Background Existing studies have confirmed that fine particulate matter (PM_2.5)is one of the important factors inducing pulmonary fibrosis. Pulmonary fibrosis is the terminal stage of a major category of lung diseases characterized by the destruction of tissue structure, and eventually leading lung ventilation and ventilation dysfunction. No effective pulmonary fibrosis treatment is available yet. Objective To investigate the protective effect of salidroside on pulmonary fibrosis induced by the exposure of PM_2.5 and its molecular mechanism. Methods Seventy 7-week-old male C57BL/6 mice were randomly divided into four groups: control group (intratracheal instillation of normal saline + saline by gavage, n=25), Sal group (intratracheal instillation of normal saline + Sal 60 mg·kg⁻¹ by gavage, n=10), PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ + saline by gavage, n=10), and Sal + PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ +Sal 60 mg·kg⁻¹ by gavage, n=10). The mice were administered by gavage once daily, intratracheal instillation once every 3 d, and every 3 d constituted an experimental cycle. At the end of the 26-30th cycles, 3 mice in the control group and 3 mice in the PM_2.5 group were randomly sacrificed, and the lung tissues were collected for Masson staining to verify whether the pulmonary fibrosis model was successfully established. After 30 cycles, the model was successfully constructed. After 1 week of continuous observation, the mice were sacrificed, and the blood and lung tissues of the mice were collected to make lung tissue sections. Assay kits were correspondingly employed to detect oxidative stress indicators such as serum malondialdehyde (MDA) and superoxide dismutase (SOD). Western blotting was used to detect the expression of fibrosis-related proteins (Collagen-III, α-SMA), mitochondrial dynamics-related proteins (MFN1, Drp1), and mitophagy-related proteins (PINK1, Parkin, and LC3). Results Compared with the control group, the weight gain rate of the PM_2.5 group was slowed down (P<0.05), which was alleviated by the Sal intervention (P<0.05). The lung coefficient increased after the PM_2.5 exposure (P<0.05), which was alleviated by Sal intervention. Compared with the control group, the PM_2.5 group showed severe alveolar structure damage, inflammatory cell infiltration, and blue collagen deposition, and significantly increased the lung injury score, collagen volume fraction (CVF), Szapiel score, and Ashcroft score (P<0.05), as well as serum oxidative stress levels (P<0.05). The protein expression levels of Collagen-III, α-SMA, Drp1, PINK1, Parkin, and LC3 II/I were increased (P<0.05), and the expression of MFN1 was decreased (P<0.05). Compared with the PM_2.5 group, the Sal intervention alleviated lung injury, reduced inflammatory cell infiltration and collagen deposition, showing decreased lung injury score, CVF, Szapiel score, and Ashcroft score (P<0.05), and decreased serum oxidative stress levels (P<0.05); the protein expression levels of Collagen-III, α-SMA, PINK1, Parkin, and LC3 II/I were decreased (P<0.05), the expression level of Drp1 was decreased, and the expression level of MFN1 was increased. Conclusion In the process of pulmonary fibrosis induced by PM_2.5 exposure in mice, Sal may affect mitochondrial autophagy through PINK1/Parkin pathway and play a protective role. The specific mechanism needs to be further verified.

