The Different Effects of Skeletal Muscle and Fat Mass on Height Increment in Children and Adolescents Aged 6-11 Years: A Cohort Study From China.

Objective: This study aimed to investigate the contribution of body composition including skeletal muscle mass (SMM) and body fat mass (BFM) to longitudinal growth among children and adolescents aged 6-11 years old. Methods: This cohort study was conducted from the annual health examination between 2019 and 2020. Annual height gain and weight gain and changes in SMM and BFM were calculated and compared between sexes, different nutritional status, and growth curve shifting mode. Spearman analyses and multiple linear regression analysis were performed to identify the impact of SMM, BFM, or body mass index (BMI) on height gain. Results: Of the 584 subjects, the annual height gains of boys (4.76 cm in the 6-9-year group and 4.63 cm in the 10-11-year group) were significantly lower than those of girls (5.48 and 5.74 cm, respectively). Spearman analysis showed that SMM gain and height gain were positively and significantly correlated in each examination of all children (r = 0.535 for boys and 0.734 for girls, p < 0.001). Conversely, BFM and height gains were negatively (r = -0.5240 for boys and -0.232 for girls, p < 0.001) correlated. Multiple linear regression analysis identified SMM gain as an independent predictor (95% CI: 1.20,1.44) of height gain after adjusting for age, gender, BMI, BFM gain, and percentage of body fat (PBF). Conclusion: SMM gains, rather than BFM gains, were associated with height gains in children and adolescents aged 6-11 years. Monitoring SMM changes in routine healthcare might motivate children and adolescents to achieve dietary and exercise recommendations, thereby growing taller without gaining excessive weight.

Effectiveness of ultrasound-guided percutaneous transhepatic puncture for the diagnosis of low-level alpha-fetoprotein liver cancer patients.

BACKGROUND: Globally, liver cancer is the most frequent fatal malignancy. The aim of the present study was to explore the effectiveness of ultrasound (US)-guided percutaneous transhepatic puncture in patients with low-level alpha-fetoprotein (AFP) liver cancer. METHODS: A total of 300 patients with primary liver cancer (PLC) (with AFP level ≤200 ng/mL and who underwent fine-needle aspiration) who were admitted to Central South University Xiangya School of Medicine Affiliated Haikou Hospital from January 2016 to December 2020 were selected to participate in the present study. Data, such as the expression of AFP and the biological characteristics of cells related to follow-up information, were retrospectively analyzed. RESULTS: Patients with AFP content <50 ng/mL accounted for 27% of total patients. Patients with tumors <20 mm accounted for 11% of total patients. There were 88 patients with 0-50 ng/mL AFP, 75 patients with 51-100 ng/mL AFP, 57 patients with 101-150 ng/mL AFP, and 83 patients with 200 ng/mL AFP. The sensitivity of detection was ≥90%, specificity was 100%, PPV was 100%, and NPV was ≥90%. In the present study, 34 patients with tumors <20 mm in size underwent US-guided percutaneous transhepatic puncture. The sensitivity of the treatment was 93.33%, 100% specificity, 100% PPV, and 64.35% NPV. The sensitivity of US-guided percutaneous transhepatic puncture was 97.65%, 100% specificity, 100% PPV, and 55.42% NPV in 266 patients with tumor size >20 mm. Implantation and metastasis accounted for 5% of complications, and gastrointestinal bleeding accounted for 7%. Among the adverse reactions, nausea and vomiting accounted for 15%, diarrhea accounted for 10%, and bone marrow suppression accounted for 8%. CONCLUSIONS: US-guided percutaneous transhepatic puncture has high sensitivity, high specificity, and is relatively safe, with a low complication rate in patients with low-level AFP liver cancer, and has certain clinical diagnostic value.

The protective effect of Trillin LPS-induced acute lung injury by the regulations of inflammation and oxidative state.

