Objective: To understand the level of nutritional literacy and its influencing factors among schoolage children in grades 4-9 in Guizhou Province, and to explore the relationship between nutritional literacy and physical health, so as to provide reference for improving nutritional literacy and physical health of schoolage children. Methods: Using multistage stratified cluster sampling method, 1 155 schoolage children in grades 4-6 in elementary school and grades 7-9 in secondary schools in three prefectural and municipal cities of Guizhou Province (Zunyi, Tongren, and Bijie) were sampled from February to July 2023, and were surveyed for nutritional literacy by using the "Food and Nutritional Literacy Questionnaire for Chinese Schoolage Children", and their physical health data (data on body measurement indicators, such as height, weight, lung capacity, and vertical jump) were obtained from the physical health surveillance platform. Pearson correlation analysis and binary Logistic regression modeling were used to explore the association between nutritional literacy and physical health. Results: The nutritional literacy score of the study population was (63.50±8.63), and the scores of each level of nutritional literacy in descending order were interactivity (66.09±13.99), functionality (63.84±8.80), and criticism (61.15±14.65); and the scores of cognitive domain of nutritional literacy, and skill domain were (64.71±10.77) (62.97±9.21); food selection, food preparation, and food intake dimension scores were (64.68±13.52) (56.39±12.17) (63.63±10.04), respectively. Differences in the total nutritional literacy scores of schoolaged children who were only children or not, by gender, ethnicity, grade level, primary caregiver, primary caregivers education, and family economic situation were statistically significant (t/F=2.88, -3.28, 5.02, 18.32, 4.67, 32.47, 32.53, P<0.05); the physical health pass rate was 85.8%, and the mean scores of the total physical health score, physical form, physical function, and physical fitness dimensions were (71.86±10.52) (93.29±12.06) (72.12±14.42) (67.26±13.13), respectively; after controlling for confounders, the nutritional literacy scores were positively correlated with physical health (OR=1.03, 95%CI=1.01-1.05, P<0.05). Conclusion Nutritional literacy scores of schoolage children in grades 4-9 in Guizhou Province are low, and there is a positive correlation between nutritional literacy and physical health in this school age children.

BACKGROUND:Cadmium is a common environmental pollutant,which can damage multiple organs and tissues,such as the kidney and bone,but its effect on annulus fibrosus cells in the intervertebral disc has been less reported. OBJECTIVE:To investigate the effect of cadmium chloride on the senescence of annulus fibrosus cells and the role of PI3K/Akt signaling pathway. METHODS:Annulus fibrosus cells from Sprague-Dawley rat intervertebral discs were harvested and passage 3 cells were intervened with different concentrations of cadmium chloride(0,1,5,10,20 μmol/L).Cell viability and proliferation were detected by cell counting kit-8 assay.Transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis were performed on annulus fibrosus cells with or without cadmium chloride addition.Passage 3 annulus fibrosus cells were divided into control group,cadmium chloride group and LY294002 group.Cell proliferation rate was detected by EdU method,positive cell rate was detected by senescence-associated β-galactosidase staining,and expressions of senescence-associated proteins(p16,p21 and p53)and p-Akt at protein and mRNA levels were measured by western blot,RT-PCR and immunofluorescence. RESULTS AND CONCLUSION:5 μmol/L cadmium chloride could inhibit the proliferation of annulus fibrosus cells.Results from the Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis showed that the main signal transduction pathways included PI3K/Akt,cell cycle and p53 signaling pathways,which were related to cell senescence and proliferation.PI3K/Akt signaling pathways with significant differential expression were selected for validation.Compared with the control group,the EdU-positive rate was significantly decreased in the cadmium chloride group(P<0.05),while the β-galactosidase-positive rate,the expression of senescence-associated proteins(p16,p21 and p53)and p-Akt significantly increased(P<0.05).Compared with the cadmium chloride group,the EdU-positive rate and p-Akt expression were significantly decreased in the LY294002 group(P<0.05),while the β-galactosidase-positive rate and the expression of senescence-associated proteins(p16,p21 and p53)significantly increased(P<0.05).To conclude,cadmium chloride can regulate the senescence of annulus fibrosus cells by activating the PI3K/Akt signaling pathway,thereby inducing the occurrence and progression of intervertebral disc degeneration.

