Glucose 6-phosphate dehydrogenase deficiency and Southeast Asian-specific mutations lower HbA levels in a Thai population: implications for diabetes diagnosis.

Aims/hypothesis: Glucose 6-phosphate dehydrogenase (G6PD) deficiency, the most common inherited enzymopathy, can affect HbA levels and the diagnosis of type 2 diabetes. This cross-sectional study aimed to investigate the association between G6PD deficiency, its common mutations (G6PD Viangchan, G6PD Mahidol) and HbA levels in a Thai cohort.

Methods: Blood samples from 1007 healthy hospital staff were collected during annual health checkups.

Inhibition of non-small cell lung cancer (NSCLC) proliferation through targeting G6PD.

Background: Mounting evidence has linked cancer metabolic reprogramming with altered redox homeostasis. The pentose phosphate pathway (PPP) is one of the key metabolism-related pathways that has been enhanced to promote cancer growth. The glucose 6-phosphate dehydrogenase (G6PD) of this pathway generates reduced nicotinamide adenine dinucleotide phosphate (NADPH), which is essential for controlling cellular redox homeostasis.

Single-Drop Blood Detection of Common Mutations in Thailand Based on Allele-Specific Recombinase Polymerase Amplification with CRISPR-Cas12a.

Glucose 6-phosphate dehydrogenase (G6PD) deficiency is the most common inherited enzymopathy. Identification of the G6PD deficiency through screening is crucial to preventing adverse effects associated with hemolytic anemia following antimalarial drug exposure. Therefore, a rapid and precise field-based G6PD deficiency diagnosis is required, particularly in rural regions where malaria is prevalent.

Effect of neonatal reticulocytosis on glucose 6-phosphate dehydrogenase (G6PD) activity and G6PD deficiency detection: a cross-sectional study.

Background: Screening for G6PD deficiency in newborns can help prevent severe hemolysis, hyperbilirubinemia, and bilirubin encephalopathy, as recommended by the World Health Organization (WHO). It has been speculated that the presence of a high number of reticulocytes in newborns interferes with the diagnosis of G6PD deficiency since reticulocytes contain higher amounts of G6PD enzyme than mature erythrocytes. Therefore, the purposes of this study were to assess the effect of reticulocytosis in the determination of blood G6PD activity in Thai newborns by using a novel automated UV-based enzymatic assay and to validate the performance of this assay for the detection of G6PD deficiency in newborn samples.

Haematological profile of malaria patients with G6PD and PKLR variants (erythrocytic enzymopathies): a cross-sectional study in Thailand.

Background: Glucose 6-phosphate dehydrogenase (G6PD) and pyruvate kinase (PKLR) deficiencies are common causes of erythrocyte haemolysis in the presence of antimalarial drugs such as primaquine and tafenoquine. The present study aimed to elucidate such an association by thoroughly investigating the haematological indices in malaria patients with G6PD and PKLR variants.

Methods: Blood samples from 255 malaria patients from Thailand, Myanmar, Laos, and Cambodia were collected to determine haematological profile, G6PD enzyme activity and G6PD deficiency variants.

Evaluating the performance of automated UV enzymatic assay for screening of glucose 6-phosphate dehydrogenase deficiency.

Introduction: A precise and reliable screening assay for glucose 6-phosphate dehydrogenase (G6PD) deficiency would greatly help avoiding unwanted outcomes due to bilirubin neurotoxicity in neonatal jaundice and antimalarial-induced haemolytic anaemia in malaria patients. Currently, available assays are laborious and require sophisticated laboratory expertise. This study aimed to evaluate the performance of a recently introduced automated screening assay for G6PD deficiency by comparing with a routine spectrophotometric assay.

Valproic acid attenuates nitric oxide and interleukin-1β production in lipopolysaccharide-stimulated iron-rich microglia.

Iron accumulation in activated microglia has been consistently reported in neurodegenerative diseases. Previous results suggest that these cells facilitate neuroinflammation leading to neuronal cell death. Therefore, chemical compounds that alleviate the activation of iron-rich microglia may result in neuroprotection.

The effects of okra (Abelmoschus esculentus Linn.) on the cellular events associated with Alzheimer's disease in a stably expressed HFE neuroblastoma SH-SY5Y cell line.

