Adolescent ; Heart Valve Diseases ; etiology ; Heart Valves ; pathology ; Humans ; Lupus Erythematosus, Systemic ; complications ; pathology ; Male

Objective To explore the correlation of the ER and HER-2 expression status with the short-term effect of paclitaxel and epirubicin (TE) chemotherapy advanced breast cancer. Methods Past Immunohistochemical data of 42 advanced breast cancer patients after paclitaxel combined epirubicin treatment were analyzed retrospectively. Patients were divided into four sub-groups: ER +, HER-2-group; ER +, HER-2 + group; ER-, HER-2-group; ER-, HER-2 + group. All affecting patients with complete clinical and pathological data were observed for the factors short-term effect of TE chemotherapy and for chemotherapy adverse. Results The whole 42 patients completed at least two cycles of chemotherapy, and then got efficacy evaluation. Recent response rate of the patients who got TE chemotherapy was 23 cases (54.8%).RR with different metastatic sites (P=0.038) and the number of metastasis (P=0.036) were significantly different. The mainly adverse events of chemotherapy were alopecia for 36 cases (85.7%), myelosuppression for 29 cases (69.1%), Peripheral neuritis for 10 cases (23.9%). ER,HER-2 expression in the Different sub-groups and the RR showed linear distribution (P= 0.027).RR values (83.3%) in patients of ER-, HER-2 + group was significantly higher than that of the ER +, HER-2-group (25.6%) (P=0.045). Conclusion Advanced breast cancer patients with ER-, HER-2 + were more sensitive to TE chemotherapy.ER and HER-2 expression status was a predictor of efficacy of the chemotherapy. It may be helpful to consider ER and HER-2 expression status in choosing reasonable chemotherapy.

Platelet activating factor (PAF) is a biologically active membrane phospholipid mediator. In this study we investigated the effects of PAF on the lymphocyte proliferation, production of IL-2, natural killer cytotoxic factor (NKCF) and colony stimulating factor (CSF) by BALB/c mice splenocytes in vitro. The results showed that PAF inhibited lymphocyte proliferation at concentrations of 10-10~ 10-7 mol/L. CTLL-2, YAC-1 and munne bone marrow cells were used for the assays of IL-2, NKCF and CSF, respectively. Production of IL-2, NKCF and CSF from ConA stimulated murine splenocytes was significantly inhibited by PAF at 10-7 mol/L. Inhibition of spleen cells proliferation and secretion may play an important role in the pathological effects of PAF.

Objective To explore the mechanism of Huagan Jiedu decoction in treatment of chronic hepatitis B by testing the influence of the decoction on Serum IL-2, IL-4 and IFN-γ of rat models of chronic hepatic injury. Methods The model of Chronic hepatic injury was established by subcutaneously injecting 40% CCl4-olive oil solution in rats according to the ratio of 3ml per kg. of body weight. 60 healthy rats were divided randomly into a normal group, a model group, a low dose of Huagan Jiedu decoction group, a large dose of Huagan Jiedu decoction group, and a control group (Qingre Jiedu tablet group), 15 cases in each group. The Serum IL-2, IL-4 and IFN-γ were detected in each group separately. Results Compared with the normal group, the Serum IL-2 and IFN-γ were decreased (t=2.401, 2.337, P=0.0349, 0.0378) and the Serum IL-4 was increased (t=2.896, P=0.00861 ) in the model group; Compared with the model group, the Serum IL-2 and IFN-γ were increased (t=2.417, 2.344, P=0.0341, 0.0372, P＜0.05; t=3.114, 2.988, P=0.0052, 0.0068) in the large Huagan Jiedu decoction group and the control group, while the Serum IFN-γ was increased (t=3.049, P=0.0062) in the low dose of Huagan Jiedu decoction group and the Serum IL-4 was decreased (t=3.102, 3.017, 2.979, P=0.0061, 0.0065, 0.0069)in both Huagan Jiedu decoction groups and the control group. Conclusion Large dose of Huagan Jiedu decoction has sound therapeutic effects on rats with chronic hepatic injury by decreaseing the content of the Serum IL-4 and increasing IL-2 and IFN-γ, and adjusting th1/th2 balance.

