Metabolic dysfunction-associated steatohepatitis (MASH), a severe type of metabolic dysfunction-associated steatotic liver disease (MASLD), is a leading etiology of end-stage liver disease worldwide, posing significant health and economic burdens. microRNA-320 (miR-320), a ubiquitously expressed and evolutionarily conserved miRNA, has been reported to regulate lipid metabolism; however, whether and how miR-320 affects MASH development remains unclear. By performing miR-320 in situ hybridization with RNAscope, we observed a notable downregulation of miR-320 in hepatocytes during MASH, correlating with disease severity. Most importantly, miR-320 downregulation in hepatocytes exacerbated MASH progression as demonstrated that hepatocyte-specific miR-320 deficient mice were more susceptible to high-fat, high-fructose, high-cholesterol diet (HFHC) or choline-deficient, amino acid-defined, high-fat diet (CDAHFD)-induced MASH compared with control littermates. Conversely, restoration of miR-320 in hepatocytes ameliorated MASH-related steatosis and fibrosis by injection of adeno-associated virus 8 (AAV8) carrying miR-320 in different types of diet-induced MASH models. Mechanistic studies revealed that miR-320 specifically regulated fibroblast growth factor 1 (FGF1) production in hepatocytes by inhibiting regulator factor X1 (RFX1) expression. Notably, knockdown of Rfx1 in hepatocytes mitigated MASH by enhancing FGF1-mediated AMPK activation. Our findings underscore the therapeutic potential of hepatic miR-320 supplementation in MASH treatment by inhibiting RFX1-mediated FGF1 suppression.

Villitis of unknown etiology (VUE) occurs in up to 15% of term placentas. Patients with VUE exhibit increased incidence of gestational diabetes mellitus, gestational hypertension, and preeclampsia, with demonstrated recurrence risk. VUE contributes to various adverse pregnancy outcomes. Its pathogenesis involves abnormal maternal immune responses against fetal allografts and may relate to unidentified microbial infections. Currently, VUE diagnosis relies exclusively on placental pathological examination. Clinical management remains primarily symptomatic, though immunomodulatory therapies show potential. This review summarizes recent advances in VUE epidemiology, pathogenesis, clinical significance, pathological features, and preventive strategies, aiming to enhance clinical understanding of this condition.

Objective To investigate the influence of herbal compatibility on the chemical composition of Banxia Houpo Decoction(BHD)using ultra-performance liquid chromatography-tandem mass spectrometry(UPLC-MS)coupled with multivariate statistical analysis,and to evaluate the neuroprotective effects of key differential components against neuroinflammation and neuronal injury using cellular models.Methods(1)UPLC-MS analysis of chemical constituents in co-decoction and separated decoction(individual herbs decocted separately then combined)of Banxia Houpo Decoction,followed by orthogonal partial least squares-discriminant analysis(OPLS-DA)to identify differential components before and after herbal compatibility(2)BV2 microglia were stimulated with lipopolysaccharide(LPS)to establish a neuroinflammation model.Cell viability was assessed using the Cell Counting Kit 8(CCK-8)assay.Nitric oxide(NO)levels were measured by the Griess method,while TNF-α and IL-1β concentrations were quantified via enzyme-linked immunosorbent assay(ELISA).(3)SH-SY5Y neuronal cells were co-cultured with conditioned medium from LPS-stimulated BV2 cells(LPS-CM)to model neuronal injury.Cell viability was evaluated using the CCK-8 assay.Results UPLC-MS/OPLS-DA identified 11 differential components between compatibility methods,with honokiol and magnolol showing significant post-compatibility increases.In the neuroinflammation model,LPS stimulation elevated NO,TNF-α and IL-1 β levels in BV2 cells,which were suppressed by 5,10 μg/mL honokiol or magnolol.In the neuronal injury model,LPS-CM induced SH-SY5Y apoptosis,while 5,10 μg/mL honokiol or magnolol attenuated this damage.Conclusion Herbal compatibility significantly enhances honokiol and magnolol content in BHD.These components inhibit microglial inflammatory responses and neuronal apoptosis,suggesting their role as primary active constituents mediating BHD's neuroprotective effects.

The clinical characteristics of a neonatal patient with movement disorder and arthrogryposis (NDEEMA) caused by gain-of-function mutation of the SCN1A gene were reported in this article. The 1-year-and-9-month-old boy started seizures since 2 hours after birth. He had funnel-breast, dislocation of the hip, and bipedal varus. Genetic testing showed SCN1A gene de novo missense mutation c.706A>G(p.Ile236Val), causing overall gain-of-function effect. The frequency of seizures decreased significantly after treatment of oxcarbazepine.

