Autophagy is the cell biology process in which cytoplasmic components are degraded in lysosomes to maintain cellular homeostasis,it is involved in the pathophysiology of several kidney diseases (podocytopathies,IgA nephropathy,diabetic nephropathy,hereditary kidney disease),but its specific effect is still controversial.Most studies suggest that autophagy plays a protective role in kidney diseases,in the future,it may become a new target for the prevention and treatment of kidney disease.

Objective: To investigate the effects of hepatitis B virus (HBV) X protein (HBx) on the expression of tumor necrosis factor-α (TNF-α) in glomerular mesangial cells (GMCs) and the underlying intracellular signal pathways. Methods: The plasmid pCI-neo-X that carries the X gene of hepatitis B virus was transfected into cultured GMCs. HBx expression in the transfected GMCs was assessed by Western-blot. TNF-α protein and mRNA were assessed by ELISA and semi-quantitative RT-PCR, respectively. Three kinase inhibitors-U0126, an inhibitor of extracellular signal-regulated kinases (ERKs);lactacystin, an inhibitor of nuclear factor-κB (NF-κB);and SB203580, a selective inhibitor of p38 MAP kinase (p38 MAPK) were used to determine which intracellular signal pathways may underlie the action of HBx on TNF-αexpression in transfected GMCs. Results:A significant increase in HBx expression in pCI-neo-X transfected GMCs was detected at 36 h and 48 h, which was not affected by any of those kinase inhibitors mentioned above. A similar increase in the expression of both TNF-αprotein and mRNA was also observed at 36 h and 48 h, which was significantly decreased in the presence of U0126 or lactacytin, but not SB203580. Conclusions:HBx upregulates TNF-αexpression in cultured GMCs, possibly through ERKs and NF-κB pathway, but not p38 MAPK pathway.

Kidney remodeling is a response to intrinsic or extrinsic triggers of kidney injury.The response potentialy control life-threatening dangers and to regain homeostasis,including tissue repair,inflammation to control the risk of infection,epithelial repair,scar resolution or minimization.Mesangial cell involved in clotting,fibrinolysis,triggering glomerular inflammation and mesangioproliferative disorders.Mesangial cell may play an important role in the devoloping of glomerular diseases and in controlling the risks of these diseases.

ObjectiveTo compare the therapeutic effec between sustained low-efficiency dialysis (SLED) and continuous blood purification (CBP) in critically ill patients.MethodsAccording to the treatment ways,96 critically ill patients were divided into SLED group and CBP group.A comparison was made on the biochemical indicators,in-hospital duration,hemodynamic parameters,acute physiology and chronic health evaluation (APACHE-Ⅱ ),the survival and the mortality rates.ResultsAfter treatment,the levels of serum creatine kinase isozyme MB (CK-MB),creatine kinase (CK),creatinine (Cr),glutamic-oxalacetic transaminase (AST),glutamate-pyruvate transaminase (ALT),APACHE Ⅱ score on the 1st,2nd and 7th day were lower than those prior to the treatment in both groups ( P ＜0.05).There were no statistical differences in in-hospital duration, biochemical indicators, APACHEⅡscore,hemodynamic parameters,the survival rate and the mortality rate between the two groups (P ＞ 0.05 ).ConclusionsSLED has similar hemodynamic stability with CBP,and the two methods have similar treatment effects in critically ill patients.However,SLED can be relatively economical and convenient for critically ill patients in clinical.

Attention deficit hyperactivity disorder (ADHD) is one of the common neurodevelopmental disorders in childhood characterized by inattention,hyperactivity,impulsivity,cognitive impairment and learning difficulties and has a negative effect on children.The specific pathogenesis of ADHD is not fully clear.Recent studies have found that there are interactions between monoaminergic system and hypothalamic-pituitary-adrenal axis,in which the machanism is associated with transcription factors,such as Spl、KLF11、R1.This article reviews the characteristics of the monoaminergic system and hypothalamic-pituitary-adrenal axis in attention deficit hyperactivity disorder,and the machanism with transcription factors.

