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Objective To investigate the prevalence of parasitic infections in human stool samples from a hospital in Chenzhou City, Hunan Province, so as to provide insights into the management of intestinal parasitic diseases. Methods Stool samples were collected from patients admitted to a hospital in Chenzhou City from September 2020 to March 2021, subjected to physiological saline smearing and microscopy for detection of intestinal parasites. The prevalence of parasitic infections and the species of parasites were descriptively analyzed. Results The overall prevalence of intestinal parasitic infections was 1.61% in the 10 728 stool samples, and there were 3 samples with mixed infections of two parasite species. A total of seven parasite species were identified, including Blastocystis hominis (162 cases, 1.55%), Giardia lamblia (5 cases, 0.05%), Dientamoeba fragilis (5 cases, 0.05%), Endolimax nana (one case, 0.01%), Iodamoeba bütschlii (one case, 0.01%), Strongyloides stercoralis (one case, 0.01%) and Trichomonas hominis (one case, 0.01%). The prevalence of intestinal parasitic infection was significantly higher among women than in men (2.14% vs. 1.25%; χ2 = 13.01, P < 0.01), and a high prevalence rate was seen among patients at ages of 20 to 30 years (2.99%) and 80 years and older (2.86%); however, no age-specific prevalence of intestinal parasitic infection was detected (χ2 = 12.45, P > 0.05). Conclusions The overall prevalence of intestinal parasitic infection was low among patients admitted to a hospital in Chenzhou City, and gender-specific prevalence was found. Food-borne and opportunistic parasites were predominant intestinal parasites, including B. hominis, G. lamblia and D. fragilis.
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Objective: To prepare adipose-derived stem cells (ADSCs) and chitosan chloride (CSCl) gel complex to study the biocompatibility and the feasibility of repairing the wounds of deep partial thickness scald in rats. Methods: ADSCs were prepared by enzymogen digestion and differential adherence method from the subcutaneous adipose tissue of SPF grade 6-week-old male Sprague Dawley (SD) rats. Temperature sensitive CSCl gel was prepared by mixing CSCl, β glycerol phosphate, and hydroxyethyl cellulose in 8∶2∶2.5 ratio. The proliferation of ADSCs was measured by cell counting kit 8 (CCK-8) assay and the survival of ADSCs was detected by the Live/Dead flurescent staining in vitro. A deep partial thickness burn animal model was made on the back of 72 SPF grade 6-week-old male SD rats by boiled water contact method and randomly divided into 3 groups ( n=24). Group A was blank control group, group B was CSCl hydrogel group, group C was ADSCs/CSCl gel group. The wound closure rate at 3, 7, 14, 21 days was observed after operation. The number of inflammatory cells at 7 days and epidermal thickness at 21 days were observed by HE staining after operation. The angiogenesis at 7 days was evaluated by immunohistochemistry staining with CD31 expression. Results: CSCl had a temperature sensitivity, at 4℃, the temperature-responsive hydrogel was liquid and became solid at 37℃. The CCK-8 assay and Live/Dead flurescent staining confirmed that ADSCs could grow and proliferate in the ADSCs/CSCl hydrogel complex. General observation showed the wound closure ratio in group C was superior to groups A and B after operation ( P<0.05). HE staining showed that at 7 days after operation, the wound healing of the three groups entered fibrous proliferation stage. Collagen deposition and inflammatory cell infiltration were observed in the dermis of each group. The proportion of inflammatory cells in group C was significantly lower than that in groups A and B, and in group B than in group A ( P<0.01). At 21 days after operation, the fibrous connective tissues of neoepithelium and dermis in groups B and C were arranged neatly, and fibroblasts and neocapillaries could be seen. In group A, neoepidermis could also be seen, but the fibrous connective tissues in dermis were arranged disorderly and sporadic capillaries could be seen. The thickness of neonatal epidermis in group C was significantly larger than that in groups A and B, and in group B than in group A ( P<0.01). CD31 immunohistochemistry staining showed that the neovascularization could be seen in all groups. The number of neovascularization in group C was significantly higher than that in groups A and B, and in group B than in group A ( P<0.05). Conclusion: The ADSCs/CSCl hydrogel complex has a good biocompatibility and possessed positive effects on promoting the deep partial thickness scald wound repairing in rats.