Inflammation response and oxidative stress have been reported to be involved in the pathogenesis of acute lung injury (ALI). Accordingly, anti-inflammatory treatment is proposed to be a possible efficient therapeutic strategy for ALI. The purpose of our present study was to evaluate the anti-inflammatory efficacy of trillin (Tr) on ALI induced by lipopolysaccharide (LPS) in mice and explore the underlying mechanism. BALB/c mice received Tr (50, 100 mg/kg) intraperitoneally 1 h prior to the intratracheal instillation of lipopolysaccharide (LPS) challenge. Pretreatment with Tr at the dose of 50, 100 mg/kg markedly ameliorated lung wet-to-dry weight (W/D) ratio, myeloperoxidase (MPO) activity and pulmonary histopathological conditions. In addition, the protective efficacy of Tr might be attributed to the down-regulations of neutrophil infiltration, malondialdehyde (MDA), inflammatory cytokines and the up-regulations of super-oxide dismutase (SOD), catalase(CAT), glutathione(GSH), Glutathione Peroxidase(GSH-Px) in bronchoalveolar lavage fluid (BALF). Meanwhile, our study revealed some correlations between (NF-E2-related factor 2) Nrf2/heme oxygenase (HO)-1/nuclear factor-kappa B (NF-κB) pathways and the beneficial effect of Tr, as evidenced by the significant up-regulations of HO-1 and Nrf2 protein expressions as well as the down-regulations of p-NF-κB and p-inhibitor of NF-κB (IκB) in lung tissues. Taken together, our results indicated that Tr exhibited protective effect on LPS-induced ALI by the regulations of related inflammatory events via the activations of Nrf2, HO-1 and NF-κB pathway. The current study indicated that Tr could be a potentially effective candidate medicine for the treatment of ALI.

Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway.

The purpose of this study was to investigate the protective effect of PD against lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explore its potential mechanism. In vivo, PD and dexamethasone were intraperitoneally administered 1h before LPS stimulation. Then, mice were sacrificed at 6h post-LPS stimulation. Neutrophil number, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) in bronchoalveolar lavage fluid (BALF) were determined, as well as lung wet to dry ratio (W/D) and polymorphonuclear (MPO) activity. The protein expressions of Toll like receptor 4 (TLR4), myeloid differentiating factor 88 (MyD88), IL-1R-associated kinases 1 (IRAK1), IRAK4, inhibitor of nuclear factor kappa-B kinase (IKK)α, p-IKKα, IKKß, p-IKKß, inhibitor of NF-κB (IκBα), p-IκBα and NF-κB in lung tissues were assessed. Besides, we detected the IL-6, IL-1ß, IL-8, TNF-α levels and TLR4, MyD88, NF-κB protein expressions in LPS-induced BEAS-2B cells. Consequently, PD significantly inhibited the levels of W/D, MPO, neutrophils number, TNF-α, IL-6, IL-1ß and reversed TLR4-MyD88-NF-κB signaling pathway in lung tissues. In vitro assays, PD effectively negatively mediated the inflammatory cytokines and ameliorated the high expressions of TLR4, MyD88, NF-κB caused by LPS simulation in Human bronchial epithelial BEAS-2B cells. This study indicated that PD played a protective role in LPS-induced ALI and BEAS-2B cells. The results supported further study of PD as potential candidate for acute lung injury.

Inhibitory Effects of Polydatin on Lipopolysaccharide-Stimulated RAW 264.7 Cells.

The purpose of this study was to evaluate the effects of polydatin (PD) on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions at protein and transcriptional levels, as well as the production of prostaglandin E2 (PGE2) and nitric oxide (NO) in lipopolysaccharide (LPS)-induced macrophage RAW 264.7 cells. To elucidate the underlying mechanism responsible for these symptoms, we investigated the phosphorylation of mitogen-activated protein kinase (MAPK) pathway and nuclear factor-κB (NF-κB) expression. NO was analyzed with the Griess method. PGE2 was measured by enzyme-linked immunosorbent assay (ELISA). iNOS and COX-2 messenger RNA (mRNA) were identified by qPCR assay. iNOS, COX-2, NF-κB, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 protein expressions were detected with Western blot. The results revealed that PD effectively inhibited NO and PGE2 production, and it is not surprising that PD reduced iNOS and COX-2 expression at protein and transcriptional levels. Additionally, PD significantly ameliorated the activation of NF-κB and the phosphorylation of MAPKs in LPS-induced RAW 264.7 macrophages. These findings suggested that PD exerted potent anti-inflammatory activity in macrophages.