[Accumulation, subcellular distribution, and chemical forms of zinc in three tree species]. / 锌在3ç§ä¹”æœ¨ä¸­çš„ç§¯ç´¯åŠå ¶äºšç»†èƒžåˆ†å¸ƒå’ŒåŒ–å­¦å½¢æ€.

In order to explore the mechanism underlying zinc (Zn) accumulation and tolerance in woody garden species, the effects of different Zn concentrations (0, 250, 500, 1000, 2000 mg·kg-1) on leaf, branch, root biomass and leaf ultrastructure of Koelreuteria paniculata, Ailanthus altissima, and Ginkgo biloba were studied in a pot pollution simulation experiment. The concentration of Zn in plant organs, the subcellular distribution and chemical forms of Zn in leaves and roots were further analyzed. The results showed that all the three species could survive under diffe-rent Zn concentrations, but the biomass of leaves, stems and roots decreased compared with the control. Excessive Zn could lead to cell deformation, cell wall rupture and organelle disintegration of leaves in K. paniculata and A. altissima, while the cells in leaves of G. biloba could maintain normal morphology, indicating that G. biloba had a better tolerance to Zn than K. paniculata and A. altissima. With the increases of Zn concentration, Zn concentration in the organs of the three species showed an increasing trend, and the Zn concentration in K. paniculata and A. altissima was significantly higher than that in G. biloba, indicating that the Zn accumulation ability of K. paniculata and A. altissima was stronger than that of G. biloba. Zn was mainly distributed in the cell walls of leaves and roots, accounting for 26.9%-71.8% and 28.1%-82.6%, respectively. Under the treatment with the highest Zn concentration (2000 mg·kg-1), Zn concentration in the soluble components (mainly vacuoles) could be higher than that in the cell walls. In addition, Zn mainly existed in NaCl-, HAc- and HCl-extracted forms in leaves, accounting for 57.4%-82.7%, and Zn mainly existed in NaCl- and HAc-extracted forms in roots, accounting for 42.8%-67.2%, all of which were forms with relatively low activity. Therefore, cell wall retention, vacuoles segregation and accumulating Zn in less active forms might be important mechanisms underlying Zn accumulation and tolerance in the three trees.

Circ_0057558 promotes nonalcoholic fatty liver disease by regulating ROCK1/AMPK signaling through targeting miR-206.

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver disorders that is featured by the extensive deposition of fat in the hepatocytes. Current treatments are very limited due to its unclear pathogenesis. Here, we investigated the function of circ_0057558 and miR-206 in NAFLD. High-fat diet (HFD) feeding mouse was used as an in vivo NAFLD model and long-chain-free fatty acid (FFA)-treated liver cells were used as an in vitro NAFLD model. qRT-PCR was used to measure levels of miR-206, ROCK1 mRNA, and circ_0057558, while Western blotting was employed to determine protein levels of ROCK1, p-AMPK, AMPK, and lipogenesis-related proteins. Immunohistochemistry were performed to examine ROCK1 level. Oil-Red O staining was used to assess the lipid deposition in cells. ELISA was performed to examine secreted triglyceride (TG) level. Dual-luciferase assay was used to validate interactions of miR-206/ROCK1 and circ_0057558/miR-206. RNA immunoprecipitation was employed to confirm the binding of circ_0057558 with miR-206. Circ_0057558 was elevated while miR-206 was reduced in both in vivo and in vitro NAFLD models. miR-206 directly bound with ROCK1 3'-UTR and suppressed lipogenesis and TG secretion through targeting ROCK1/AMPK signaling. Circ_0057558 directly interacted with miR-206 to disinhibit ROCK1/AMPK signaling. Knockdown of circ_0057558 or overexpression of miR-206 inhibited lipogenesis, TG secretion and expression of lipogenesis-related proteins. ROCK1 knockdown reversed the effects of circ_0057558 overexpression. Injection of miR-206 mimics significantly ameliorated NAFLD progression in vivo. Circ_0057558 acts as a miR-206 sponge to de-repress the ROCK1/AMPK signaling and facilitates lipogenesis and TG secretion, which greatly contributes to NAFLD development and progression.

[Adenovirus pneumonia with hemophagocytic lymphohistiocytosis in children: a clinical analysis of 7 children].

