Dexamethasone may affect the occurrence of parenteral nutrition-associated cholestasis in preterm neonates.

Introduction: Glucocorticoids are currently used for the co-therapeutic management of autoimmune hepatitis and some cholestatic diseases. Thus far, we do not know the efficacy of glucocorticoids in the treatment of parenteral nutrition-associated cholestasis. We aimed to analyze whether the administration of late postnatal dexamethasone for treating bronchopulmonary dysplasia influence the occurrence of parenteral nutrition-associated cholestasis in preterm neonates.

Evaluation of the diagnostic value of gastric juice aspirate culture for early-onset sepsis in newborns 28-35 weeks' gestation.

The aim of the study was to discuss the diagnostic value of gastric aspirate culture of early-onset sepsis in premature neonates. A retrospective study was conducted for 600 premature neonates of predisposing high-risk factors (gestation age from 28 to 35 weeks) hospitalized in neonatal unit of the First Affiliated Hospital of Wenzhou Medical University. The culture of gastric aspirate was performed within 24 h after birth.

Sex Differences in Progression of Diabetic Cardiomyopathy in OVE26 Type 1 Diabetic Mice.

OVE26 mice are a widely used transgenic model of early-onset type 1 diabetes. These mice overexpress calmodulin in their pancreatic cells, develop severe diabetes within the first weeks of life, and progress to severe diabetic complications including diabetic nephropathy and diabetic cardiomyopathy (DCM). To date, diabetic nephropathy in OVE26 mice has been well explored, leaving the progression of DCM and the gender impact in this type 1 diabetes model still unrevealed.

Diabetic‑induced alterations in hepatic glucose and lipid metabolism: The role of type 1 and type 2 diabetes mellitus (Review).

Diabetes mellitus (DM) is a growing health concern in society. Type 1 and type 2 DM are the two main types of diabetes; both types are chronic diseases that affect glucose metabolism in the body and the impaired regulation of glucose and lipid metabolism promotes the development and progression of DM. During the physiological metabolism process, the liver serves a unique role in glucose and lipid metabolism.

Sex differences in progression of diabetic nephropathy in OVE26 type 1 diabetic mice.

Aims: OVE26 mice (FVB background), genetically overexpressing calmodulin in pancreatic beta cells, develop early onset type 1 diabetes, leading to progressive diabetic nephropathy (DN), with features of established human DN. The role of gender in characteristics of renal lesions has remained unexplored.

Methods: Male and female OVE26 mice were compared to age and sex matched wild-type, nondiabetic FVB mice at ages of 4, 12, 24 and 36 weeks.

Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time.

To detect the changes in the liver function in both male and female OVE26 mice from young to adults for better understanding of type 1 diabetes-induced hepatic changes, OVE26 mice and wild-type FVB mice were raised in the same environment without any intervention, and then killed at 4, 12, 24 and 36 weeks for examining liver's general properties, including pathogenic and molecular changes. The influence of diabetes on the bodyweight of male and female mice was different. Both male and female OVE26 mice did not obtain serious liver injury or non-alcoholic fatty liver disease, manifested by mild elevation of plasma alanine transaminase, and less liver lipid content along with significantly suppressed lipid synthesis.

HDAC3 inhibition in diabetic mice may activate Nrf2 preventing diabetes-induced liver damage and FGF21 synthesis and secretion leading to aortic protection.

Vascular complications are common pathologies associated with type 1 diabetes. In recent years, histone deacetylation enzyme (HDAC) inhibitors have been shown to be successful in preventing atherosclerosis. To investigate the mechanism for HDAC3 inhibition in preventing diabetic aortic pathologies, male OVE26 type 1 diabetic mice and age-matched wild-type (FVB) mice were given the HDAC3-specific inhibitor RGFP-966 or vehicle for 3 mo.

Exacerbation of diabetic cardiac hypertrophy in OVE26 mice by angiotensin II is associated with JNK/c-Jun/miR-221-mediated autophagy inhibition.

Both diabetes and angiotensin II (Ang II) excess trigger cardiac remodeling and dysfunction, and diabetic cardiomyopathy. We hypothesized that cardiac hypertrophy associated with the development of diabetic cardiomyopathy is worsened by increased Ang II. Male type 1 diabetic OVE26 and wild-type mice were given Ang II (sc.