Most organisms contain glutamate dehydrogenase (E.C. 1.4.1.2-1.4.1.4). In eukaryotes, the enzyme is mainly present in mitochondria. This enzyme plays a vital role in the metabolism of nitrogen and carbon and the signaling pathway. Studies have found that glutamate dehydrogenase has a certain relationship with the occurrence and development of tumors, which is significant for tumor research, but reviews on its relationship with human tumors are rare. This review summarized the relationship between glutamate dehydrogenase and breast cancer, glioma, colorectal cancer and ovarian cancer, etc, thus providing assistance for related research.
Carbon ; Glioma ; Glutamate Dehydrogenase ; Humans ; Mitochondria ; Nitrogen

Child ; Glutamate Dehydrogenase ; genetics ; Humans ; Hyperinsulinism ; genetics ; Male ; Mutation

Various commercial assays have recently been developed for detecting glutamate dehydrogenase (GDH) and/or toxin A/B to diagnose Clostridioides difficile infection (CDI). We compared the performance of two assays for the simultaneous detection of C. difficile GDH and toxin A/B, using 150 stool samples: C. DIFF QUIK CHEK COMPLETE (QCC; TechLab, Blacksburg, VA, USA) and RIDASCREEN Clostridium difficile GDH (RC-GDH) and Toxin A/B (RC-Toxin A/B; R-Biopharm, Darmstadt, Germany). For GDH detection, QCC and RC-GDH showed satisfactory sensitivity (95.7% and 94.3%, respectively) and specificity (92.5% and 93.8%, respectively) compared with C. difficile culture. For toxin A/B detection, QCC showed higher sensitivity than RC-Toxin A/B (60.0% vs 33.3%, P < 0.001) compared with toxigenic C. difficile culture. When the results of QCC or RC-GDH+RC-Toxin A/B were used as the first step of a two-step algorithm for diagnosing CDI, QCC permitted more accurate discrimination than RC of positive or negative results for CDI (77.3% and 65.3%, respectively). QCC is useful for the simultaneous detection of C. difficile GDH and toxin A/B as a part of the two-step algorithm for diagnosing CDI.
Clostridium difficile ; Discrimination (Psychology) ; Glutamate Dehydrogenase ; Glutamic Acid ; Sensitivity and Specificity

OBJECTIVETo explore the pathophysiological and biomechanical features of skeletal muscular injury for providing a rational basis for its treatment, prevention and rehabilitation.

METHODSIn 70 adult rabbits, the left tibialis anterior (TA) muscle was stretched to injury, while the right TA muscle served as control. Histological, enzymohistochemical and biomechanical changes were observed on days 0, 1, 2, 3, and 7 after injury. Cytochrome oxidase (CCO), acid phosphatase (ACP), ATPase, succinate dehydrogenase (SDH), malate dehydrogenase (MDH), NADH-diaphorase (NADHD), glutamatedehydrogenase (GDH), alpha-glycerophosphate dehydrogenase (alpha-GPD) and lactate dehydrogenase (LDH) were measured. The examined biomechanical parameters included maximal contractile force, ultimate load, length, energy absorption, tangent stiffness, and rupture site.

RESULTSPartial or complete rupture of TA muscle occurred near the muscle-tendon junction. There was an intense inflammatory reaction on day 1 and 2 after injury. Endomysium fibrosis and myotube formation were observed on day 3, and developed further on day 7. The activity of cell oxidases (CCO, ATPase, MDH, alpha-GPD, SDH, NADHD and GDH) showed a significant drop from day 0 to 2, and resumed with different levels on day 3. The increment of enzymatic activities continued on day 7 and the levels of NADHD and alpha-GPD reached to the levels of control muscle. Maximal contractile force was 70.17%+/-3.82% of controls immediately after injury, 54.82%+/-3.09% at 1 day, 66.41%+/-4.36% at 2 days, 78.39%+/-4.90% at 3 days and 93.64%+/-5.02% at 7 days. Ultimate load was 85.78%+/-7.54% of controls at the moment of injury, 61.44%+/-5.91% at 1 day, 49.17%+/-4.26% at 2 days, 64.43%+/-5.02% at 3 days, and 76.71%+/-6.46% at 7 days.