The clinical characteristics of a neonatal patient with movement disorder and arthrogryposis (NDEEMA) caused by gain-of-function mutation of the SCN1A gene were reported in this article. The 1-year-and-9-month-old boy started seizures since 2 hours after birth. He had funnel-breast, dislocation of the hip, and bipedal varus. Genetic testing showed SCN1A gene de novo missense mutation c.706A>G(p.Ile236Val), causing overall gain-of-function effect. The frequency of seizures decreased significantly after treatment of oxcarbazepine.

Villitis of unknown etiology (VUE) occurs in up to 15% of term placentas. Patients with VUE exhibit increased incidence of gestational diabetes mellitus, gestational hypertension, and preeclampsia, with demonstrated recurrence risk. VUE contributes to various adverse pregnancy outcomes. Its pathogenesis involves abnormal maternal immune responses against fetal allografts and may relate to unidentified microbial infections. Currently, VUE diagnosis relies exclusively on placental pathological examination. Clinical management remains primarily symptomatic, though immunomodulatory therapies show potential. This review summarizes recent advances in VUE epidemiology, pathogenesis, clinical significance, pathological features, and preventive strategies, aiming to enhance clinical understanding of this condition.

Objective:To explore the early-stage language characteristics of children with autism spectrum disorder (ASD), global developmental delay (GDD), and developmental language disorder (DLD) at the same deve-lopmental level, thus providing references for their diagnosis.Methods:Clinical data of 719 children, involving 382 ASD patients, 198 DLD patients and 139 GDD patients presented to the Children′s Hospital Affiliated to Chongqing Medical University from January 2018 to January 2020 were retrospectively analyzed. Chi- square test was used to compare the developmental distribution of 3 groups.Variance analysis was used to analyze difference of developmental levels among 3 groups.Correlation analysis was used to analyse relationship between language and nonverbal abilities.At the same developmental, student′s t test was used to compare ASD with GDD, ASD with DLD in language ability, and difference of expression with receptive and visual related language. Results:The nonverbal developmental levels of ASD, GDD, DLD children were significantly different ( χ2=414.64, P<0.01). Language abilities were correlated with non-verbal developmental levels( r=0.60, P<0.05). The receptive and visual-related language abilities of ASD children with abnormal developmental level were more delayed compared with that of expressive language ( t=6.97, 3.58, 13.29, 6.85, 9.09, 7.27, all P<0.01). Expressive language of DLD children with normal developmental level was worse than visual-related and receptive language( t=-2.21, -3.61, all P<0.05). In GDD children with mild delayed development, receptive language was worse than expressive and visual-related language ( t=4.12, -4.24, all P<0.01), GDD children with moderate and worse development had worse visual-related and receptive language than the expression ( t=2.46, 2.68, all P<0.01). No significant differences in the expressive, receptive and visual-related language were detected in ASD and DLD children with normal development level and those with delayed development level (all P>0.05). Receptive and visual related language of ASD children with marginal delayed development level were significantly worse than those of DLD children ( t=-4.64, -4.60, all P<0.01), whereas no significant diffe-rence in the expression was detected ( P>0.05). In ASD children with mild delayed developmental level, the receptive and visual-related language were worse than those of GDD children( t=-4.11, -4.68, all P<0.01), whereas no significant difference in the expression was detected ( P>0.05). Conclusions:In early childhood, ASD children with abnormal developmental levels present severe delay in receptive and visual related language.DLD children with normal development have an obvious delay in expressive language.The language abilities of GDD children are globally delayed, especially the receptive language.In the marginal and mild delayed developmental level, ASD is featured by obvious delay of receptive and visual-related language.In normal and worse delayed development levels, the development of language in ASD, DLD and GDD children is similar.

OBJECTIVE To investigate the effects of osthole （OST） on renal interstitial fibrosis in diabetic nephropathy （DN） model mice. METHODS The diabetic mice model was established by the tail vein injection of streptozotocin once， and the DN model was established by feeding for 12 weeks after successful modeling of diabetes. Diabetic model mice were randomly divided into model group， low-dose， moderate-dose， high-dose groups （20， 40， 80 mg/kg） of OST， with 10 mice in each group. After successful modeling of diabetes， the mice were given corresponding drugs or solvent （model group） intragastrically， once a day， for consecutive 12 weeks， and the normal control group was set up at the same time. After the last administration， the levels of fasting blood glucose， 24 h urinary protein， serum creatinine （Scr） and blood urea nitrogen were tested in each group. Masson staining was used to observe the deposition of collagen fibers in renal interstitium； the expressions of E-cadherin and vimentin in renal cortex were detected by immunohistochemical staining. The protein expressions of follistatin-like protein 1 （Fstl1） and Snail family transcriptional repressor 1 （Snail1）， the phosphorylation of protein kinase B （Akt） （calculated by p-Akt/Akt） in the renal cortex were detected by Western blot. RESULTS Compared with normal control group， the levels of fasting blood glucose， 24 h urinary protein， Scr and blood urea nitrogen， collagen fiber deposition ratio of renal interstitium， the expression of vimentin， protein expressions of Fstl1 and Snail1， p-Akt/Akt in renal cortex were increased significantly （P＜0.01）， as well as the expression of E-cadherin was decreased significantly （P＜0.01）. Compared with model group， above indexes of OST groups were reversed significantly （P＜0.05 or P＜0.01）. CONCLUSIONS Preventive use of OST can effectively reduce fasting blood glucose level， protect renal function and inhibit epithelial-mesenchymal transition of DN model mice， and delay the progression of renal interstitial fibrosis ， the mechanism of which may be associated with the suppression of Fstl1/Akt/Snail1 signaling pathway.

