[A case of acute fish gallbladder poisoning with multiple organ dysfunction].

Fish bile poisoning may damage human liver and kidney, causing degeneration and necrosis. Can also damage brain cells and heart muscle, resulting in nervous system and cardiovascular system lesions. This paper reports a case of a patient who developed multiple organ dysfunction syndrome (MODS) after oral administration of fish bile with Xiexin folk prescription for eye disease. In January 2020, he went to the poisoning and occupational diseases department of the emergency department of Qilu hospital. After receiving hemoperfusion, continuous renal replacement therapy (CRRT) and symptomatic support treatment, the patient was improved and discharged. CRRT combined with HP is one of the rapid and effective methods for the treatment of acute fish bile poisoning.

[Interventional effect of metformin on pulmonary inflammation and pulmonary fibrosis in silicotic rats].

Objective: To investigate the interventional effect of metformin on pulmonary inflammation and pulmonary fibrosis in silicotic rats. Methods: In April 2019, 48 Wistar male rats of SPF grade were randomly divided into negative control group, metformin control group, silicon dioxide (SiO2) model group, low, medium and high dose metformin intervention group according to the random number table method, 8 rats in each group. The SiO2 model group and the low, medium and high dose metformin intervention groups were given 1 ml 50 mg/ml of SiO2 by intratracheal instillation, the negative control group and the metformin control group were given 1 ml normal saline by intratracheal instillation. 24 hours later, the low, medium and high dose metformin intervention groups and the metformin control group were treated with 100, 200, 400 and 400 mg/kg metformin daily, the control and SiO2 model groups received normal saline daily. Then the rats were sacrificed at the 28th day after SiO2 exposure. The changes of rat body weight and pathological examination of rat lung tissue were observed, and the lung organ coefficient, the content of hydroxyproline (HYP) , the expression levels of inflammatory factors transforming growth factor beta1 (TGF-ß1) , tumor necrosis factor-alpha (TNF-α) , interleukin-1beta (IL-1ß) and the protein expression of E-cadherin (E-Cad) , Vimentin, α-SMA were detected. Results: Compared with the negative control group, SiO2 model group had a significant decrease in the body weight of rats (P<0.05) , lung organ coefficient, alveolitis and fibrosis scores, HYP content and the levels of TGF-ß1, TNF-α, IL-1ß were all significantly increased (P<0.05) . Compared with the SiO2 model group, the weights of the rats in the medium and high dose intervention group of metformin increased significantly (P<0.05) . And after intervention with different doses of metformin, the lung organ coefficient, alveolitis and fibrosis scores, HYP content and the levels of TGF-ß1, TNF-α and IL-1ß were significantly decreased (P<0.05) . Immunohistochemistry and Western blotting results showed that compared with the negative control group, the expression of E-Cad of the SiO2 model group was decreased, and the expression levels of Vimentin and α-SMA were significantly increased (P<0.05) . After metformin intervention, the expression of E-Cad was significantly increased, the expression levels of Vimentin and α-SMA were significantly decreased (P<0.05) . Conclusion: Metformin can reduce lung tissue inflammation and fibrosis in rats exposed to SiO2 dust, which may be related to reducing the expression of inflammatory factors in lung tissue and inhibiting the EMT process.

[Nursing care of esophagitis dissecans superficialis caused by acute paraquat poisoning].

The clinical data of 13 patients with esophageal dissecans superficials (EDS) induced by paraquat (PQ) in Qilu Hospital from March 2016 to April 2019 were analyzed retrospectively. EDS usually occurs on the 3rd to 9th day after taking poison, and the esophageal mucosa is different in size, color and character, in 10 cases of death, 1 case of pharyngeal pain basically disappeared on the 19th day after EDS onset, but died on the 27th day after taking poison, and 9 cases of death survived 5~19th days after taking poison, the overall cure rate was low; The pharyngeal pain symptoms of 3 surviving patients basically disappeared on day 15, 16 and 17 of EDS, and all patients had no discomfort after eating, and were cured gradually.