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Objective@#To observe effects of exogenous high mobility group protein box 1 (HMGB1) on angiogenesis in ischemic zone of early scald wounds of rats.@*Methods@#Thirty-six Sprague-Dawley rats were divided into HMGB1 group and simple scald (SS) group according to the random number table, with 18 rats in each group. Comb-like copper mould was placed on the back of rats for 20 s after being immersed in 100 ℃ hot water for 3 to 5 min to make three ischemic zones of wound. Immediately after scald, rats in HMGB1 group were subcutaneously injected with 0.4 μg HMGB1 and 0.1 mL phosphate buffer solution (PBS), and rats in SS group were subcutaneously injected with 0.1 mL PBS from boarders of ischemic zone of scald wound. At post scald hour (PSH) 24, 48, and 72, 6 rats in each group were collected. Protein expressions of vascular endothelial growth factor (VEGF) in ischemic zone of wound at PSH 24, 48, and 72 and protein expressions of CD31 in ischemic zone of wound at PSH 48 and 72 were detected by immunohistochemistry. The number of microvessel in CD31 immunohistochemical sections of ischemic zone of wound at PSH 48 and 72 was calculated after observing by the microscope. The mRNA expressions of VEGF and CD31 in ischemic zone of wound were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction at PSH 24, 48, and 72. Data were processed with analysis of variance of factorial design, t test, and Bonferroni correction.@*Results@#(1) At PSH 24, 48, and 72, protein expressions of VEGF in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=7.496, 4.437, 5.402, P<0.05 or P<0.01). At PSH 48 and 72, protein expressions of CD31 in ischemic zone of wound of rats in HMGB1 group were 0.038 8±0.007 9 and 0.057 7±0.001 2 respectively, significantly higher than 0.013 4±0.004 9 and 0.030 3±0.004 0 of rats in SS group (t=10.257, 15.055, P<0.01). (2) At PSH 48 and 72, the number of microvessel in ischemic zone of wound of rats in HMGB1 group was obviously more than that of rats in SS group (t=3.536, 4.000, P<0.05). (3) At PSH 24, 48, and 72, mRNA expressions of VEGF in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=4.406, 3.821, 3.356, P<0.05). At PSH 24 and 48, mRNA expressions of CD31 in ischemic zone of wound of rats in HMGB1 group were significantly higher than those of rats in SS group (t=4.113, 3.466, P<0.05). At PSH 72, mRNA expressions of CD31 in ischemic zone of wound of rats in 2 groups were close (t=0.010, P>0.05).@*Conclusions@#Exogenous HMGB1 can promote angiogenesis in ischemic zone of early scald wounds of rats by increasing expressions of VEGF and CD31.
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Objective To explore the methods and effects of parents chaperone for premature infants with bronchopulmonary dysplasia(BPD)in neonatal intensive care unit(NICU).Methods Convenience sampling method was used to recruit premature infants diagnosed with BPD admitted from January 2014 to October 2016 in NICU in a tertiary hospital,and 41 premature infants were recruited and divided into the control group (n=19) and the experimental group(n=22) according to the time sequence of admission.Infants in the experimental group was accompanied by parents when diagnosed as BPD,and under the guidance of specialty nurses,parents performed daily care,observation of condition,treatment assistance,and early intervention;infants in the control group were provided traditional nursing mode,nurses performed nursing care,and parents were allowed to visit through the window for one hour each time,three times every week.Parental anxiety was compared between two groups at 1 day before discharge,and follow-up compliance and weight gain of infants were compared at 3 days,7 days,2 weeks,4 weeks after discharge.Results Parental anxiety at 1 day before discharge,and follow-up compliance and weight gain of infants in the experimental group were all better than those in the control group,and the differences were statistically significant(P＜0.05).Conclusion Parents chaperone can improve parents' ability of caring,reduce parents' anxiety and improve follow-up compliance after discharge,so as to improve quality of life of premature infants with BPD.