Objective: To study the effect of ketogenic diet (KD) on vascular endothelial function in children with intractable epilepsy. Methods: Clinical informations of 14 children with intractable epilepsy in Fujian Medical University Affiliated Union Hospital from May 2014 to March 2018 were collected.Their blood index values were tested and retested before and after 3 months of KD treatment, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), low density lipoprotein (LDL), nitric oxide (NO), endothelin-1 (ET-1), and von Willebrand factor (vWF). These data were statistically analyzed by using repeated measurement analysis of variance. Results: (1)Changes in blood lipid levels: the levels of TG and TC increased slightly [(1.08±0.14) mmol/L, (5.19±0.64) mmol/L vs.(0.97±0.10) mmol/L, (4.57±0.29) mmol/L]and the level of HDL decreased slightly [(1.19±0.08) mmol/L vs.(1.31±0.08) mmol/L]after 3 months of KD treatment, but the differences were not statistically significant in the above indexes (all P>0.05). The level of LDL before KD was significantly lower than that after 3 months of KD [(2.93±0.25) mmol/L vs.(3.73±0.40) mmol/L ], and the difference was statistically signi-ficant(P=0.034). (2)Assessment of vascular endothelial function: compared with before KD, all the levels of NO [(60.84±5.29) μmol/L vs.(66.45±5.39) μmol/L ], ET-1 [(1.24±0.30) ng/L vs.(2.13±0.78)ng/L] and vWF [(150.53±12.97) μg/L vs.(137.57±13.10) μg/L]had no statistically significant changes after 3 months of KD(all P>0.05). Conclusions KD treatment lasting 3 months in children with intractable epilepsy can raise the level of LDL, but can′t change the vascular endothelial function.

Th17 cell is a newly developed CD4 +T cell subsets,play a pro-inflammatory role and participate in the pathogenesis of many autoimmune diseases mainly through secretion of cytokines such as interleukin-17 (IL-17),many of the biological effects of Th17 cells are closely related to the IL-17,this article reviews the relation-ship between Th17/IL-17 axis and related cytokines and kidney the pathogenesis of disease,in order to more in-depth understanding of the pathogenesis of kidney disease,provide the basis for looking for new targets of diagnosis and treatment of kidney disease and new treatment strategies.

The X gene of HBV encodes a 17-KD protein, termed HBx, which has been shown to function as a transcriptional trans-activator of a variety of viral and cellular promoter/enhancer elements. The aim of this study was to investigate the effect of HBx on gene expression of interleukin (IL)-1β and IL-6, and proliferation of rat mesangial cells in vitro. The X gene of HBV was amplified by PCR assay, and inserted into the eukaryotic expression vector pCI-neo. The structure of recombinant pCI-neo-X plasmid was proved by restrict endonuclease digestion and sequencing analysis. pCI-neo-X was transfected into cultured rat mesangial cell line in vitro via liposome. HBx expression in transfected mesangial cells was detected by Western blot. The IL-1β and IL-6 mRNA expression in those cells was assayed by semiquantitative RT-PCR. Mesangial cell proliferation was tested by MTT. The results showed that HBx was obviously expressed in cultured mesangial cell line at 36th and 48th h after transfection. The expression of IL-1β and IL-6 mRNA was simultaneously increased. The cell proliferation was also obvious at the same time. It was concluded that HBx gene transfection could induce IL-1β and IL-6 gene expression and mesangial cell proliferation. HBx may play a critical role in mesangial cell proliferation through upregulation of the IL-1β and IL-6 gene expression.

Autism spectrum disorder(ASD)is a severe neurodevelopmental disorder of children that leads to disability which lacks of effective treatment.The specific pathogenesis of ASD remains unclear,which may involve in multiple factors.In recent years,many studies have shown that children with ASD have gastroin-testinal(GI)abnormalities and some special diet therapies can effectively ameliorate the symptoms of ASD. These diets include gluten free diet,sensitive or harmful food removing therapy and ketogenic diet.The patients with ASD have GI inflammation or allergy,energy metabolism disorder,oxidative stress injury,neurotransmitter disturbance and dysbiosis of intestinal flora.Diet therapy may improve ASD symptoms by correcting disorders a-bove.This article reviews the application and the related mechanism of diet therapy in ASD children and the effect of diet therapy on the growth and the development of children.

Objective To explore the clinical and the genetic features of infantile neuroaxonal dystrophy (INAD).Methods The clinical and laboratory data,neuroimaging examination and genetic testing results of one child with INAD were retrospectively analyzed.Results A 2 years old boy presented motor and verbal dexterity regression and hypotonia.Laboratory findings revealed decreased total iron-binding capacity in serum with increased glutamic oxaloacetic transaminase (AST) and lactic dehydrogenase (LDH).Myoelectrography showed neurogenic impairments of the arms and legs,and the color doppler ultrasound of the heart,video-EEG and brain MRI results were normal.A homozygous mutation of c.1077G＞A was found in PLA2G6 gene of the infant.The infant's parents were heterozygous mutation carriers at this locus.Conclusions PLA2G6 gene mutations cause INAD.