[Preliminary analysis of differential expression of miRNA-423-5p and miRNA-26a-5p in lung tissue of early silicotic rats].

Objective: To screen the changes of microRNA (miRNA) expression profiles in lung tissues of early silicosis rats, and provide a basis for functional analysis of differential microRNA. Methods: SPF Wistar male rats were randomly divided into a negative control group and SiO(2)-exposed groups, with 30 rats in each group. The model of silicosis in rats was established by intratracheal instillation of 1 ml SiO(2) suspension, and the control rats were treated with 1mL in the same way to sterilize normal saline. The lung tissues of two group were collected at the 1, 7, 14, 21, 28 d after SiO(2)-exposed. Three of the rat lung tissues were used for pathological observation, and the other three were used to screen differentially expressed miRNAs in lung tissue by miRNA microarray technology. miRNA chip screening and RT-qPCR were used to verify the expression levels of miRNA-423-5p and miRNA-26a-5p in the two groups. miRNA-423-5p and miRNA-26a-5p are predicted by target genes and analyzed by GO (gene ontology) enrichment analysis and KEGG (kyoto encyclopedia of genes and genomes) pathway analysis. Results: In the control group, the inflammatory response of lung tissue 21 and 28 days was significantly reduced compared with 1, 7 and 14 days, and the inflammatory cells infiltrated in the lung tissue of the SiO(2)-exposed rats. The rats in the control group had a small amount of collagen at 21 and 28 days, but a large amount of collagen fiber deposition began to appear in the lung tissue of rats exposed to SiO(2) after 21 days. Compared with the control group, the expression levels of micro RNA-423-5p was significantly up-regulated and the expression of microRNA-26a-5p was significantly down-regulated in the SiO(2)-exposed rats lung tissues dust at different time points (P<0.05) . Conclusion: The up-regulation of miRNA-423-5p and the down-regulation of miRNA-26a-5p in lung tissues of early silicotic rats may be related to the occurrence and development of early silicosis.

[Expression changes of miRNA-29b-3p and miRNA-34c-3p in lung tissue of rats exposed to silica and A549 cells].

Objective: To investigate the role of microRNA-29b-3p (miRNA-29b-3p) and miRNA-34c-3p in the process of pulmonary fibrosis, we detected the expression levels of miRNA-29b-3p and miRNA-34c-3p in the lung tissue of rats exposed to silica and A549 cells. Methods: SPF male Wistar rats were randomly divided into 1, 7, 14, 21, 28 d control group and silica (SiO(2)) dusting group, with 6 rats in each group. One-time non-exposure method was used to infuse 1ml SiO(2) suspension. The rat SiO(2) dusting group was established in the liquid, and the control rats were intratracheally injected with 1 ml of sterile physiological saline in the same manner. The lung tissues of each group were collected at the corresponding time points after dusting. Three of the rats were taken out for pathological observation, and the other three were used to screen differentially expressed miRNAs in lung tissue by miRNA microarray technology. A549 cells were cultured at the in vitro cell level and divided into control group, SiO(2) stimulation group and TGF-ß(1) stimulation group, and cells were collected at 12, 24 and 48 h after treatment. The expression levels of miRNA-29b-3p and miRNA-34c-3p in rat lung tissue and A549 cells were verified by real-time PCR (qRT-PCR), target gene prediction of miRNA-29b-3p and miRNA-34c-3p and perform GO enrichment analysis and KEGG pathway analysis. Results: The weight growth rate of the control group was significantly higher than that of the SiO(2) dusting group. Compared with the control group, the lung mass and lung coefficient of the SiO(2) dusting group were significantly increased (P<0.05). The inflammatory response of the lungs in the control group was significantly reduced at 21 and 28 days, and the inflammatory cells infiltrated in the lung tissue of the SiO2 group. The rats in the control group had a small amount of collagen at 21 and 28 days. A large amount of collagen fiber deposition began to appear in the lung tissue of rats exposed to SiO(2) for 21 days. Compared with the control group, the expression levels of miRNA-29b-3p and miRNA-34c-3p in the SiO(2) dusting group were significantly down-regulated, and there was significant difference compared with the control group (P<0.05). The expression levels of miRNA-29b-3p and miRNA-34c-3p in A549 cells treated with SiO(2) and human recombinant TGF-ß1 were significantly lower than those in the control group at 24 h and 48 h, and the difference was statistically significant (P<0.05). Conclusion: Down-regulation of miRNA-29b-3p and miR-34c-3p in rat lung tissue A549 cells may be associated with the development of early silicosis and is expected to be an indicator of early silicosis diagnosis and prognosis.

