A Celecoxib-Loaded Emulsion Gel for Enhanced Drug Delivery and Prevention of Postoperative Adhesion.

Postoperative adhesions are a common complication following abdominal surgery, affecting over 90% of patients and leading to significant morbidity. Current anti-adhesion strategies, such as the use of physical and chemical barriers, have limitations such as short retention time, mechanical fragility, and inefficient drug delivery. This study developed a pectin-based emulsion gel loaded with celecoxib to prevent adhesions and provide localized pain relief.

Fulvic acid inhibits the differentiation of 3T3-L1 adipocytes by activating the Ca/CaMKⅡ/AMPK pathway.

Type 2 diabetes increases the risk of developing obesity. Although fulvic acid alleviates back fat thickness in pigs, the mechanism underlying its anti-obesity effect remains unclear. Therefore, we investigated the anti-obesity mechanism of fulvic acid using 3T3-L1 adipocytes.

Role of cytosolic and endoplasmic reticulum Ca in pancreatic beta-cells: pros and cons.

Pancreatic beta cells utilize Ca to secrete insulin in response to glucose. The glucose-dependent increase in cytosolic Ca concentration ([Ca]) activates a series of insulin secretory machinery in pancreatic beta cells. Therefore, the amount of insulin secreted in response to glucose is determined in a [Ca]-dependent manner, at least within a moderate range.

Lupenone attenuates thapsigargin-induced endoplasmic reticulum stress and apoptosis in pancreatic beta cells possibly through inhibition of protein tyrosine kinase 2 activity.

Aims: Prolonged high levels of cytokines, glucose, or free fatty acids are associated with diabetes, elevation of cytosolic Ca concentration ([Ca]), and depletion of Ca concentration in the endoplasmic reticulum (ER) of pancreatic beta cells. This Ca imbalance induces ER stress and apoptosis. Lupenone, a lupan-type triterpenoid, is beneficial in diabetes; however, its mechanism of action is yet to be clarified.

Spoligotype Variation of Strains Prevailing in Korea.

Tuberculosis (TB) is an ongoing global health problem, including in South Korea. To manage TB efficiently, it is necessary to understand the epidemiology, transmission route, and characteristics of prevailing strains. In this study, we investigated microevolutions over time in the spoligotype patterns of isolated from TB patients in Korea.

Oxidative stress resulting from the removal of endogenous catalase induces obesity by promoting hyperplasia and hypertrophy of white adipocytes.

Obesity is regarded as an abnormal expansion and excessive accumulation of fat mass in white adipose tissue. The involvement of oxidative stress in the development of obesity is still unclear. Although mainly present in peroxisomes, catalase scavenges intracellular HO at toxic levels.

Orexin A-induced inhibition of leptin expression and secretion in adipocytes reducing plasma leptin levels and hypothalamic leptin resistance.

Orexin A (OXA) is a neuropeptide associated with plasma insulin and leptin levels involved in body weight and appetite regulation. However, little is known about the effect of OXA on leptin secretion in adipocytes and its physiological roles. Leptin secretion and expression were analysed in 3T3-L1 adipocytes.

Proteomics approach to identify serum biomarkers associated with the progression of diabetes in Korean patients with abdominal obesity.

Type 2 diabetes is a metabolic disease with a group of metabolic derangements and inflammatory reactants in the serum. Despite the substantial public health implications, markers of diabetes progression with abdominal obesity are still needed to facilitate early detection and treatment. In this study, we performed a proteomic approach to identify differential target proteins underlying diabetes progression in patients with abdominal obesity.

Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice.

Hydrogen peroxide (HO) produced endogenously can cause mitochondrial dysfunction and metabolic complications in various cell types by inducing oxidative stress. In the liver, oxidative and endoplasmic reticulum (ER) stress affects the development of non-alcoholic fatty liver disease (NAFLD). Although a link between both stresses and fatty liver diseases has been suggested, few studies have investigated the involvement of catalase in fatty liver pathogenesis.

