Determinants of Hypoglycemia in Premature Vietnamese Infants: A Case-Control Study.

Background Premature infants are more likely to experience hypoglycemia. Early recognition and prompt therapy are essential to avoiding neurological sequelae in the future. This study aimed to identify the determinants of hypoglycemia in premature Vietnamese infants. Methodology This was a case-control study conducted at the Neonatal Intensive Care Unit, The Women and Children Hospital of An Giang, Vietnam. Hypoglycemia was defined as a plasma glucose value of less than 2.6 mmol/L (47 mg/dL) after two hours postpartum. Maternal and neonatal information was collected and analyzed. Both bivariate and multiple logistic regression models were used to identify the risk factors of neonatal hypoglycemia (NH) Results A total of 65 cases and 195 controls were included in the study. Gestational diabetes mellitus (GDM) (adjusted odds ratio [AOR] 3.78, 95% confidence interval [CI] 1.69-8.52; P < 0.001) and excessive gestational weight gain (GWG) (AOR 2.80, 95% CI 1.12-6.98; P < 0.026) were associated with NH in the multiple logistic regression model. An observed positive interaction between gestational hypertension and GDM on NH yielded an odds ratio (OR) of 6.29 (95% CI 2.46-16.64). Conclusions GDM, excessive GWG, and the interaction between gestational hypertension and GDM were the determinants of hypoglycemia in premature infants.

Retail fresh vegetables as a potential source of Salmonella infection in the Mekong Delta, Vietnam.

From July 2017 to Jan 2019, a total of 572 retail fresh vegetables were collected to clarify the contamination of Salmonella in the Mekong Delta, Vietnam. Salmonella was isolated from 74 (12.9%) of 572 samples. The isolation rate of Salmonella from retail fresh vegetables in the rainy season (15.3%) was significantly higher than that in the dry season (7.6%) (P < 0.05). Of 74 Salmonella isolates, Salmonella Weltevreden was the most predominant serovar (35.1%) identified from retail fresh vegetables in all of the wet markets. All S. Weltevreden isolates (100%) were susceptible to nine antibiotics examined. Thus, retail fresh vegetables were considered as an important potential vehicle of Salmonella transmission to humans in the Mekong Delta. These results provide important data for preventing and controlling human salmonellosis in this area.

The gut hormone ghrelin partially reverses energy substrate metabolic alterations in the failing heart.

BACKGROUND: The gut-derived hormone ghrelin, especially its acylated form, plays a major role in the regulation of systemic metabolism and exerts also relevant cardioprotective effects; hence, it has been proposed for the treatment of heart failure (HF). We tested the hypothesis that ghrelin can directly modulate cardiac energy substrate metabolism. METHODS AND RESULTS: We used chronically instrumented dogs, 8 with pacing-induced HF and 6 normal controls. Human des-acyl ghrelin [1.2 nmol/kg per hour] was infused intravenously for 15 minutes, followed by washout (rebaseline) and infusion of acyl ghrelin at the same dose. (3)H-oleate and (14)C-glucose were coinfused and arterial and coronary sinus blood sampled to measure cardiac free fatty acid and glucose oxidation and lactate uptake. As expected, cardiac substrate metabolism was profoundly altered in HF because baseline oxidation levels of free fatty acids and glucose were, respectively, >70% lower and >160% higher compared with control. Neither des-acyl ghrelin nor acyl ghrelin significantly affected function and metabolism in normal hearts. However, in HF, des-acyl and acyl ghrelin enhanced myocardial oxygen consumption by 10.2±3.5% and 9.9±3.7%, respectively (P<0.05), and cardiac mechanical efficiency was not significantly altered. This was associated, respectively, with a 41.3±6.7% and 32.5±10.9% increase in free fatty acid oxidation and a 31.3±9.2% and 41.4±8.9% decrease in glucose oxidation (all P<0.05). CONCLUSIONS: Acute increases in des-acyl or acyl ghrelin do not interfere with cardiac metabolism in normal dogs, whereas they enhance free fatty acid oxidation and reduce glucose oxidation in HF dogs, thus partially correcting metabolic alterations in HF. This novel mechanism might contribute to the cardioprotective effects of ghrelin in HF.

OPA3, mutated in 3-methylglutaconic aciduria type III, encodes two transcripts targeted primarily to mitochondria.

3-Methylglutaconic aciduria type III (3-MGCA type III), caused by recessive mutations in the 2-exon gene OPA3, is characterized by early-onset bilateral optic atrophy, later-onset extrapyramidal dysfunction, and increased urinary excretion of 3-methylglutaconic acid and 3-methylglutaric acid. Here we report the identification of a novel third OPA3 coding exon, the apparent product of a segmental duplication event, resulting in two gene transcripts, OPA3A and OPA3B. OPA3A deficiency (as in optic atrophy type 3) causes up-regulation of OPA3B. OPA3 protein function remains unknown, but it contains a putative mitochondrial leader sequence, mitochondrial sorting signal and a peroxisomal sorting signal. Our green fluorescent protein tagged OPA3 expression studies found its localization to be predominantly mitochondrial. These findings thus place the cellular metabolic defect of 3-MGCA type III in the mitochondrion rather than the peroxisome and implicate loss of OPA3A rather than gain of OPA3B in disease etiology.