[Lung fibrosis and changes in autophagy-related proteins in rats exposed to silica dust].

Objective: To explore the changes in the autophagy marker microtubule-associated protein 1 light chain 3 (LC3) and yeast autophagy-related gene 6 (Beclin1) in rat lungs exposed to free silica (SiO(2)) dust for different periods. Methods: A total of 72 male specific pathogen-free Wistar rats were randomly divided into solvent control group and SiO(2) model group. The SiO(2) model group received one-time non-exposed intratracheal instillation of suspension of SiO(2) particles to establish a model of silicosis. The solvent control group received an equal amount of saline. Six rats each were sacrificed at 1, 7, 14, 21, 28, and 60 days after model establishment. The pathological changes and fibrosis of rat lungs at different time points were evaluated by H&E staining and Masson staining, respectively. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of transforming growth factor-ß (TGF-ß) , interleukin-1 (IL-1) , and tumor necrosis factor-α (TNF-α) in lung tissue homogenate. Western blot was used to determine the relative expression levels of LC3 and Beclin1 in the lung tissue. Results: The results of H&E staining showed that the model group had continuous inflammation in the lung tissue from day 1 to day 60, and the inflammatory scores were significantly higher in the model group than in the control group (P<0.05) . The results of Masson staining showed that rats in the model group had a small amount of collagen fibers in the lung tissue on day 14 and a large amount of collagen fibers on day 60. The fibrosis score was significantly higher in the model group than in the control group (P<0.05) . No collagen fibrosis was observed in the lung tissue in the control group. The results of ELISA showed that the model group had significantly higher levels of IL-1, TNF-α, and TGF-ß in lung tissue homogenate than the control group at each time point after exposure (P<0.05) . The results of Western blot showed that the model group had decreased expression of Beclin1 protein in the lung tissue on days 7, 14, 21, 28, and 60, which was significantly higher than that of the control group (P<0.05) . The model group also had a decreased ratio of LC3II/LC3I on days 1, 7, 14, 21, 28, and 60, which were significantly higher than that of the control group (P<0.05) . Conclusion: In the rat model of silicosis induced by free SiO(2) dust, the expression levels of autophagy-related proteins, LC3 and Beclin1, are correlated with different stages of silicosis. In the early stage of silicosis, the lung tissue has inflammation, substantially increased ratio of LC3II/LC3I and expression of Beclin1, and active autophagy. With the progression of silicosis, the ratio of LC3II/LC3I and expression level of Beclin1 gradually decrease and autophagy becomes weak.

[The anti-inflammatory effect of hesperetin on lung damage induced by paraquat in rats].