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Objective To investigate the changes in molecule levels of Ras-ERK signal pathway of K562 cells treated with simvastatin in vitro,and to illustrate that simvastatin inducing the changes in molecule levels of Ras- ERK signal pathway is involved in regulation of proliferation and apoptosis of K562 cells. Methods K562 cells,the chronic myelocytic leukemia(CML) cell lines,were cultured and treated with simvastatin in vitro and proliferation activity of K562 cells was detected by MTT. The changes of apoptosis rate and cell cycle of K562 cells were measured by flow cytometry(FCM). The molecular changes of Ras-ERK signal pathway were analyzed by RT- PCR in transcriptional level. Results The proliferation of K562 cells was inhibited by simvastatin,and G_0-G_1 arrested in K562 cells and significant apoptosis rate was observed with FCM. Most molecules of Ras- ERK signal pathway expressed differentially at transctiptional level. Conclusion Simvastatin probablely inhibit proliferation and induces apoptosis of K562 cells,depending on Ras-ERK signal pathway which is involved in cell proliferation and apoptosis.
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AIM: To probe into tau hyperphosphorylation at PHF- 1 sites induced by glycogen synthase kinase - 3β(GSK- 3β) in vivo. METHODS: Twenty - one rats were randomly allocated to three groups as follows: GSK - 3β transfection group, vector group and control group; 0.1 μg/3μL GSK- 3β- HA plasmid or vector was injected bilaterally into cerebrum of the rats respectively, rats without injection were controls. Western blotting and immunohistochemical staining of cortex were carried out to detect the expression of GSK- 3β- HA plasmid and tau phosphorylation using phosphorylation- dependent tau antibody PHF- 1. RESULTS: After transfection with GSK- 3β- HA for 48 h, GSK - 3β - HA was expressed in GSK- 3β transfection group; and hyperphosphorylated tau at PHF- 1 sites accumulated in neurons in the transfected areas. The hyperphosphorylated tau colocalized largely with GSK- 3β expressed by the transfected GSK- 3β plasmid. CONCLUSIONS: Transfection with GSK- 3βin vivo can induce tau hyperphosphorylation involving the pathogenesis of neurodegenerative disorders. These data further prove that GSK- 3β is a key kinase to induce tau hyperphosphorylation and may be a therapeutic target for tauopathy- related neurodegenerative diseases.
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AIM: To probe into tau hyperphosphorylation at PHF-1 sites induced by glycogen synthase kinase-3? (GSK-3?) in vivo. METHODS: Twenty-one rats were randomly allocated to three groups as follows: GSK-3? transfection group, vector group and control group; 0.1 ?g/3 ?L GSK-3?-HA plasmid or vector was injected bilaterally into cerebrum of the rats respectively, rats without injection were controls. Western blotting and immunohistochemical staining of cortex were carried out to detect the expression of GSK-3?-HA plasmid and tau phosphorylation using phosphorylation-dependent tau antibody PHF-1. RESULTS: After transfection with GSK-3?-HA for 48 h, GSK-3?-HA was expressed in GSK-3? transfection group; and hyperphosphorylated tau at PHF-1 sites accumulated in neurons in the transfected areas. The hyperphosphorylated tau colocalized largely with GSK-3? expressed by the transfected GSK-3? plasmid. CONCLUSIONS: Transfection with GSK-3? in vivo can induce tau hyperphosphorylation involving the pathogenesis of neurodegenerative disorders. These data further prove that GSK-3? is a key kinase to induce tau hyperphosphorylation and may be a therapeutic target for tauopathy-related neurodegenerative diseases.