To improve patient-centered pharmaceutical management and pharmaceutical service capabilities in the pharmaceutical department of medical institutions,automation and information technology are indispensable.The Pharmacy Administration-Automation and Information Technology is one of the social organization standards of the Chinese Hospital Association as part 4-4 of Pharmaceutical Administration and Pharmaceutical Practice in Healthcare,which standardizes 32 key elements in four aspects:basic requirements for automation construction in medical institutions,construction of automation hardware equipment,construction of intelligent information platform,and quality management and continuous improvement.It can be used to guide medical institutions at all levels to select and optimize pharmacy automation equipment and information platforms.This article introduced the construction methods and contents of the pharmacy automation and information technology standards,to deepen the understanding of peers on this standard and promote its implementation.This article aimed to promote the modernization,informatization,and intelligence of pharmaceutical services in medical institutions,and improve the quality and efficiency of overall medical pharmaceutical administration and service.

Objective: To isolate and identify the undescribed compounds from the fruits of Cinnamomum migao and evaluate its nitric oxide inhibition potential. Methods: The chromatographic techniques of silica gel, Sephadex, and HPLC were used for isolation and purification of the compounds, while HR-ESI-MS, 1D NMR, 2D NMR, ECD, and X-ray diffraction techniques were used to characterize and confirm the isolated compounds. Moreover, the anti-inflammatory activity of the isolated compounds was carried out to check inhibitory potential against the production of nitric oxide with RAW264.7 cells stimulated by LPS. Results: Camganoid A (1), a novel sesquiterpene possessing an unprecedented skeleton, and camganoid B (2), containing a unique eight-membered sesquiterpene moiety with a new carbon skeleton, were isolated and identified from the fruits of C. migao. The absolute configurations of 1 and 2 were confirmed by single crystal X-ray diffraction and electronic circular dichroism (ECD) calculations. Among these compounds, compound 1 exhibited potent inhibitory activity against the production of nitric oxide with IC

Objective: To investigate the effect of 1q21 amplification (1q) on the therapeutic response and prognosis of bortezomib(Btz) in the treatment of newly diagnosed multiple myeloma (MM) patients. Methods: A total of 180 newly diagnosed MM were included for analyses of clinical characteristics, cytogenetics, objective response rate (ORR), progression-free survival (PFS) and overall survival (OS), retrospectively. Gene expression profiling (GEP) was analyzed using publicly available R2 platform. Results: ① In 180 patients, 1q was found in 51.1% cases. Of them, 174 patients had complete follow-up data, including 88 cases with 1q and 86 without 1q (non-1q). ②Incidence of 1q was positively associated with percentage of IGH rearrangement (72.2%, P=0.017) and 1p deletion (1p) (27.8%, P=0.040). ③ The median PFS was 15.0 and 20.3 months for the 1q group and non-1q group, and the median OS was 29.4 and 44.0 months, respectively. Both PFS and OS of 1q group was significantly shorter than those of the non-1q group (P=0.029 and 0.038, respectively). Multivariate analysis further revealed that 1q was an independent prognostic factor for both PFS (HR=1.910, 95% CI 1.105-3.303, P=0.020) and OS (HR=2.353, 95% CI 1.090-5.078, P=0.029). ④ In 91 evaluable cases with 1q, very good partial remission (VGPR) rate was higher after treatment with Btz than those without Btz (62.1% vs 40.0%, P=0.032). Of note, the patients with 1q who received auto-HSCT after induction with Btz had significantly longer PFS than those without auto-HSCT (19 months vs 13 months, P=0.048). ⑤GEP analysis revealed that 1q21 amplification predominantly up-regulated expression of >50% genes within 1q21 region, and also altered expression of 28% genes in chromosome 1 and 10% genes in whole genome, particularly related to DNA repair and cell cycle. Conclusions 1q is an independent adverse prognostic factor in patients with newly diagnosed MM. It is often associated with 1p deletion and IGH rearrangement. Patients with 1q respond well to Btz-based regimen, but they fail to gain long-term benefit from this treatment itself. However, auto-HSCT following Btz induction might improve survival of patients with 1q, suggesting a potential strategy to treat this high-risk subset of MM. GEP analysis warrants further attention in understanding the mechanisms underlying the high-risk of 1q.

