Glycemic control as the main determinant factor of serum VEGF levels in type 2 diabetes mellitus patients.

Diabetes mellitus (DM) is a main endocrine disorder that may cause vascular complications as the disease progresses. Vascular endothelial growth factor (VEGF) has been linked to the development of micro and macrovascular diabetic complications. This study aimed to assess several factors including blood pressure, body mass index, lipid profile, kidney function, and glycemic control that may provide the rise of serum VEGF levels in type 2 DM subjects.

Excess mortality attributable to antimicrobial-resistant bacterial bloodstream infection at a tertiary-care hospital in Indonesia.

The burden of antimicrobial-resistant (AMR) infections in low and middle-income countries (LMICs) is largely unknown. Here, we evaluate attributable mortality of AMR infections in Indonesia. We used routine databases of the microbiology laboratory and hospital admission at Dr.

Performance of Xpert MTB/RIF and sputum microscopy compared to sputum culture for diagnosis of tuberculosis in seven hospitals in Indonesia.

Introduction: Tuberculosis (TB) is a major public health concern in Indonesia, where the incidence was 301 cases per 100,000 inhabitants in 2020 and the prevalence of multi-drug resistant (MDR) TB is increasing. Diagnostic testing approaches vary across Indonesia due to resource limitations. Acid-fast bacilli (AFB) smear is widely used, though Xpert MTB/RIF has been the preferred assay for detecting TB and rifampicin resistance since 2012 due to higher sensitivity and ability to rapidly identify rifampicin resistance.

Lipocalin 2 could predict circulating MMP9 levels in patients with breast cancer.

Objectives: Breast cancer is the most prevalent carcinoma found in Indonesian women, and its incidence remains high worldwide. Lipocalin 2 has been linked with the progression of breast cancer. Matrix metalloproteinase 9 (MMP9) is an enzyme that has an important role in angiogenesis.

Anthropometric features in predicting insulin resistance among non-menopausal Indonesian adult females.

Introduction: The prevalence of obesity is increasing worldwide in high, low, and middle-income countries such as Indonesia. Obesity rate is higher in females in Indonesia. Obesity has important contribution in the occurrence of insulin resistance (IR) and type 2 diabetes mellitus.

Body Mass, Total Body Fat Percentage, and Visceral Fat Level Predict Insulin Resistance Better Than Waist Circumference and Body Mass Index in Healthy Young Male Adults in Indonesia.

The incidence of obesity which leads to insulin resistance (IR) and metabolic disorder is increasing in developing countries, including Indonesia. Male adults have a higher risk of abdominal obesity than females. This is associated with cardiometabolic disorders.

Inhibition of antibody production in vivo by pre-stimulation of Toll-like receptor 4 before antigen priming is caused by defective B-cell priming and not impairment in antigen presentation.

Stimulation of Toll-like receptor 4 (TLR4) induces not only innate but also adaptive immune responses, and has been suggested to exert adjuvant effects. Additional to such positive effects, pre-stimulation of TLR4 induces endotoxin tolerance where animals are unresponsive to subsequent lethal challenges with lipopolysaccharide (LPS). We examined the effects of pre-stimulation of TLR4 using an agonistic anti-TLR4 mAb (UT12) on antibody production in vivo.

Preparation and characterization of agonistic monoclonal antibodies against Toll-like receptor 4-MD-2 complex.

Ligands for toll-like receptors (TLR) are known to induce a variety of immune responses. Selective induction of desirable responses would be important for the treatment of individual diseases with various pathogenesis. For this purpose, we established six MAbs against the TLR4/MD-2 complex (UT MAbs) from TLR4(-/-) mice or MD-2(-/-) mice.

Penta-acylated lipopolisaccharide binds to murine MD-2 but does not induce the oligomerization of TLR4 required for signal transduction.

A mutant lipopolysaccharide (LPS) lacking a myristate chain in lipid A was shown to be non-pathogenic both in humans and mice. The mutant penta-acylated LPS from the lpxM-strain did not induce TNF-alpha production in murine peritoneal macrophages, or activation of NF-kappaB in transfected cells expressing murine TLR4/MD-2. We prepared a recombinant murine MD-2 in Escherichia coli (E.

Induction of long-term lipopolysaccharide tolerance by an agonistic monoclonal antibody to the toll-like receptor 4/MD-2 complex.

We have established an agonistic monoclonal antibody, UT12, that induces stimulatory signals comparable to those induced by lipopolysaccharide (LPS) through Toll-like receptor 4 and MD-2. UT12 activated nuclear factor kappaB and induced the production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in peritoneal exudative cells. In addition, mice injected with UT12 rapidly fell into endotoxin shock concomitant with the augmentation of serum TNF-alpha and IL-6 levels, followed by death within 12 h.

Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment.

Toll-like receptors (TLRs) are best known for their ability to recognize microbial or viral components and initiate innate immune responses. We showed here that TLRs and their coreceptors were expressed by multipotential hematopoietic stem cells, whose cell cycle entry was triggered by TLR ligation. TLR expression also extended to some of the early hematopoietic progenitors, although not the progenitor cells dedicated to megakaryocyte and erythroid differentiation.

Identification of a novel isoform of MD-2 that downregulates lipopolysaccharide signaling.

MD-2 is an association molecule of Toll-like receptor 4 and is indispensable for the recognition of lipopolysaccharide. Here we report the identification of mRNA for an alternatively spliced form of MD-2, named MD-2B, which lacks the first 54 bases of exon 3. When overexpressed with MD-2, MD-2B competitively suppressed NF-kappaB activity induced by LPS.