OBJECTIVE: To study the clinical features of children with adenovirus pneumonia and hemophagocytic lymphohistiocytosis (HLH). METHODS: A retrospective analysis was performed on the mediacal data of 7 children with adenovirus pneumonia and HLH from March to September, 2019. RESULTS: The age of these children ranged from 11 months to 5 years, and among these children, 5 were aged <2 years and 5 were boys. None of these children had underlying diseases. All children were hospitalized due to persistent high fever and cough, and the peak temperature of fever was 39°C to 41°C. With disease progression, 7 children developed hepatomegaly and 6 developed splenomegaly. Routine blood test results showed reductions in two or three lineages of blood cells, with increases in serum ferritin (SF), C-reactive protein (CRP), procalcitonin (PCT), and lactate dehydrogenase (LDH). Phagocytosis of blood cells was observed in 6 children. Radiological examination of lungs showed pneumonia changes. All 7 children were diagnosed with human adenovirus type 7 infection based on pathogenic metagenome detection. No abnormality was found by HLH gene detection and the children were diagnosed with secondary HLH. All children received intravenous immunoglobulin. Among these children, 4 received dexamethasone and etoposide chemotherapy, 3 received dexamethasone alone, and 4 received plasma exchange. Of the 7 children, 2 died and 5 were recovered. Compared with those who survived, the children who died had significantly greater reductions in the three lineages of blood cells and significantly greater increases in serum levels of CRP, PCT, SF, and LDH. CONCLUSIONS: The children with adenovirus pneumonia and HLH have main clinical features of persistent high fever, progressive reductions in two or three lineages of peripheral blood cells, and involvement of other organ systems, including hepatosplenomegaly. Significant increases in serum levels of CRP, PCT, SF, and LDH may suggest a poor prognosis.

LncRNA NEAT1 promotes hepatic lipid accumulation via regulating miR-146a-5p/ROCK1 in nonalcoholic fatty liver disease.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a severe liver disease, which influences the health of people worldwide. However, the specific mechanism of the disease remains unknown, and effective treatments are still lacking. It was reported that Nuclear enriched abundant transcript 1 (NEAT1) obviously was up-regulated in NAFLD model. But the role and underlying mechanism of NEAT1 in NAFLD is unclear. METHODS: HepG2 cells were treated by free fatty acids (FFA) and C57BL/6J mice were treated by high-fat diet to establish NAFLD in vitro and in vivo models, respectively. Cell transfection was applied to regulate the expression of NEAT1, ROCK1, and miR-146a-5p. Western blotting and qRT-PCR were used for measuring expression of protein and mRNA level, respectively. Dual luciferase assay was used to detect the target relationship. Oil Red O staining was used to measure the lipid accumulation. HE staining was used for observing pathological feature of liver tissues. RESULTS: High levels of NEAT1 and ROCK1, and low level of miR-146a-5p were identified in NAFLD models. NEAT1 could target miR-146a-5p to promote ROCK1 expression. Knockdown of NEAT1, overexpression of miR-146a-5p and knockdown of ROCK1 inhibited lipid accumulation through activating AMPK pathway. CONCLUSION: NEAT1 may regulate NAFLD through miR-146a-5p targeting ROCK1, and further affect AMPK/SREBP pathway. This study may provide a new thought for the treatment of NAFLD.

[Association between acanthosis nigricans and metabolic syndrome in children with obesity].

OBJECTIVE: To investigate adipokines levels in obese children with acanthosis nigricans (AN) and to explore the relationship between AN and metabolic syndrome (MS). METHODS: A cross-sectional study was performed on 109 obese children and 47 age- and gender-matched normal controls. The obese children were divided into two groups with AN and without AN. Serum levels of adiponectin, leptin, TNF-α and retinol-binding protein 4 (RBP4) were measured using ELISA. Multiple logistic regression analysis was performed to estimate the association of clinical parameters with MS. RESULTS: Waist-hip ratio, systolic blood pressure, triglyceride, fasting insulin and insulin resistance index (HOMA-IR) were significantly higher in obese children with AN than in those without AN and normal controls (P<0.05). The obese children with AN and without AN had lower adiponectin levels than normal controls (P<0.05), on the contrary, the obese children with AN had higher leptin levels than those without AN and normal controls (P<0.05). Multiple logistic regression analysis revealed that AN (OR=3.469, 95%CI: 1.518-7.929) and BMI (OR=7.108, 95%CI: 2.359-21.416) were independent risk factors for MS. CONCLUSIONS: As a visible marker of insulin resistance, AN is associated with abnormal adipokines secretion. Reducing the incidence of AN and losing weight may prevent obesity associated MS.

[Research advances on CIDEC in insulin resistance].

Childhood obesity has been rising dramatically in recent years and most patients are insulin resistant. Recent studies have indicated that cell death-inducing DFF45-like effector C (CIDEC) is responsible for the development of insulin resistance. CIDEC regulates adipogenesis, lipid storage and lipolysis, thus protecting insulin target tissues from lipotoxity. This paper reviews current findings on the structure and function of CIDEC, its transcriptional and post-translational regulations, and the underlying mechanism of CIDEC causing insulin resistance. As a novel lipid droplet protein, CIDEC may be a drug target for treatment of insulin resistance and relevant metabolic disorders.