-structured and open-ended interviews was used. Interviews with mothers of hospitalized children and nurses in the PICU were conducted at a national university hospital in South Korea. Results Five integrated categories were identified concerning nurses' and mothers' perceptions of partnership. Five common domains were derived by merging the partnership categories perceived by each PICU mother and nurse: expectation of trust, sharing and communication, participation in care, equality in the relationship, and coordination of opinion However, there were significant differences in the composition of the categories of these common domains. Conclusion These results may facilitate more effective partnerships between parents and PICU nurses. Efforts should be taken to promote the formation of trust between nurses and parents and create an environment that is conductive to regular open communication in particular, steps should be taken to reduce gaps in awareness concerning this partnership and information sharing, nursing methods, and decision-making.

Exosomes derived from mesenchymal stem cells have shown promise in treating metabolic disorders, yet their specific mechanisms remain largely unclear. This study investigates the protective effects of exosomes from human umbilical cord Wharton's jelly mesenchymal stem cells (hWJMSCs) against adiposity and insulin resistance in high-fat diet (HFD)-induced obese mice. HFD-fed mice treated with hWJMSC-derived exosomes demonstrated improved gut barrier integrity, which restored immune balance in the liver and adipose tissues by reducing macrophage infiltration and pro-inflammatory cytokine expression. Furthermore, these exosomes normalized lipid metabolism including lipid oxidation and lipogenesis, which alleviate lipotoxicity-induced endoplasmic reticulum (ER) stress, thereby decreasing fat accumulation and chronic tissue inflammation in hepatic and adipose tissues. Notably, hWJMSC-derived exosomes also promoted browning and thermogenic capacity of adipose tissues, which was linked to reduced fibroblast growth factor 21 (FGF21) resistance and increased adiponectin production. This process activated the AMPK-SIRT1-PGC-1α pathway, highlighting the role of the FGF21–adiponectin axis. Our findings elucidate the molecular mechanisms through which hWJMSC-derived exosomes counteract HFD-induced metabolic dysfunctions, supporting their potential as therapeutic agents for metabolic disorders. [ABSTRACT FROM AUTHOR]

The advancement of semiconductor technology nodes requires precise control of their manufacturing process, including plasma etching, which is highly important in terms of the yield, cost, and device performance. Endpoint detection (EPD) is an imperative technique for controlling this process. Here, we propose a novel EPD scheme based on multivariate kernel density estimation (MKDE). The proposed approach is developed by extending the conventional unsupervised learning MKDE method to supervised learning. The performance of the proposed scheme is validated on randomly selected optical emission spectroscopy data collected from an industrial semiconductor manufacturing process. Because the proposed approach uses target values (labeling) of data, it demonstrates enhanced EPD performance compared to the conventional MKDE method, even without threshold presetting.

Hepatobiliary abnormality and metabolic disorders are frequently observed complications in patients with inflammatory bowel diseases (IBD). Given that microbiota dysbiosis is a common pathophysiological feature of both IBD and metabolic diseases, we examined how the IBD-induced dysbiosis affects the host metabolism and contributes to the development of associated metabolic diseases using germ-free (GF) mice transplanted with fecal microbiota of DSS-induced colitis mice. There was no significant change in inflammation or barrier integrity in the gut of GF mice that received microbiota from colitis mice compared to their counterparts that were transplanted with microbiota from non-colitis healthy mice. Interestingly, it was observed that the GF recipients of colitis-induced altered microbiota showed a significant decrease in the weight of adipose tissues including mesenteric, epididymal, subcutaneous, and brown fat without any change in body weight, which was accompanied by abnormalities in adipose tissue functions such as fat storage and adiponectin production. Transplantation of colitis-induced altered microbiota also disrupted hepatic lipid metabolism in the GF recipient mice, which was observed by increases in synthesis and accumulation of cholesterol and bile acids in hepatocytes and a decrease in plasma HDL-cholesterol. Additional observations including elevated plasma levels of insulin, decreased hepatic production of FGF21, and decreased levels of fecal short chain fatty acids (SCFAs) and hepatic expression of SCFA receptors led to a conclusion that the transplantation of the colitis-associated dysbiotic microbiota was causally associated with impairments of insulin action and FGF21-adiponectin axis, possibly due to the low SCFA-producing capacity of the colonized microbiota, leading to metabolic abnormalities including adipose tissue dysfunction and dysregulated hepatic lipid metabolism. Our findings suggest potential mechanisms that explain how colitis-associated gut dysbiosis may contribute to the development of metabolic dysfunctions, which could be applied to clinical practice to improve the efficacy of treatment of IBD patients with comorbid metabolic disorders or vice versa.

