This paper aimed at exploring for a scientific method of clinical skill strength-ening training by comparison and analysis on the training examination results of 121 clinical students in Clinical College,Wuhan University of Science and Technology before practice.It was found that the examination achievements of check-up is the lowest in the whole items as a re-sult of lack of normative and precise operation,and style of study is a primary reason to impact class average achievements.Relevant measures are put forward.The study results are available to improve clinic teaching quality.

This paper is to report the investigation on the metabolic behavior of Staphylococcus aureus (S. aureus) after given Qingkailing injection, and with the aim of seeking for a new quality control method based on biological assessment. The growth thermogenic curves of S. aureus were determined by microcalorimetry and analyzed by computer. The results showed that in the concentration range of (0-5.00%), the growth thermogenic curves of S. aureus were declined and removed back with increasing dosage of Qingkailing injection; the main parameters (T1, T2, k1, P1, P2 and I) and the dosage of Qingkailing injection have good correlation. The 50% inhibiting dosage is 3.26 %, and the optimal inhibiting dosage is 5.47%. Difference could be detected among the Qingkailing injection samples from different factories and different batches. It is proved that Qingkailing injection could inhibit the metabolic behavior of S. aureus, and microcalorimetry might be applied in the quality assessment of Qingkailing injection.

Background Lead exposure induces microglial cell death, of which the mechanism is unclear. Ferroptosis is a new death form and its role in microglia death has not been reported. Objective To investigate the role of ferroptosis in microglia following lead exposure in order to provide a theoretical basis for the mechanism of lead neurotoxicity. Methods Microglial cell line BV-2 cells were co-cultured with 0, 10, 20 and 40 μmol·L⁻¹ lead acetate for 24 h. The 40 μmol·L⁻¹ lead acetate group with iron chelator (DFO) was named the 40+DFO group. Changes in BV-2 cell morphology after lead exposure were observed under an inverted microscope; tissue iron kit and glutathione kit were used to detect intracellular iron and glutathione (GSH) respectively; flow cytometry was applied to detect lipid reactive oxygen species (lipid ROS) immunofluorescence intensity. Western blotting and qPCR were adopted to detect the expressions of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), transferrin receptor 1 (TFR-1), divalent metal transporter 1 (DMT1), ferroportin 1 (FPN1) protein and mRNA. Results Compared with the control group, the number of BV-2 cells decreased with increasing doses of lead and the cells showed a large, round amoeboid shape. The intracellular levels of iron of BV-2 cells were (1.08±0.04), (1.29±0.03), and (1.72±0.10) mg·g⁻¹ (calculated by protein, thereafter) in the 10, 20, and 40 μmol·L⁻¹ lead acetate groups, respectively, significantly higher than that in the control group (P<0.05), and the intracellular level of iron in the 40+DFO group, (1.34±0.10) mg·g⁻¹, was lower than that in the 40 μmol·L⁻¹ lead acetate group, (1.72±0.03) mg·g⁻¹ (P<0.05). Compared with the control group, the TFR-1 and DMT1 protein and mRNA expressions were increased in BV-2 cells in the 10, 20, 40 μmol·L⁻¹ lead acetate groups (P<0.05), especially in the 40 μmol·L⁻¹ lead acetate group; the FPN1 protein expression did not change significantly, but the FPN1 mRNA expressions in BV-2 cells in the 10, 20, 40 μmol·L⁻¹ lead acetate groups were significantly decreased (P<0.05). Compared with the control group, the intracellular GSH level decreased and the lipid ROS content increased in all three lead acetate groups; compared with the 40 μmol·L⁻¹ lead acetate group, the GSH level increased by 12.30% and the lipid ROS content decreased by 13.00% in the 40+DFO group (P<0.05). The expressions of GPX4 protein were reduced to 50.00%, 35.00%, and 17.00% of that of the control group in the 10, 20, and 40 μmol·L⁻¹ lead acetate groups respectively, while the expressions of GPX4 mRNA were also significantly reduced; the expressions of SLC7A11 protein and mRNA in the 20 and 40 μmol·L⁻¹ lead acetate groups were lower than that in the control group, with the most significant decrease in the 40 μmol·L⁻¹ lead acetate group (P<0.05). Conclusion Lead exposure could induce ferroptosis in BV-2 cells, in which iron transport imbalance and oxidative damage might be involved.