Background Salidroside (SAL) has a protective effect on multiple organ systems. Exposure to fine particulate matter (PM_2.5) in the atmosphere may lead to disruptions in gut microbiota and impact intestinal health. The regulatory effect of SAL on the gut microbiota of mice exposed to PM_2.5 requires further investigation. Objective To evaluate gut microbiota disruption in mice after being exposed to PM_2.5 and the potential effect of SAL. Methods Forty male C57BL/6 mice, aged 6 to 8 weeks, were randomly divided into four groups: a control group, an SAL group, a PM_2.5 group, and an SAL+PM_2.5 group, each containing 10 mice. In the SAL group and the SAL+PM_2.5 group, the mice were administered SAL (60 mg·kg⁻¹) by gavage, while in the control group and the PM_2.5 group, sterile saline (10 mL·kg⁻¹) was administered by gavage. In the PM_2.5 group and the SAL+PM_2.5 group, PM_2.5 suspension (8 mg·kg⁻¹) was intratracheally instilled, and in the control group and SAL group, sterile saline (1.5 mL·kg⁻¹) was intratracheally administered. Each experiment cycle spanned 2 d, with a total of 10 cycles conducted over 20 d. Histopathological changes in the ileum tissue of the mice were observed after HE staining. Colon contents were collected for gut microbiota sequencing and short-chain fatty acids (SCFAs) measurements. Results The PM_2.5 group showed infiltration of inflammatory cells in the ileum tissue, while the SAL+PM_2.5 group exhibited only a small amount of inflammatory cell infiltration. Compared to the control group, the PM_2.5 group showed decreased Shannon index (P<0.05) and increased Simpson index (P<0.05), indicating that the diversity of gut microbiota in this group was decreased; the SAL+PM_2.5 group showed increased Shannon index compared to the PM_2.5 group (P<0.05) and decreased Simpson index (P<0.05), indicating that the diversity of gut microbiota in mice intervened with SAL was increased. The principal coordinates analysis (PCoA) revealed a significant separation between the PM_2.5 group and the control group, while the separation trend was less evident among the control group, the SAL group, and the SAL+PM_2.5 group. The unweighted pair-group method with arithmetic means (UPGMA) clustering tree results showed that the control group and the SAL group clustered together first, followed by clustering with the SAL+PM_2.5 group, and finally, the three groups clustered with the PM_2.5 group. The PCoA and UPGMA clustering results indicated that the uniformity and similarity of the microbiota in the PM_2.5 group were significantly decreased. Compared to the control group, the PM_2.5 group showed decreased abundance of phylum Bacteroidetes and Candidatus_Saccharimonas (P<0.05) and increased abundance of phylum Proteobacteria, genus Escherichia, genus Bacteroides, genus Prevotella, genus Enterococcus, and genus Proteus (P<0.05). Compared to the PM_2.5 group, the SAL+PM_2.5 group showed decreased abundance of phylum Proteobacteria, phylum Actinobacteria, genus Prevotella, and genus Proteus (P<0.05), and increased abundance of Candidatus_Saccharimonas (P<0.05). The PM_2.5 group showed reduced levels of propionic acid, valeric acid, and hexanoic acid compared to the control group (P<0.05), while the SAL+PM_2.5 group showed increased levels of propionic acid, isobutyric acid, butyric acid, valeric acid, and hexanoic acid compared to the PM_2.5 group (P<0.05). Conclusion Exposure to PM_2.5 can cause pathological alterations, microbial dysbiosis, and disturbing production of SCFAs in intestinal tissue in mice. However, SAL can provide a certain degree of protective effect against these changes.

Objective To observe the clinical efficacy of artificial liver plasma bilirubin adsorption for treatment of patients with severe viral hepatitis B (HBV). Methods A retrospective study was conducted, the 120 patients with severe HBV B and their historical data of having undergone treatment of artificial liver plasma bilirubin adsorption admitted to Department of Respiration of Mianyang Central Hospital from August 2015 to August 2017 were collected, and there were 68 cases in the cirrhotic group and 52 cases in the non-cirrhotic group. The indexes of liver function and coagulation function before and after the treatment of artificial liver plasma bilirubin adsorption were collected; the differences of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamine transferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total protein (TP), albumin (Alb), globulin (Glo), prothrombin time (PT), prothrombin activity (PTA), total bilirubin (TBil) and indirect bilirubin (IBil), total bile acid (TBA), etc were compared between cirrhotic group and the severe hepatitis B non-cirrhotic group. Results The levels of ALT, AST, ALP, LDH after artificial liver plasma bilirubin adsorption therapy were lower than those before the treatment [ALT (U/L): 138.8±26.2 vs. 993.4±185.2, AST (U/L): 121.7±119.9 vs. 798.7±226.8, ALP (U/L): 129.7±8.1 vs. 178.9±14.1, LDH (μmol·L-1·s-1·L-1): 4.50±0.32 vs. 8.15 ±1.75, all P < 0.05], PTA was higher than that before the treatment [(43.2±25.6)% vs. (30.0±16.1)%, P < 0.05]. After the treatment, the decline rate of ALP, TBil, and TBA of non-cirrhotic group was higher than those in cirrhotic group (ALP: 34.20% vs. 17.80%, TBil: 39.10% vs. 18.10%, TBA:30.70% vs. 5.00%, P < 0.05), the elevation rate of PTA in non-cirrhotic group was also higher than that in cirrhotic group (52.50% vs. 25.10%, P < 0.05). Conclusion Artificial liver plasma bilirubin adsorption therapy is effective for treatment of patients with severe HBV B, particularly the effect being good on the early severe viral HBV B non-cirrhotic group.