Objective: To investigate the anti-inflammatory effect of hesperetin (HSP) on lung damage induced by paraquat (PQ) in rats by detecting the levels of inflammatory makers in rat lung tissues. Methods: 140 Wistar male rats were randomly divided into negative control group, HSP control group, HSP control group, paraquat model group, pirfenidone (PDF) positive control group, and 100, 200, 400 mg/kg HSP treatment groups. All groups were exposed to 50mg/kg paraquat by oral gavage except for the negative control group and HSP control group. After 24 hours, the rats in each group were given drug intervention once daily. 10 rats were randomly sacrificed at 7th day and 28th day after exposure to paraquat respectively. 3 rats were randomly selected from them and HE, Masson staining were used to observe the pathological changes in the lungs of each group. Each group randomly selected 6 rats at two time points to detect the levels of TGF-ß(1), TNF-α, IL-4, IL-10, IL-1ß and IFN-γ in rat lung tissues. Results: Histopathological examination found that the lung injury were reduced in the rats of PDF positive control group and all HSP treatment groups. Compared with the negative control group, the levels of TGF-ß1, IL-1ß, TNF-α, IL-4, and IL-10 in rat lung tissues were significantly increased (P<0.05, P<0.01) after PQ exposure at two points in time, and there was no significant difference in the level of IFN-γ in lung tissues compared with the negative control group (P>0.05) . The levels of TGF-ß1, IL-1ß, IL-4, IL-10 and TNF-α in the lung tissues of rats on the 7th day in different dose treatment groups of HSP were reduced compared with those in the PQ model group with varying degrees (P<0.05, P<0.01) . The level of IFN-γ in lung tissues of rats were not significantly different from that of model group (P>0.05) . The levels of TGF-ß(1) and TNF-α in lung tissue of rats on the 28th day in PDF positive control group and different dose treatment groups of HSP were reduced compared with those in the PQ model group with varying degrees (P<0.05, P<0.01). The levels of IFN-γ in the rat lung tissues were increased compared with those in the PQ model group (P<0.05). Besides, there were no significant in the levels of IL-1ß, IL-4 and IL-10 in lung tissues compared with PQ model group (P>0.05). Conclusion: HSP can reduce lung damage induced by PQ in rats by inhibiting the release of inflammatory factors and promoting the secretion of anti-inflammatory factors.

[Effect of mitogen-activated protein kinase signaling pathway on apoptosis induced by chloroacetic acid in human normal bronchial epithelial 16HBE cells].

Objective: The aim of this study was to investigate the effect of mitogen-activated protein kinase (MAPK) signaling pathway on apoptosis induced by chloroacetic acid in human normal bronchial epithelial 16HBE cells. Methods: 16HBE cells were exposed to 0.5, 1.0, 1.5, 2.0, 2.5, 3.0 and 3.5 mmol/L chloroacetic acid for 24 h in vitro. The cytotoxicity induced by chloroacetic acid was assessed by CCK-8 and LDH assays. Cell apoptosis was detected by Annexin V-FITC and PI staining. The protein expression levels of phosphorylation of p38, ERK1/2 and JNK were determined by western blotting. 16HBE cells were pretreated with MAPK signaling pathway specific inhibitors including SB203580, U0126 and SP600125 for 1 h, and these cells were subsequently treated with 2.5 mmol/L chloroacetic acid for 24 h. The expressions of p-p38, p-ERK1/2 and p-JNK as well as the changes of cell viability and apoptosis were measured after pretreated with inhibitors for 1 h. Results: The cell viability by CCK-8 and LDH methods gradually reduced in a dose-dependent manner when chloroacetic acid concentrations elevated (P<0.05) , and their correlation coefficients were -0.902 and -0.825, respectively. The detection efficiency of CCK-8 assay significantly increased compared with LDH assay (P<0.05) . The cell apoptosis rates, which were (17.2±4.0) %, (24.6± 4.2) %, (39.3 ± 5.7) % in 1.5, 2.0, 2.5 mmol/L chloroacetic acid-treated groups, were higher than that of the control group[ (5.6 ± 3.0) %] (P<0.05) . There was a time-or dose-dependent change in the protein expressions of p-p38, p-ERK1/2 and p-JNK. Compared with the control, the levels of p-p38 had 2.1 and 2.6-fold increases in 16 and 24 h treated groups (P<0.01) , while the levels of p-ERK1/2 distinctly decreased by 37% and 52% (P<0.01) . In comparison with the control group, the expressions of p-p38 had 1.9 and 2.6-fold increases in 1.5 and 2.5 mmol/L treatment groups (P<0.01) , whereas the expressions of p-ERK1/2 significantly decreased by 40% and 50% (P<0.01) . No significant change was observed in p-JNK protein expression between the chloroacetic acid-treated and control groups. In comparison with the vehicle control and the exposed group, p-p38, p-ERK1/2, p-JNK protein expressions significantly declined in the inhibitor controls and inhibitor groups. Compared with the controls, the cell survival rates had significant reductions of 28%, 18%, 36% and 26% respectively in chloroacetic acid treated group, SB203580 group, U0126 group and SP600125 group, and the apoptosis rates in the abovementioned groups were 7, 4, 8 and 7 times. Compared with chloroacetic acid-treated group, the cell viability increased by 14% in SB203580 group and decreased by 11% in U0126 group, and the cell apoptosis rates decreased by 36% in SB203580 group and increased by 18% in U0126 group (P<0.05) . But no significant changes were observed in cell viability and apoptosis between SP600125 and chloroacetic acid-treated group. Conclusion: Chloroacetic acid might activate p38 MAPK signaling pathway and inhibit ERK1/2 MAPK signaling pathway. The signaling pathways of p38 and ERK1/2 MAPK are involved in 16HBE cell apoptosis induced by chloroacetic acid, but JNK is not involved in chloroacetic acid-induced 16HBE cell apoptosis.