CONCLUSIONSEndomysium fibrosis and scar formation at the injured site are responsible for frequent recurrence of skeletal muscle injury. Recovery of tensile load slower than that of maximal contractile force may be another cause. Whether the injured muscle returns to normal exercise is mainly determined by the tensility on which the muscle-tendon can bear rather than the maximal contractile force.

Acid Phosphatase ; analysis ; Adenosine Triphosphatases ; analysis ; Animals ; Biomechanical Phenomena ; Dihydrolipoamide Dehydrogenase ; analysis ; Electron Transport Complex IV ; analysis ; Glutamate Dehydrogenase ; analysis ; Glycerolphosphate Dehydrogenase ; analysis ; L-Lactate Dehydrogenase ; analysis ; Malate Dehydrogenase ; analysis ; Muscle, Skeletal ; injuries ; pathology ; physiology ; Rabbits ; Succinate Dehydrogenase ; analysis

Congenital hyperinsulinism (CHI), the most important cause of hyperglycemia in early infancy, is a heterogenous disease characterized by dysregulation of insulin secretion. Mutations in five proteins have been associated with CHI: sulfonyl urea receptor 1; Kir 6.2; glucokinase; glutamate dehydrogenase and mitochondrial enzyme short-chain 3-hydroxyacyl-coenzyme A dehydrogenase. Early recognition of hypoglycemia, diagnosis of CHI and appropriate management of the hypoglycemia are of the utmost importance to prevent neurologic damage. We report a case of persistent hyperinsulinemic hypoglycemia in 8-month-old male infant. This patient has no mutation in previously mentioned genes. Treatment with diazoxide was successful without any severe side effects in this patient.
Congenital Hyperinsulinism* ; Diagnosis ; Diazoxide* ; Glucokinase ; Glutamate Dehydrogenase ; Humans ; Hyperglycemia ; Hyperinsulinism ; Hypoglycemia ; Infant ; Insulin ; Male ; Oxidoreductases ; Urea

In May 2015, we conducted a voluntary online survey on laboratory diagnostic assays for Clostridium difficile infection (CDI) across clinical microbiology laboratories in Korea. Responses were obtained from 66 laboratories, including 61 hospitals and five commercial laboratories. Among them, nine laboratories reported having not conducted CDI assays. The toxin AB enzyme immunoassay (toxin AB EIA), nucleic acid amplification test (NAAT), and C. difficile culture, alone or in combination with other assays, were used in 51 (89.5%), 37 (64.9%), and 37 (64.9%) of the remaining 57 laboratories, respectively, and 23 (40.4%) of the laboratories performed all three assays. Only one laboratory used the glutamate dehydrogenase assay. Nine laboratories used the toxin AB EIA as a stand-alone assay. The median (range) of examined specimens in one month for the toxin AB EIA, NAAT, and C. difficile culture was 160 (50–2,060), 70 (7–720), and 130 (9–750), respectively. These findings serve as valuable basic data regarding the current status of laboratory diagnosis of CDI in Korea, offering guidance for improved implementation.
Clinical Laboratory Techniques ; Clostridium difficile ; Clostridium ; Glutamate Dehydrogenase ; Immunoenzyme Techniques ; Korea ; Nucleic Acid Amplification Techniques

To understand a mechanism of underlying cognitive deficit in schizophrenia, the risk factors, cognitive function, blood dopamine concentrations and glutamate dehydrogenase activities of male schizophrenics with tardive dyskinesia(N=30) were compared with those of schizophrenics without tardive dyskinesia(N=30). The result were as following ; 1) The age, duration of illness and duration of medication were significantly more in schizophrenics with tardive dyskinesia than schizophrenics without tardive dyskinesia(respectively p<0.005, p<0.0001, p<0.0001). 2)The scores of MMSE, TIQ, VIQ and PIQ were significantly lower in schizophrenics with tradive dyskinesia than schizophrenics without tardive dyskinesia(respectively p<0.0001). 3) plasma dopamine concentrations were tended to be higher, and serum glutamate dehydrogenase activities were tended to be lower in schizophrenics with tardive dyskinesia than schizophrenics without tardive dyskinesia. 4) The cognitive deficit seemed to be negatively correlated with duration of illness and duration of illness and duration of medication(respectively gamma=-0.496, gamma=-0.615).
Dopamine ; Dyskinesias ; Glutamate Dehydrogenase ; Humans ; Male ; Movement Disorders* ; Plasma ; Risk Factors ; Schizophrenia*