It has been known that the Alzheimer's disease(AD)is related closely with a synaptic failure,and the p21-activated kinase(PAK)is well documented to play an important role in the regulation of the synaptie functions.However,the relationship between thePAK and the pathology of AD is unclear.In the present study,we examined the expressions of the PAK3(one subtype ofPAK),phospho-rylated-PAK(pPAK) and β-amyloid42(Aβ42,β-amyloid with 42 peptides)in an APP/PS1 double transgenie mouse model of AD andthe morphologies of geurOtlS in the hippocampus at different ages.The Western Blot results showed that the expression of PAK remainedunchanged,while,the expression of pPAK decreased largely at the age of 32 weeks and further decreased significantly with aging in thehippocampus of the APP/PS1 transgenic mouse.A1342 levels in the hippocampus were detected to increase as early as the age of 22 weeks,and kept the increase to continue with aging.The morphological results showed no obvious neuron loss in the sections of Nissl staining,while serious distonion and disorder of the dendrites of the hippocampal neurons were observed on the sections of Gelgi staining in theAPP/PS1 transgenic mouse.The present results suggested that it seemed something wrong in the processes of phospholization of PAK,butnot in the expression of the PAK itself;the toxic Aβ42 might affect the PAK in its phospholization,which in turn directly influence thedendritic development in the hippocampal neurons and cause the dendrites distorting and disordering.

Objective To determine the serum gastrin level, the expression of gastrin in colorectal carcinoma cells and observe the ultrastructure of gastrin secretory granule in colorectal carcinoma cells,in order to explore the relationship between gastrin and clinical behavior of colorectal carcinoma. Methods The serum gastrin and gastrin expression in colorectal carcinoma tissues of the 53 cases were examined by using radio-immunity analysis(RIA), immunohistochemistry and immunoelectron microscopic technique. Results Compared with control group,the preoperative level of serum gastrin in colorectal group was significantly increased, especially in well-differentiation adenocarcinoma . In the tissue of colorectal carcinoma, the gastrin expression rate was 56.6%. The expression rate of well-differentiated adenocaroinoma was higher than that in moderate and poor differentiation adenocarcinoma. Immunoelectron microscopy showed that the granules of protein A-gold (PAG) could be seen in different electro- density secretion granules in carcinoma cells, in intercellular space and on the surface of membrane of microvillus.Conclusions The level of serum gastrin and the expression of gastrin in cancer tissues in colorectal carcinoma patients are increased. The colorectal carcinoma cells may synthesize and secrete gastrin themselves, which may be correlated with clinical behavior of colorectal carcinoma.

Fifty adult lower limbs were studied macromicroscopically to reveal the extrinsic blood vessels of the menisci of the knee joint. It was found that the menisci were supplied from 2 sources, the genicular branches (except the superior lateral genicular branch) of the popliteal artery, and the descending branch of the descending genicular artery. A pair of additional genicular branches with independent stems from the popliteal artery, named as the posterior medial and the posterior lateral genicular arteries by the authors, constantly supplied the posterior part of both the menisci. The arterial branches formed a circular anastomotic arch around the menisci with small branches springing from the arch and getting into the menisci. The arterial arch communicated with the femoral and the popliteal arteries and became an important stem of a reentry channol in cases of popliteal artery occlusion.