It has been reported that persons carrying the H63D variant in their hemochromatosis (HFE) gene are at increased risk of Alzheimer's disease (AD). We investigated the possibility that okra (Abelmoschus esculentus) and quercetin could mitigate this risk factor by examining its effect on AD-associated cellular events in HFE stably expressing SH-SY5Y cells. Treatment of H63D HFE cells either with okra or quercetin significantly decreased reactive oxygen species (ROS), hydrogen peroxide (H2O2), and protein oxidation compared to untreated cells.

Characterization of putative Japanese encephalitis virus receptor molecules on microglial cells.

Japanese encephalitis virus (JEV) a mosquito-borne flavivirus is a major cause of viral encephalitis in Asia. While the principle target cells for JEV in the central nervous system are believed to be neurons, microglia are activated in response to JEV and have been proposed to act as a long lasting virus reservoir. Viral attachment to a host cell is the first step of the viral entry process and is a critical mediator of tissue tropism.

Increased cellular iron levels affect matrix metalloproteinase expression and phagocytosis in activated microglia.

Activation of microglia could be beneficial and yet simultaneously harmful depending upon nature of pathological milieu. Regardless of disease-specific etiology, iron accumulation, particularly in activated microglia, is a notable feature associated with a series of neuropathologies, including Alzheimer's diseases. Although mounting evidence supports the role of iron in oxidative brain injury, knowledge on its regulatory role in neuroinflammation is still scarce.

The H63D HFE gene variant promotes activation of the intrinsic apoptotic pathway via mitochondria dysfunction following β-amyloid peptide exposure.

Numerous epidemiological studies suggest that the expression of the HFE allelic variant H63D may be a risk factor or genetic modifier for Alzheimer's disease (AD). The H63D variant alters cellular iron homeostasis and increases baseline oxidative stress. The elevated cellular stress milieu, we have proposed, may alter cellular responses to genetic and environmental determinants of AD.

Highly permissive infection of microglial cells by Japanese encephalitis virus: a possible role as a viral reservoir.

Japanese encephalitis virus (JEV), a mosquito-borne Flavivirus, is a major cause of acute encephalitis, and neurons have been proposed to be the principle JEV target cells in the central nervous system. However, clinically, infection with JEV leads to increased levels of cytokines and chemokines in the serum and cerebrospinal fluid (CSF) the levels of which correlate with the mortality rate of patients. This research aimed to study the role of microglial cells in JEV infection.

Iron increases MMP-9 expression through activation of AP-1 via ERK/Akt pathway in human head and neck squamous carcinoma cells.

Head and neck squamous cell carcinoma (HNSCC) is a highly invasive cancer that is capable of distant metastasis and is a cause of great morbidity and mortality worldwide. Over-expression of matrix metalloproteinase-9 (MMP-9) is implicated in the invasion and metastasis of HNSCC. There is increasing evidence of an association between iron overload and cancer progression.

In vitro biocompatibility of schwann cells on surfaces of biocompatible polymeric electrospun fibrous and solution-cast film scaffolds.

The in vitro responses of Schwann cells (RT4-D6P2T, a schwannoma cell line derived from a chemically induced rat peripheral neurotumor) on various types of electrospun fibrous scaffolds of some commercially available biocompatible and biodegradable polymers, i.e., poly(3-hydroxybutyrate) (PHB), poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV), polycaprolactone (PCL), poly(l-lactic acid) (PLLA), and chitosan (CS), were reported in comparison with those of the cells on corresponding solution-cast film scaffolds as well as on a tissue-culture polystyrene plate (TCPS), used as the positive control.

In vitro biocompatibility of electrospun poly(3-hydroxybutyrate) and poly(3-hydroxybutyrate-co-3-hydroxyvalerate) fiber mats.

In the present contribution, the potential for use of the ultrafine electrospun fiber mats of poly(3-hydroxybutyrate) (PHB) and poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) as scaffolding materials for skin and nerve regeneration was evaluated in vitro using mouse fibroblasts (L929) and Schwann cells (RT4-D6P2T) as reference cell lines. Comparison was made with PHB and PHBV films that were prepared by solution-casting technique. Indirect cytotoxicity assessment of the as-spun PHB and PHBV fiber mats with mouse fibroblasts (L929) and Schwann cells (RT4-D6P2T) indicated that the materials were acceptable to both types of cells.

Estrogen enhances the inhibitory effect of iron on microglial nitric oxide production.

Abnormal iron accumulation has been consistently reported in specific brain regions of many neurodegenerative diseases. At cellular level, iron is unusually observed in microglia, immune effector cell of the brain. Most evidence has provided that upon activation, microglia produces neurotoxins and different kinds of inflammatory mediators.