Objective To study the therapeutic effects of Xileisan Pessary on rats with cervicitis based on the idea of treating different diseases with the same therapy. Methods Vagina perfusion of hydroxybenzene mucilage was used to establish rat cervicitis models. Rats were randomly divided into normal group, model group, positive medicine group, low-, medium-, and high-dose Xileisan Pessary groups. Rats with cervicitis were treated with Xileisan Pessary from the next day after modeling for 10 days. The amount of neutrophilic granulocytes and leukocytes were detected by blood routine analysis meter; cervial histopathologic examination was conducted by HE staining. Results Compared with normal group, the numbers of granulocyte and leucocyte increased significantly in the model group (P<0.01). Compared with the model group, the numbers of granulocyte and leucocyte in the low-dose Xileisan Pessary group showed a decreasing trend (P<0.05, P<0.01); cervical inflammation mucosal epithelium and tissue necrosis were signally alleviated; granulocyte in the medium-dose Xileisan Pessary group showed a decreasing trend (P>0.05);the content of leucocyte hardly changed;granulocyte in the high-dose Xileisan Pessary group increased observably (P<0.01); the number of leucocyte showed an increasing trend (P>0.05), and the numbers of granulocyte and leucocyte in positive medicine group decreased observably (P<0.01), and cervical inflammation mucosal epithelium and tissue necrosis were also signally alleviated. Conclusion Xileisan Perssary can relieve the inflammation of cervix and repair injured mucosa. It has the function of treating different diseases with the same therapy.

OBJECTIVE: To explore the effects of lead exposure on inflammatory damage of hippocampus and cognitive impairment in diabetic rats. METHODS: The specific pathogen free(SPF) male healthy Wistar rats were randomly divided into control group and lead-exposed group. The SPF male Goto-Kakisaki Wistar rats rats were randomly divided into diabetes group and diabetes lead-exposed group, with 10 rats in each group. Rats in lead-exposed group and diabetes lead-exposed group were continuously exposed to lead acetate water with a mass fraction of 0.025% for 9 weeks. Rats in control group and diabetes group were given distilled water. The body weight and blood glucose level of rats were measured before lead exposure and at 1, 3, 5, 7 and 9 weeks after exposure. After the exposure, Morris water maze test was used to evaluate the learning and memory ability of rats. The lead levels in whole blood and hippocampal tissues were detected by inductively coupled plasma mass spectrometry, and the expression of mRNA and protein expression of inflammatory factors in hippocampal tissues of rats were detected by real-time fluorescence quantitative polymerase chain reaction and enzyme-linked immunoadsorption, respectively. RESULTS: At the end of lead exposure, the difference of body mass of rats in the diabetes group and the diabetes lead-exposed group was not statistically significant compared with that in the same group before exposure(all P values were >0.05); but the body mass of rats in these two groups was lower than that of the control group and the lead-exposure group(all P values were <0.05). The blood glucose levels of rats were higher in the diabetic group and the diabetes lead-exposed group than that in the control group and the lead-exposed group, respectively(all P values were <0.05). Morris water maze test showed that the escape latency of rats in the 1 st, 2 nd and 3 rd day were longer in diabetes group and the diabetes lead-exposed group than that in the control group and the lead-exposed group(all P values were <0.05). The number of times of crossing platforms were less in the lead-exposed group and the diabetes group than that of the control group(all P values were <0.05). The number of times of crossing platforms was more in the diabetes lead-exposed group than that in the other 3 groups(all P values were <0.05). The levels of lead in blood and hippocampus of rats were higher in the lead-exposed group than those in the control group(all P values were <0.05), and those in the diabetes lead-exposed group were higher than that in the other 3 groups(all P values were <0.05). The relative expression of mRNA of interferon-γ(ifn-γ) and interleukin(il)-6 in hippocampal tissues of rats was higher in the lead-exposed group and the diabetes group than that of the control group(all P values were <0.05). The relative expression of mRNA of tumour necrosis factor-α(tnf-α) and il-1β in the hippocampal tissues of rats was higher in the diabetes group than that of the control group and the lead-exposed group, respectively(all P values were <0.05). The relative expression of mRNA of ifn-γ, tnf-α, il-1β and il-6 in hippocampal tissues of rats was higher in the diabetes lead-exposed group than that of the other 3 groups(all P values were <0.05). The relative protein expression of IFN-γ, TNF-α, IL-4 and IL-6 in hippocampal tissues of rats was higher in lead-exposed group than that of the control group(all P values were <0.05). The relative protein expression of IFN-γ, TNF-α, IL-1β and IL-6 in hippocampal tissues of rats was higher in diabetes group than that of the control group(all P values were <0.05). The relative protein expression of IFN-γ, IL-1β and IL-6 in hippocampal tissues of rats was higher in diabetes group than that of the other 3 groups(all P values were <0.05). CONCLUSION: Diabetes can promote the lead accumulation in the blood and hippocampus of rats. The combined effect of lead exposure and diabetes can up-regulate the expression of pro-inflammatory cytokines in the hippocampal tissues of rats, aggravate the inflammatory response, and have a synergistic effect on the cognitive impairment in rats.