Purpose This study compared infant mortality and its associated factors between Korean and immigrant women using vital statistics gathered by Statistics Korea. Methods Birth and death statistics from the period between 2009 and 2019 were extracted from the census of population dynamics data of the Microdata Integrated Service, Korea. Statistical data were derived from a complete survey and infant mortality was analyzed from mortality statistics data. Descriptive statistics were used for comparison. Results The average infant mortality rate (IMR) of Korean women was 2.7 in Koreawhich, did not change significantly between 2009 and 2019; however, the IMR of immigrant women increased significantly in 2018 to 4.2 and subsequently decreased to 2.6 in 2019. Moreover, the age of Korean and immigrant women at the time of infant death gradually increased from 31.1 years and 25.9 years in 2009 to 32.8 years and 30.9 years in 2019, respectively. The gestational age was lower for deceased infants born to immigrant women (mean, 31.04 weeks; standard deviation [SD], 6.42; median, 30.00 ) compared to those born to Korean women (mean, 31.71 weeks; SD, 6.48; median, 32.00). Immigrant women (91.7%) received slightly fewer antenatal care visits compared to Korean women (93.1%). Conclusion It is vital to devise a plan to lower the IMR of immigrant women in Korea. Moreover, it is necessary to explore the factors related to infant mortality among immigrant women within the context of Korean societal situation, culture, and home environment.

Abstract The balance between activities of fear neurons and extinction neurons in the basolateral nucleus of the basal amygdala (BAL) has been hypothesized to encode fear states after extinction. However, it remains unclear whether these neurons are solely responsible for encoding fear states. In this study, we stably recorded single-unit activities in the BAL during fear conditioning and extinction for 3 days, providing a comprehensive view on how different BAL neurons respond during fear learning. We found BAL neurons that showed excitatory responses to the conditioned stimulus (CS) after fear conditioning (‘conditioning-potentiated neurons’) and another population that showed excitatory responses to the CS after extinction (‘extinction-potentiated neurons’). Interestingly, we also found BAL neurons that developed inhibitory responses to the CS after fear conditioning (‘conditioning-inhibited neurons’) or after extinction (‘extinction-inhibited neurons’). BAL neurons that showed excitatory responses to the CS displayed various functional connectivity with each other, whereas less connectivity was observed among neurons with inhibitory responses to the CS. Intriguingly, we found correlative neuronal activities between conditioning-potentiated neurons and neurons with inhibitory responses to the CS. Our findings suggest that distinct BAL neurons, which are responsive to the CS with excitation or inhibition, encode various facets of fear conditioning and extinction.

Abstract Considering high prevalence of non-alcoholic fatty liver diseases (NAFLD) in patients with inflammatory bowel disease (IBD), this study aimed to elucidate molecular mechanisms for how intestinal inflammatory conditions are causally linked to hepatic steatosis and dyslipidemia. Both younger and older mice treated with acute or chronic dextran sodium sulfate (DSS) developed colitis, which was evidenced by weight loss, colon length shortening, and elevated disease activity index and inflammation score. They also showed decreased expression of intestinal barrier function-related proteins and elevated plasma lipopolysaccharide level, indicating DSS-induced barrier dysfunction and thereby increased permeability. Interestingly, they displayed phenotypes of hepatic fat accumulation and abnormal blood lipid profiles. This DSS-induced colitis-associated lipid metabolic dysfunction was due to overall disruption of metabolic processes including fatty acid oxidation, lipogenesis, lipolysis, reverse cholesterol transport, bile acid synthesis, and white adipose tissue browning and brown adipose tissue thermogenesis, most of which are mediated by key regulators of energy homeostasis such as FGF21, adiponectin, and irisin, via SIRT1/PGC-1α- and LXRα-dependent pathways. Our study suggests a potential molecular mechanism underlying the comorbidity of NAFLD and IBD, which could provide a key to understanding how the two diseases are pathogenically linked and discovering critical therapeutic targets for their treatment.

Clinically, prostate cancer is infamous for its histological and molecular heterogeneity, which causes great challenges to pinpoint therapy and pharmaceutical development. To overcome these difficulties, researchers are focusing on modulating tumor microenvironment and immune responses in addition to genetic alteration and epigenetic regulation. Here, we aimed to identify potential biomarkers or modulators of prostate cancer by investigating genes specifically altered in prostate cancer cells treated with established anti-cancer agents. Glycerol kinase 1 (GK1) is phosphotransferase encoded on the X chromosome, is associated with the synthesis of triglycerides and glycerophospholipids, and has been mainly studied for X-linked metabolic disorder GK deficiency (GKD). Interestingly, our DNA microarray analysis showed that several anti-cancer agents highly induced the expression of GK1, especially GK1a and GK1b isoforms, in human prostate cancer PC-3 cells. To elucidate the relationship between GK1 and cancer cell death, a human GK1b-specific expression vector was constructed and transfected into the PC-3 cells. Surprisingly, GK1b overexpression dramatically reduced cell viability and significantly accelerated apoptotic cell death. These findings suggest that GK1b may serve as a promising modulator and biomarker of cell death in prostate cancer, offering potential avenues for therapeutic intervention. [ABSTRACT FROM AUTHOR]