Epigenetic modification of IGF2/H19 imprinting control region regulates PGC-1α/PI3K/AKT2 pathway in a rat model of intrauterine growth restriction.

Background: Intrauterine growth restriction (IUGR) is associated with adverse metabolic outcomes during adulthood. Histone modifications and changes in DNA methylation-affected genes are important for fetal development. This study aimed to confirm the epigenetic mechanisms in IUGR.

Predominance of A2063G mutant strains in the Mycoplasma pneumoniae epidemic in children: A clinical and epidemiological study in 2023 in Wuhan, China.

Objectives: The prevalence of respiratory infectious diseases has changed in the post-COVID-19 epidemic era, and mycoplasma pneumoniae (MP) infection in children has attracted wide attention.

Methods: Children hospitalized for pneumonia in Wuhan, China, in 2023 were enrolled. Respiratory secretions were obtained for the targeted next-generation sequencing (tNGS) including mutation of MP.

Challenges of PICC placement via the popliteal vein under ultrasound guidance in a patient with severe burns: A case report.

Peripherally inserted central catheters are widely used in patients with extensive burns, with the guidelines recommending insertion through unburned skin. This case report describes a patient who was burned over 88% of their surface area and suffered severe inhalation injury. For him, the popliteal vein was the only vein on unburned skin available for catheter catheterization.

Structural characterization and anti-lipotoxicity effects of a pectin from okra (Abelmoschus esculentus (L.) Moench).

Okra (Abelmoschus esculentus (L.) Moench) is rich in various bioactive ingredients and used as a medicinal plant in traditional medicine. In the present study, to find the polysaccharide with anti-lipotoxicity effects from okra and clarify its structure, a pectin OP-1 was purified from okra, which had a backbone containing →4)-α-GalpA-(1 → residues, and 1,5-Ara linked the main chain through the O-3 of the residue →3,4)-α-GalpA-(1→, and the C-6 of residue 1, 4-α-GalpA replaced by methyl ester.

Isosilybin regulates lipogenesis and fatty acid oxidation via the AMPK/SREBP-1c/PPARα pathway.

It is well known that the excessive accumulation of lipid in hepatocytes is one of the important causes of non-alcoholic fatty liver disease (NAFLD). The purpose of this study was to explore the effects of isosilybin on lipid metabolism in free fatty acids (FFAs) or TO901317-induced HepG2 cells. Cells were treated with FFAs (oleic acid: palmitic acid, 2:1) or TO901317 to induce steatosis in vitro.

Association of Low Birth Weight and Premature Birth With the Risk of Metabolic Syndrome: A Meta-Analysis.

The association of preterm or low birth weight (LBW) with the risk of metabolic syndrome is still unclear. This study aimed to assess the association between preterm or LBW and metabolic syndrome risk according to study or participants' characteristics. PubMed, Web of Science, and EMBASE were searched for epidemiologic studies on the association published up to April 30, 2020.

Effects of rs2260863 polymorphisms on warfarin maintenance dose in very elderly, frail Han-Chinese population.

This study was conducted to investigate the effects of , , and  and nongenetic factors on warfarin maintenance dose in a very elderly, frail Han-Chinese population.  16 variants of , , and were genotyped. Univariate analysis and multivariable regression model were performed for the associations of gene variants and warfarin maintenance dose.

[Effect of recombinant adenovirus Ad-mir-22 on glucose uptake in HepG2 cells].

The recombinant adenoviruses expressing miR-22 (Ad-miR-22) was constructed and the effect of Ad-miR-22 on insulin signal pathway and glucose uptake in HepG2 cells was analyzed. MiR-22 gene was amplified by PCR from human hepatocytes and cloned into the pAdTrack-CMV vector to generate the shuttle plasmid pAdT-22. The positive colonies were confirmed by PCR and sequencing.

Diagnosis of intellectual disability/global developmental delay via genetic analysis in a central region of China.

Background: Advanced technology has become a valuable tool in etiological studies of intellectual disability/global developmental delay (ID/GDD). The present study investigated the role of genetic analysis to confirm the etiology in ID/GDD patients where the cause of the disease was uncertain in central China.

Methods: We evaluated 1051 ID/GDD children aged 6 months to 18 years from March 2009 to April 2017.

Low IGF-I Bioavailability Impairs Growth and Glucose Metabolism in a Mouse Model of Human PAPPA2 p.Ala1033Val Mutation.

Bioactive free IGF-I is critically important for growth. The bioavailability of IGF-I is modulated by the IGF-binding proteins (IGFBPs) and their proteases, such as pregnancy-associated plasma protein-A2 (PAPP-A2). We have created a mouse model with a specific mutation in PAPPA2 identified in a human with PAPP-A2 deficiency.

PAPPA2 as a Therapeutic Modulator of IGF-I Bioavailability: and Evidence.

Context: Pregnancy-associated plasma protein A2 (PAPPA2) is a protease that cleaves IGF-binding protein (IGFBP)-3 and IGFBP-5, liberating free IGF-I. Five patients from two families with genetic mutations in presented with growth retardation, elevated total IGF-I, and IGFBP-3 but decreased free IGF-I.

Objective: To determine whether plasma transfusion or recombinant human (rh)PAPPA2 could increase free IGF-I in patients with PAPPA2 deficiency or idiopathic short stature (ISS).