OBJECTIVE: To investigate the effects of lead exposure and high fat diet on the hippocampal inflammatory factors and learning-memory in rats. METHODS: A total of 40 specific pathogen free male SD rats were randomly divided into control group,high fat diet group,lead exposure group,combine exposure group,10 rats in each group. Rats in control group were given regular diet and rats in high-fat diet group were given high-fat diet. Rats in lead exposure group were given regular diet and water with 400 mg/L lead acetate. Rats in combine exposure group were given high fat diet and water with 400 mg/L lead acetate. Body weight was measured every other week. The exposure period was 9 weeks. Morris water maze was applied to measure the learning-memory. The content of total cholesterol,triglyceride(TG),low density lipoprotein cholesterol(LDL) and high density lipoprotein cholesterol(HDL) in serum were detected by using microplate reader. The lead content of hippocampus was detected by inductively coupled plasma mass spectrometer. Enzyme-linked immuno sorbent assay was used to detect the content of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,IL-4,IL-6 and interferon-γ(IFN-γ). RESULTS: Beginning from the third week,the body weight of rats in high fat diet and combine exposure group were significantly higher than that in control group(P < 0. 05). In addition,the body weight of rats in combine exposure group were higher than that in lead exposure group(P < 0. 05). Escape latency and the frequency of crossing platform of rats in high fat diet group,lead exposure group and combine exposure group were significant changed compared with those in control group(P < 0. 05). The escape latency of rats in combine exposure group increased compared with those in high fat diet group and lead exposure group(P < 0. 05). In addition,serum TG and LDL content in high-fat diet group and combine exposure group increased and HDL decreased compared with the control exposure group and lead exposure group(P < 0. 05). Compared with the control group and high fat diet group,the content of lead in hippocampus of lead exposure group and combine exposure group substantially increased(P < 0. 05). The levels of TNF-γ,IL-6,IL-1β,IFN-γ of hippocampus in high fat diet group,lead exposure group and combine exposure group were significantly higher than those in control group(P < 0. 05). Besides,the levels of IL-4 of hippocampus in lead exposure group and combine exposure group were higher than that in control group(P < 0. 05). IL-1β content of rats hippocampus in combine exposure group was higher than that in high-fat diet group or lead exposure group(P < 0. 05). CONCLUSION: Combine lead and high-fat diet exposure can exert a synergy in decrease of learning-memory in rats. IL-1β might involved in the process of synergic neurotoxicity induced by lead and high fat diet.