Catalase and nonalcoholic fatty liver disease.

Obesity and insulin resistance are considered the main causes of nonalcoholic fatty liver disease (NAFLD), and oxidative stress accelerates the progression of NAFLD. Free fatty acids, which are elevated in the liver by obesity or insulin resistance, lead to incomplete oxidation in the mitochondria, peroxisomes, and microsomes, leading to the production of reactive oxygen species (ROS). Among the ROS generated, HO is mainly produced in peroxisomes and decomposed by catalase.

Epac2a-knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress.

Exchange protein directly activated by cAMP (Epac) 2a-knockout (KO) mice exhibit accelerated diet-induced obesity and are resistant to leptin-mediated adipostatic signaling from the hypothalamus to adipose tissue, with sustained food intake. However, the impact of Epac2a deficiency on hypothalamic regulation of sympathetic nervous activity (SNA) has not been elucidated. This study was performed to elucidate the response of Epac2a-KO mice to dexamethasone-induced muscle atrophy and acute cold stress.

Tomatidine inhibits tumor necrosis factor-α-induced apoptosis in CC myoblasts via ameliorating endoplasmic reticulum stress.

In this study, we examined the effect of tomatidine on tumor necrosis factor (TNF)-α-induced apoptosis in CC myoblasts. TNF-α treatment increased cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase (PARP) protein levels in a dose- and time-dependent manner. Pretreatment of cells with 10 μM tomatidine prevented TNF-α-induced apoptosis, caspase 3 cleavage, and PARP cleavage.

Comparative Analysis of Protein Tyrosine Phosphatases Regulating Microglial Activation.

Protein tyrosine phosphatases (PTPs) are key regulatory factors in inflammatory signaling pathways. Although PTPs have been extensively studied, little is known about their role in neuroinflammation. In the present study, we examined the expression of 6 different PTPs (PTP1B, TC-PTP, SHP2, MEG2, LYP, and RPTPβ) and their role in glial activation and neuroinflammation.

Comparison of the tuberculin skin test and interferon gamma release assay for the screening of tuberculosis in adolescents in close contact with tuberculosis TB patients.

Background: The tuberculin skin test (TST) frequently yields false positive results among BCG-vaccinated persons thereby limiting its diagnostic value particularly in settings with high BCG vaccination rate. We determined the agreement between IGRA and TST using 2 cutoff values and identified possible relationships between the results of these tests and the development of active tuberculosis.

Methodology: Adolescents aged 11-19 years in close contact with smear-positive tuberculosis cases and with normal chest radiographs were recruited from middle and high schools in South Korea.

Saucerneol D, a naturally occurring sesquilignan, inhibits LPS-induced iNOS expression in RAW264.7 cells by blocking NF-kappaB and MAPK activation.

We evaluated the ability of saucerneol D (SD), a tetrahydrofuran-type sesquilignan isolated from Saururus chinensis, to regulate the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells. SD consistently inhibited nitric oxide (NO) production in a dose-dependent manner, with an IC(50) of 2.

Critical role of a single position in the -35 element for promoter recognition by Mycobacterium tuberculosis SigE and SigH.

Mycobacterial SigE and SigH both initiate transcription from the sigB promoter, suggesting that they recognize similar sequences. Through mutational and primer extension analyses, we determined that SigE and SigH recognize nearly identical promoters, with differences at the 3' end of the -35 element distinguishing between SigE- and SigH-dependent promoters.

The increasing racial disparity in infant mortality: respiratory distress syndrome and other causes.

Although substantial declines in infant mortality rates have occurred across racial/ethnic groups, there has been a marked increase in relative black-white disparity in the risk of infant death over the past two decades. The objective of our analysis was to gain insight into the reasons for this growing inequality on the basis of data from linked cohort files for 1989-1990 and 1995-1998. We found a nationwide reversal from a survival advantage to a survival disadvantage for blacks with respect to respiratory distress syndrome over this period.