The usefulness of malaria diagnosis by Plasmodium falciparum-GDH (NADP+), obtained by affinity chromatography, is demonstrated in ELISA assays, testing IgG antibodies against GDH (NADP+) from patients with acute malaria, who have had two or more episodes of malaria, or from sera of hyperimmune patients. GDH (NADP+) thermal stability was demonstrated in a high heat resistance assay. The immunofluorescence assay demonstrated that anti-culture (P. falciparum) supernatant serum and anti-GDH (NADP+) of Proteus spp, recognized epitopes in Venezuelan isolates, and Colombian and Brasilian malarial strains. The antigen is soluble, with high specificity, is a potent immunogen and is thermoresistant.
parasitology-protozoa ; antigen ; enzymes ; glutamate dehydrogenase ; malaria ; diagnosis ; Plasmodium berghei ; Plasmodium cathemerium ; Plasmodium falciparum ; Plasmodium vivax ; enzyme-linked immunosorbent assay

The hyperinsulinism/hyperammonemia (HI/HA) syndrome is a form of congenital hyperinsulinism. The children with HI/HA syndrome present recurrent symptomatic hypoglycemia and asymptomatic, persistent hyperammonemia, caused by mutations of the GLUD1 encoding the mitochondrial enzyme, glutamate dehydrogenase (GDH). The mutations impair sensitivity to the inhibition of GTP (guanosine triphosphate), which results in stimulation of insulin secretion from pancreatic beta-cells and increased rates of ammonia production. Leucine is known to mediate the insulin secretion. We report HI/HA syndrome with a 12-month-old male who had intermittent hypoglycemia. We revealed characteristic clinical findings of hypoglycemia induced by oral administration of protein in this patient who had mutations of GLUD1 (S445L).
Administration, Oral ; Ammonia ; Child ; Congenital Hyperinsulinism ; Glutamate Dehydrogenase ; Guanosine Triphosphate ; Humans ; Hyperammonemia ; Hyperinsulinism ; Hypoglycemia ; Infant ; Insulin ; Leucine ; Male

BACKGROUND: Clostridium difficile is the most common pathogen of antibiotic-associated diarrhea. Toxigenic strains produce toxin A and toxin B. The pathogenicity of C. difficile is due to the production of these two exotoxins. This study aimed to evaluate diagnostic value of two enzyme immunoassay by comparison of concordance rate to diagnose C. difficile-associated infection. METHODS: C. DIFF QUIK CHEK (TECHLAB, USA) that detect glutamate dehydrogenase antigen and VIDAS C. difficile Toxin A&B (BioMerieux, France) that detect toxin A and toxin B were done in 122 fecal specimens to detect C. difficile. RESULTS: In the total 122 stool specimens, 17 cases showed positive results in both tests. One specimen showed discrepancy that positive result in VIDAS C. difficile Toxin A&B (relative fluorescence value, RFV=2.93) but negative result in C. DIFF QUIK CHEK. Therefore, the concordance rate between two tests was 95.1% (116/122). Both anaerobic culture and in-house PCR for toxin B were negative in the discrepant fecal specimen and there was no clinical evidence that support C. difficile-associated diarrhea, so we concluded result in VIDAS C. difficile Toxin A&B as false positive. CONCLUSIONS: Although these two enzyme immunoassays targeted different antigen, they showed high concordance rate. The discrepant case was concluded to false positive in VIDAS C. difficile Toxin A&B test because it showed negative results in culture and PCR for toxin B and there were no clinical evidences of C. difficile-associated infection. It could be needed for analysis about conditions that cause false positive result in enzyme immunoassays to detect C. difficile toxin.
Azure Stains ; Clostridium difficile ; Diarrhea ; Exotoxins ; Fluorescence ; Glutamate Dehydrogenase ; Immunoenzyme Techniques ; Methylene Blue ; Polymerase Chain Reaction ; Xanthenes