• Microbiology and Biotechnology Letters
• /
• v.52 no.2
• /
• pp.179-188
• /
• 2024

It has been widely documented that stress conditions in aquatic ecosystems could trigger the release of stress hormone (dopamine) in fishes. Such hormone could attract pathogens (such as Aeromonas hydrophila) to initiate its infection in fishes. The major focus of this study was to investigate the effect of the catecholamine derived stress hormone (dopamine) on the motility and hemolytic activity associated with the virulence of A. hydrophila ATCC AH-1N, the causative agent of Motile Aeromonas Septicemia (MAS). The density of bacterial cells used in this study was adjusted at 106 cells/ml. The results showed that dopamine increased swimming motility of A. hydrophila ATCC AH-1N and was proportional to both dopamine hormone concentration and the incubation period. Dopamine concentration of 100 µM in the medium resulted in the highest increment of swimming ability of A. hydrophila ATCC AH-1N. The dopamine hormone was also found to affect the hemolytic activity of A. hydrophila ATCC AH-1N. The optimum hemolytic activity of the pathogen was found at 50 µM dopamine concentration in the medium, and this hemolytic activity was found to decrease when the concentration of dopamine at greater than 50 µM. It can be concluded from this study that dopamine hormone increased the motility and hemolysis capability, as well as the growth rate of A. hydrophila, and hence increased its virulence.

• Archives of Plastic Surgery
• /
• v.51 no.4
• /
• pp.432-440
• /
• 2024

Background The risk of flap necrosis in tissue reconstruction surgery is elevated in patients with vascular disorders, such as diabetes mellitus. Chronic hyperglycemia causes endothelial cell dysfunction and increases inflammatory process, causing vascular insufficiency. Platelet-rich plasma (PRP) contains high levels of platelets, growth factors, and fibrinogens. Its regenerative properties spark interest in supporting flap survival in relation to diabetic complications. Methods Thirty Wistar rats were divided into three groups. The first group included diabetic rats without PRP injection, which underwent flap procedure. The second group included diabetes-induced rats receiving PRP subcutaneous injection 1 day prior to flap procedure. The third group included nondiabetic rats receiving PRP injection 1 day prior to flap procedure. Flap tissue samples were taken on the seventh day to measure vascular endothelial growth factor (VEGF) levels using enzyme-linked immunosorbent assay method; angiogenesis and collagen density were measured from histopathology examination, and flap viability was analyzed using digital measurements. Results Analysis showed that flap viability, angiogenesis, and VEGF levels were significantly higher in the PRP-injected diabetic rats compared with diabetic rats that did not receive PRP. The levels of VEGF, angiogenesis, and viability of flaps in diabetic rats given PRP did not differ significantly compared with nondiabetic rats that received PRP. Conclusion Flap preconditioning through local injection of activated PRP enhances flap viability, VEGF levels and angiogenesis, in random skin flaps in diabetic rats, to the level where it does not differ significantly to nondiabetic rats that were given PRP.

• Journal of The Korean Society of Inherited Metabolic disease
• /
• v.20 no.1
• /
• pp.24-28
• /
• 2020

Type III Glycogen storage disease (Type III GSD, OMIM#232400) is a genetic metabolic disorder in which undigested glycogen accumulates in the organs due to lack of glycogen debranching enzyme caused by AGL mutation. The clinical symptoms of type III GSD include hepatomegaly, delayed growth, hypoglycemia and muscle weakness. These clinical symptoms are similar to those of other types of GSD, making it difficult to distinguish clinically. The authors report a case of type III GSD diagnosed by gene panel sequencing. A 11-month old male patient was presented with hepatomegaly. In liver biopsy, glycogen was accumulated in hepatocytes, suggesting GSDs. For differential diagnosis of types of GSD, gene panel sequencing for GSDs was performed. As a result, two novel pathogenic compound heterozygous variants: c.311_312del (p.His104Argfs*15) and c.3314+1G>A in AGL were detected and the patient was diagnosed as type III GSD. After diagnosis, he started dietary treatment with cornstarch, and has been free from complications. After two years, two same variants were also identified in the chorionic villous sampling of the pregnant mother, and the fetus was diagnosed as type III GSD. Gene panel sequencing is useful for diagnosis of disease which is indistinguishable by clinically and has high genetic heterogeneity, such as GSD. After diagnosis, familial genetic analysis can provide adequate genetic counseling and rapid diagnosis.

• Journal of The Korean Society of Inherited Metabolic disease
• /
• v.12 no.2
• /
• pp.108-112
• /
• 2012

Glycogen storage disease type III (GSD type III, OMIM #232400) is a rare autosomal recessive disease caused by a deficiency of the glycogen-debranching enzyme (GDE) with a mutation in the AGL gene (OMIM *610860). It is known to be bifunctional enzyme, that is, having two independent catalytic activities; 1,4-${\alpha}$-D-glucan 4-${\alpha}$-D-glycosyltransferase (EC 2.4.1.25) and amylo-1,6-glucosidase (EC 3.2.1.33) that occur at separate active sites on a single polypeptide chain. Most patients with GSD type III usually have symptoms related to decreased glycogenolysis in liver and muscles, such as hepatomegaly, hypoglycemia, failure to thrive, hyperlipidemia, muscle weakness and cardiomyopathy (type IIIa), however some patients show symptoms restricted to liver (type IIIb). GSD type III is diagnosed by enzyme test through liver or muscle biopsy or mutation analysis of the AGL gene. We report the case of GSD type III proven by gene study after liver biopsy, which revealed c.476delA, c.3444_3445insA in exon 6, 27 of AGL gene in Korean patient.