Effectiveness of microsatellite and single nucleotide polymorphism markers for parentage analysis in European domestic pigs.

Parentage analysis and individual identification are recent, promising methods that have been applied to evolutionary and ecological studies, as well as conservation management. Parental exclusion relying on polymorphic microsatellites has been used worldwide in parentage determination, while the low mutation rate and genotyping error rate of single nucleotide polymorphisms (SNPs) make them another important marker for pedigree tracing. Here, we compared the effectiveness of microsatellites and SNP markers in European pigs. We also measured and presented the minimum and optimal criteria for SNP markers to be used in paternity and identity analysis. Our findings may contribute to the development of techniques for future molecular evolution and conservation studies, as well as breeding programs.

Prognostic role of the systemic immune-inflammation index and pan-immune inflammation value for outcomes of breast cancer: a systematic review and meta-analysis.

OBJECTIVE: This review examined the literature for evidence on the prognostic ability of systemic immune-inflammation index (SII) and pan-immune inflammation value (PIV) for predicting overall survival (OS) and disease-free survival (DFS) in breast cancer patients. MATERIALS AND METHODS: PubMed, Embase, Scopus, and Web of Science were searched with Google Scholar for gray literature. All types of studies reporting the association between SII or PIV and OS or DFS of breast cancer were eligible. RESULTS: 13 studies on SII and 4 studies on PIV were included. Meta-analysis showed that a high SII was a significant predictor of OS (HR: 1.97 95% CI: 1.54, 2.52 I2=76%) and DFS (HR: 2.07 95% CI: 1.50, 2.86 I2=79%) in breast cancer patients. These results did not change on sensitivity analysis and were more or less stable on multiple subgroup analyses. Pooled analysis showed that high PIV was also a significant predictor of poor OS (HR: 2.63 95% CI: 1.46, 4.74 I2=71%) and DFS (HR: 1.64 95% CI: 1.23, 2.17 I2=0%) in breast cancer patients. CONCLUSIONS: High SII and PIV can predict poor OS and DFS in breast cancer patients. High heterogeneity and the observational nature of data are important limitations of the review. Further studies are needed specifically on PIV to increase the strength of the evidence.

Clinical disorders of phosphorus metabolism.

Deranged phosphorus metabolism is commonly encountered in clinical medicine. Disturbances in phosphate intake, excretion and transcellular shift account for the abnormal serum levels. As a result of the essential role played by phosphate in intracellular metabolism, the clinical manifestations of hypophosphatemia and hyperphosphatemia are extensive. An understanding of the pathophysiology of various phosphate disorders is helpful in guiding therapeutic decisions.