Objective:To determine whether insulin resistance is associated with all-cause mortality in subjects without diabetes.Methods:A total of 505 participants without diabetes, 198 with normal glucose tolerance (NGT) and 307 with impaired glucose tolerance (IGT), were recruited from the Daqing Diabetes Study. The participants were followed up for 30 years. They were stratified into three groups (tertiles) according to baseline homeostasis model assessment of insulin resistance(HOMA-IR) levels, as the HOMA-IR 0, the HOMA-IR 1 and the HOMA-IR 2 groups, to assess the predictive effect of insulin resistance on risk of all-cause mortality.Results:During the 30-year follow-up, 52, 56 and 78 participants died across the three HOMA-IR groups, respectively. The corresponding mortality per 1 000 person-years (95 %CI) were 12.12 (9.56-15.01), 13.10 (10.46-16.03) and 19.91 (16.73-23.15), respectively. Participants in the HOMA-IR 2 group had a significantly higher risk of death than those in the HOMA-IR 0 group after adjustment of age, sex and smoking status ( HR=1.97,95 %CI 1.38-2.81, P<0.001). Cox analyses showed that a one standard deviation increase in HOMA-IR was associated with a 22% increase in the mortality after adjustment of potential confounders ( HR=1.22, 95 %CI 1.08-1.39, P=0.002). Conclusions:Insulin resistance is associated with increased risk of all-cause death in Chinese people without diabetes, suggesting that improving insulin resistance could be beneficial for people without diabetic in reducing risk of long-term all-cause mortality.

Objective:To investigate the physical indices and growth status of preterm children aged 0 to 4 years with different birth weight.Methods:Following the real world research approach, the current study retrospectively collected e-chart information of 8 496 preterm children from the child health care system of the Children′s Hospital of Chongqing Medical University from December 2010 to December 2017, with 203 123 full-term children followed up during the same period as controls. Premature children were divided into normal birth weight (NBW) group, low birth weight (LBW) group, and very low birth weight (VLBW) group based on their birth weights. The weight and length development within 48 months of age of preterm boys and girls in each group were measured and recorded to establish a numerical table and analyze the growth levels, growth rate, and proportionality. The t-test or chi-square test was used for between-group comparison. Results:Of the 8 496 preterm children, 4 839 were girls and 3 657 boys, including 525 in the VLBW group, with an average birth weight of (1.28±0.14) kg, 3 862 in the LBW group, with an average birth weight of (2.07±0.28) kg, and 4 109 in the NBW group, with an average birth weight of (2.86±0.35) kg. The weight at the actual age of 2-<3 months ((5.61±0.96) vs. (5.64±0.78) kg in boys, (5.11±0.67) vs. (5.18±0.71) kg in girls) and the length at the actual age of 8-<10 months ((70.3±2.4) vs. (70.6±2.4) cm in boys, (68.9±2.2) vs. (68.9±2.4) cm in girls) in the NBW group reached the average weight and length of full-term children. The difference of physical growth before 24 months of age between LBW and control group decreased as children age, with that of LBW group approaches the average of full-term children after 24 months of age, with a weight difference of 0.64-0.95 kg and height difference of 1.3-1.7 cm. The weight and height of the VLBW group were lower than those of full-term infants (2.80-2.86 kg and 3.3-4.3 cm, respectively) at 48 months of age. During 2-12 months of age, the corresponding values of the VLBW group were higher than that of the LBW and NBW groups by 0.35 kg and 0.71 kg, respectively. However, the corresponding values of the VLBW group were lower than that of the LBW and NBW groups(0.64 kg and 0.76 kg at 0-2 months of age, 1.04 kg and 1.49 kg at 12-48 months of age, respectively). The rates of delayed development, underweight, and emaciation were the highest in the VLBW group (all P<0.01), while the rates of overweight and obesity were the highest in the NBW group, with that of the VLBW group being lower than LBW group ( P<0.01) at the age of 24-<36 months. Conclusions:Prior to 4 years of age, the time for preterm children to reach the average physical indices of full-term children differ by birth weights, hence warranting further examination of the corrected gestational age for preterm children. Normal birth weight preterm children present with the highest incidence of overweight and obesity and very low birth weight preterm children present with the highest incidence of growth disorders, marking both groups at high risks of malnutrition.