Two Siblings with a Mutation in CCDC8 Presenting with Mild Short Stature: A Case of 3-M Syndrome.

Background: Short stature can be caused by mutations in a multitude of different genes. 3-M syndrome is a rare growth disorder marked by severe pre- and postnatal growth retardation along with subtle dysmorphic features. There have only been 2 prior reports of mutations in CCDC8 causing 3-M syndrome.

Protective effects of activated protein C on neurovascular unit in a rat model of intrauterine infection-induced neonatal white matter injury.

Activated protein C (APC), a natural anticoagulant, has been reported to exert direct vasculoprotective, neural protective, anti-inflammatory, and proneurogenic activities in the central nervous system. This study was aimed to explore the neuroprotective effects and potential mechanisms of APC on the neurovascular unit of neonatal rats with intrauterine infection-induced white matter injury. Intraperitoneal injection of 300 μg/kg lipopolysaccharide (LPS) was administered consecutively to pregnant Sprague-Dawley rats at embryonic days 19 and 20 to establish the rat model of intrauterine infection- induced white matter injury.

Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level.

Intrauterine exposure to hyperglycaemia may increase the risk of later-life metabolic disorders. Although the underlying mechanism is not fully understood, epigenetic dysregulation in fetal programming has been implicated. With regard to energy homoeostasis, PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α, encoded by the PPARGC1A gene) plays a regulatory role in several biochemical processes.

Neuroprotective effects of activated protein C on intrauterine inflammation-induced neonatal white matter injury are associated with the downregulation of fibrinogen-like protein 2/fibroleukin prothrombinase and the inhibition of pro-inflammatory cytokine expression.

Maternal intrauterine inflammation or infection is an important risk factor for neonatal cerebral white matter injury (WMI) and future neurological deficits. Activated protein C (APC), a natural anticoagulant, has been shown to exhibit anti-inflammatory, anti-apoptotic, profibrinolytic and cytoprotective activities. Recent studies have demonstrated that the novel prothrombinase, fibrinogen-like protein 2 (fgl2), contributes to the pathogenesis of a number of inflammatory diseases through the generation of fibrin.

IUGR with infantile overnutrition programs an insulin-resistant phenotype through DNA methylation of peroxisome proliferator-activated receptor-γ coactivator-1α in rats.

Background: Intrauterine growth restriction (IUGR) followed by postnatal accelerated growth (CG-IUGR) is associated with long-term adverse metabolic consequences, and an involvement of epigenetic dysregulation has been implicated. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a key orchestrator in energy homeostasis. We hypothesized that CG-IUGR programed an insulin-resistant phenotype through the alteration in DNA methylation and transcriptional activity of PGC-1α.

[Analysis of a case with typical Hutchinson-Gilford progeria syndrome with scleroderma-like skin changes and review of literature].

Objective: To explore clinical, radiographical and genetic characteristics of classical Hutchinson-Gilford progeria syndrome (HGPS).

Method: Data of a case of HGPS diagnosed at Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology was analyzed and related literature was reviewed.

Result: At the age of 8 months, the affected-infant presented with characteristic manifestation such as short stature, low weight, frontal bossing, alopecia, prominent scalp veins, micrognathia with a vertical midline groove in the chin, sclerodermatous skin, knee joints contracture with a horse-riding stance, and limited range of movement of ankle joints.

A novel COMP mutation in a Chinese patient with pseudoachondroplasia.

A 2.75-year-old Chinese boy presented with typical clinical features of pseudoachondroplasia, including disproportionate short-limb short stature, brachydactyly, genu varus and waddling gait. Radiologically, tubular bones were short with widened metaphyses, irregular and small epiphyses; anterior tonguing or beaking of vertebral bodies were characteristic.

Effects of SOCS 1/3 gene silencing on the expression of C/EBPα and PPARγ during differentiation and maturation of rat preadipocytes.

Background: Suppressor of cytokine signaling-1 and -3 (SOCS-1 and SOCS-3) are two important negative regulators in the insulin-signaling pathway, and their overexpression may aggravate insulin resistance. Subjects with insulin resistance are often obese and have increased expressions of SOCS-1 and SOCS-3. We speculated that SOCS-1 and SOCS-3 may be involved in abnormal deposition of adipose tissues during insulin resistance.

Downregulating SOCS3 with siRNA ameliorates insulin signaling and glucose metabolism in hepatocytes of IUGR rats with catch-up growth.

Background: Individuals with intrauterine growth retardation (IUGR) who demonstrate a catch-up in body weight are prone to insulin resistance. High expressions of suppressor of cytokine signaling 3 (SOCS3) are thought to aggravate insulin resistance. We hypothesized that downregulating SOCS3 expression via small interfering RNA (siRNA) might have beneficial effects on insulin-resistant hepatocytes of catch-up growth IUGR rats (CG-IUGRs).

The influence of down-regulation of suppressor of cellular signaling proteins by RNAi on glucose transport of intrauterine growth retardation rats.

Intrauterine growth retardation (IUGR) has been linked to metabolic syndrome including insulin resistance, and overexpression of suppressors of cytokine signaling (SOCSs) proteins is thought to be associated with increased whole-body insulin sensitivity. The insulin-resistant IUGR rat model was established by maternal food restriction (about 30% of the normal rats). The weight, length, and homeostasis model assessment of insulin resistance (HOMA-IR) of IUGR-born rats was higher than the control group.