Objective To evaluate the role of autophagy in dexmedetomidine-induced reduction of lipopolysaccharide ( LPS)-caused inflammatory responses in macrophages of mice. Methods Mouse mac-rophage cell line RAW264. 7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups ( n=20 each ) when cell confluence reached 60％ using a random number table method: control group (group Con), LPS group, LPS plus dexmedetomidine group (group LPS+DEX), and LPS plus dexmedetomidine plus autophagy inhibitor 3-MA group (group LPS+DEX+3-MA). PBS was added and cells were cultured for 12 h in group Con. LPS at the final concentration of 1000 ng∕ml was added and cells were incubated for 12 h in group LPS. LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h in group LPS+Dex. In group LPS+Dex+3-MA, 3-MA at the final concentration of 2 mmol∕L was added and cells were incubated for 1 h, LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h. Cell viability was detected by CCK-8 assay, and the concentrations of nitrous oxide ( NO) , tumor necrosis factor-alpha ( TNF-α) and interleukin-1beta ( IL-1β) in the supernatant were determined by en-zyme-linked immunosorbent assay, and the expression of microtubule-associated protein 1 light chain 3 Ⅰ( LC3 Ⅰ) , LC3Ⅱ, P62 and Bcelin-1 was detected by Western blot. LC3Ⅱ∕LC3Ⅰ ratio was calculated. Results Compared with group Con, the cell viability was significantly decreased, the concentrations of TNF-α, IL-1β and NO and LC3Ⅱ∕LC3Ⅰratio were increased, and the expression of P62 and Beclin1 was up-regulated in group LPS (P<0. 05). Compared with group LPS, the cell viability was significantly in-creased, the concentrations of TNF-α, IL-1βand NO were decreased, LC3Ⅱ∕LC3Ⅰratio was increased, the expression of P62 was down-regulated, and the expression of Beclin1 was up-regulated in group LPS+DEX ( P<0. 05) . Compared with group LPS+Dex, the cell viability was significantly decreased, the con-centrations of TNF-α, IL-1β and NO were increased, LC3Ⅱ∕LC3Ⅰ ratio was decreased, the expression of P62 was up-regulated, and the expression of Beclin1 was down-regulated in group LPS+Dex+3-MA ( P<0. 05) . Conclusion Enhanced autophagy is involved in dexmedetomidine-induced reduction of LPS-caused inflammatory responses in macrophages of mice.

Objective To investigate the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in hydrogen-rich saline-induced reduction of lipopolysaccharide (LPS)-caused damage to mitochondria in macrophages of mice.Methods Macrophage line RAW264.7 of mice were routinely cultured and divided into 4 groups (n=6 each) using a random number table method:control group (group C),group LPS,hydrogen-rich saline plus LPS group (group LPS+H2) and hydrogen-rich saline plus LPS plus ATP group (group LPS+ATP+H2).LPS was given at the concentration of 1 μg/ml,and the cells were then incubated for 30 min in group LPS.LPS at the concentration of 1 μg/ml and hydrogen-rich saline at the concentration of 0.6 mmol/L were simultaneously given,and the cells were then incubated for 30 min in LPS+H2 and LPS+ATP+H2 groups.ATP at the concentration of 1 nmol/L was then given,and the cells were incubated for 6 h in group LPS+ATP+H2.Mitochondrial membrane potential (MMP) was determined by JC-1 staining,and respiratory control ratio (RCR) was measured using a Clark-type electrode.The expression of NLRP3,caspase-1 and apoptosisassociated speck-like protein containing C-terminal caspase recruitment domain (ASC) was determined by Western blot.The concentrations of INTERLEUKIN-1 BETA (IL-1β),IL-18 and IL-6 in the supernatant were determined by enzyme-linked immunosorbent assay.Results Compared with group C,MMP and RCR were significantly decreased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were increased,and the expression of NLRP3,caspase-1 and ASC was up-regulated in group LPS (P＜0.05).Compared with group LPS,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-l8 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+H2 (P＜0.05).Compared with group LPS+H2,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+ATP+H2 (P＜0.05).Conclusion Hydrogen-rich saline can reduce LPS-caused damage to mitochondria in macrophages of mice through inhibiting the activation of NLRP3 inflammasome.

Objective To evaluate the effect of dexmedetomidine on expression of hypoxia-inducible factor-1α (HIF-1α) during endotoxin-caused apoptosis in macrophages of mice.Methods Mouse macrophage cell line RAW264.7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups (n=16 each) when cell confluence reached 60％-70％ using a random number table method:control group (group Con),dexmedetomidine group (group Dex),lipopolysaccharide (LPS) group,and LPS plus dexmedetomidine group (group LPS+Dex).Phosphate buffer solution was added in group Con.Dexmedetomidine 1 μmol/L was added in group Dex.LPS 1 μg/ml was added in LPS and LPS+Dex groups.Dexmedetomidine 1 μmol/L was added immediately after adding LPS in group LPS+Dex.Cells were then cultured for 24 h in each group.Cell apoptosis was measured using TUNEL,mitochondrial membrane potential using JC-1,reactive oxygen species (ROS) content by ROS kit,and ATP content by ATP kit.The apoptosis rate was calculated.The expression of HIF-1α,cytochrome C (Cyt-c),caspase-9 and cleaved caspase-3 was detected by Western blot.Results Compared with group Con,the apoptosis rate and ROS content were significantly increased,ATP content and mitochondrial membrane potential were decreased,the expression of HIF-1α,Cyt-c,caspase-9 and cleaved caspase-3 was up-regulated in group LPS (P＜ 0.05),and no significant change was found in the parameters mentioned above in group Dex (P＞0.05).Compared with group LPS,the apoptosis rate and ROS content were significantly decreased,ATP content and mitochondrial membrane potential were increased,the expression of HIF-1α was up-regulated,and the expression of Cyt-c,caspase-9 and cleaved caspase-3 was down-regulated in group LPS + Dex (P＜0.05).Conclusion Dexmedetomidine can reduce endotoxin-caused oxidative stress injury to macrophages,improve mitochondrial function and inhibit mitochondrial apoptosis,and the mechanism may be related to upregulating the expression of HIF-1α in mice.

Objective To evaluate the effect of hydrogen on blood brain barrier of mice with sepsisassociated encephalopathy (SAE).Methods A total of 100 adult male ICR mice,aged 6-8 weeks,weighing 20-25 g,were divided into 4 groups (n =25 each) using a random number table method:sham operation group (group Sham),sham operation plus hydrogen group (group Sham+H),group SAE and SAE plus hydrogen group (group SAE+ H).Sepsis was induced by cecal ligation and puncture (CLP).Sham+H and SAE+H groups inhaled 2％ hydrogen for 1 h starting from 1 and 6 h after CLP,respectively.At 24 h after CLP,Evans blue (EB) was injected via the caudal vein,and then the mice were sacrificed and brain tissues were removed for measuring the EB and water contents,for examining the pathological changes of hippocampi (with a light microscope) and for detecting the expression of occludin and VE-cadherin (by Western blot).Morris water maze test was performed at days 10-16 after CLP.Results Compared with group Sham,the contents of EB and water in brain tissues were significantly increased,the expression of occludin and VE-cadherin was down-regulated,the escape latency was prolonged,and the number of crossing the original platform was reduced in SAE and SAE+H groups (P＜0.05).Compared with group SAE,the contents of EB and water in brain tissues were significantly decreased,the expression of occludin and VE-cadherin was up-regulated,the escape latency was shortened,the number of crossing the original platform was increased (P＜0.05),and the pathological changes of hippocampi were significantly attenuated in group SAE+H.Conclusion The mechanism by which hydrogen mitigates SAE may be related to reducing the damage to blood brain barrier of mice.

Objective To investigate the changes in FUNDC1/microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ) signaling pathway during sepsis-induced liver injury in mice.Methods Tbirtytwo clean-grade healthy male C57BL/6 mice,aged 6 weeks,weighing 20-25 g,were divided into sham operation group (n =8) and sepsis group (n =24) using a random number table method.Sepsis was induced by cecal ligation and puncture.Blood samples were obtained at 24 h after operation in sham operation group and at 6,12 and 24 h after establishing the model in sepsis group for determination of concentrations of alanine aminotransferase and aspartate aminotransferase in serum.Mice were then sacrificed,and the right lobe of livers was removed for examination of the pathological changes and for determination of the expression of FUNDC1 and LC3 Ⅱ by Western blot.The mitochondria in the right lobe of livers were isolated to measure the respiratory function,and respiratory control rate was calculated.Results Compared with sham operation group,the concentrations of alanine aminotransferase and aspartate aminotransferase in serum and pathological scores were significantly increased,the respiratory control rate of mitochondria was decreased,the expression of FUNDC1 was down-regulated,and the expression of LC3 Ⅱ was up-regulated at each time point after establishing the model in sepsis group (P＜0.05).Conclusion The mechanism by which sepsis induces liver injury may be related to inhibiting activation of FUNDC1/LC3 Ⅱ signaling pathway in mice.