Objective To evaluate the effects of mechanical stretch preconditioning on pathological stretch-induced activation of nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) signaling pathways in human type Ⅱ alveolar epithelial cells.Methods Human type Ⅱ alveolar epithelial cell line A549 cells cultured in vitro were randomly divided into 3 groups (n =24 each) using a random number table: control group (group Ⅰ), pathological stretch group (group Ⅱ), and mechanical stretch preconditioning group (group Ⅲ).In group Ⅰ , A549 cells were cultured routinely without receiving pathological stretch.In group Ⅱ , A549 cells were exposed to 20％ cyclic stretch at 0.3 Hz for 6 h.In group Ⅲ , A549 cells were exposed to 5％ cyclic stretch at 0.3 Hz for 60 min, and then exposed to 20％ cyclic stretch at 0.3 Hz for 6 h.After the end of the treatment, the cells were collected for determination of the cell viability (by methyl thiazolyl tetrazolium assay) and lactate dehydrogeuase (LDH)release (by colorimetric method).The concentrations of tumor necrosis factor-alpha (TNF-α),interleukin-8 (IL-8) and high mobility group box 1 (HMGB1) in the culture medium were detected using enzyme linked immunosorbent assay.The expression of total NF-κB, phosphorylated NF-κB, total STAT3 and phosphorylated STAT3 was detected using Western blot.The ratios of phosphorylated NF-κB to total NF-κB and phosphorylated STAT3 to total STAT3 were calculated to reflect the activation.Results Compared with group Ⅰ , the cell viability was significantly decreased, the amount of LDH released was increased, and the concentrations of TNF-α, IL-8 and HMGB1, and activation of NF-κB and STAT3 were increased in Ⅱ and Ⅲ groups.Compared with group Ⅱ , the cell viability was significantly increased, the amount of LDH released was decreased, and the concentrations of TNF-α, IL-8 and HMGB1, and activation of NF-κB and STAT3 were decreased in group Ⅲ.Conclusion The mechanism by which mechanical stretch preconditioning attenuates pathological stretch-induced damage to human type Ⅱ alveolar epithelial cells is related to inhibited activation of NF-κB and STAT3 signaling pathways.

Objective To evaluate the role of spinal RhoA/ROCK signaling pathway in the development of lipopolysaccharide (IP)-induced inflammatory pain(IP) in rats.Methods Fifty-two male Sprague-Dawley rats, weighing 180-220 g, were equally randomized into 4 groups using a random number table: normal saline group (group NS) , LPS group, RhoA inhibitor C3 exoenzyme group (group LC) , and ROCK inhibitor Y27632 group (group LY).Inflammatory pain was induced by injecting LPS 25 μl (300 ng) into the plantar surface of hindpaws in IP, LC and LY groups, while the equal volume of normal saline was injected instead in NS group.C3 exoenzyme 10 pg and Y27632 10 nmol were injected intrathecally at 30 min prior to LPS administration in LC and LY groups, respectively.Before LPS injection (T0) , and at 1, 3, 5, 12 and 24 h after LPS injection (T1-5) , the mechanical and thermal pain thresholds were measured.Five rats in each group were sacrificed after pain thresholds were measured at T3, and L4.5 segments of the spinal cord were removed for determination of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) mRNA expression in spinal dorsal horns by real-time reverse transcriptase-polymerase chain reaction.Results Compared with group NS, the mechanical and thermal pain thresholds were significantly decreased at T2-5in IP, LC and LY groups, and TNF-α and IL-1β mRNA expression was up-regulated at T3 in IP group.Compared with group IP, the mechanical and thermal pain thresholds were significantly increased at T2-5, and TNF-α and IL-1β mRNA expression was down-regulated at T3 in LC and LY groups.Conclusion Spinal RhoA/ROCK signaling pathway is involved in the development of LPS-induced IP in rats.

Objective: To explore whether gancyclovir (GCV) can inhibit the proliferation and induce the erythro-differ-entiation of the K562 human myeloid leukemia cell line. Methods: 562 cells were cultured with GCV for 4 days to detect cellular changes cloning efficiency, benzidine-positive rate, flow eytometry analysis, and telomerase activity. Results: When 562 cells grew in the medium containing GCV, the cellular growth and division were gradually suppressed,growth fracture decreased and further differentiation towards the cell producing hemoglobins was found. Conclusion: GCVcan inhibit proliferation and induce erythro-differentiation of K562 cells.

Objective To evaluate the efficacy and mid-term follow-up results of endovascular treatment with Willis covered stent for traumatic pseudoaneurysms located in the internal carotid artery (ICA).Methods ICA angiogmphy was performed in 38 patients with traumatic brain and neck injury.Of the 38 patients.13 delayed traumatic pseudoaneurysms were found.All the pseudoaneurysms were treated with Willis covered stents.Follow-up angiography was performed at 1,3,6 and 12 months after the procedure,and the results were categorized as complete or incomplete occlusion.Clinical manifestations were graded as full recovery,improvement,unchanged and aggravation.Results Willis covered stent placement was technically successful in all traumatic pseudoaneurysms.No procedure-related complications occurred.The initial angiographic results showed a complete occlusion in 9 patients,and an incomplete occlusion in 4.The angiographic follow-up within 3-12 months exhibited a complete occlusion in 12 patients and the parent arteries remained patency in all patients.The clinical follow-up observation demonstrated that full recovery wag obtained in 11 patients,clinical improvement in one,and unchanged condition in one.No morbidity or mortality occurred.Conclusion Willis covered stent implantation iS a feasible and practical treatment for traumatic pseudoaneurysms located in the ICA.This technique can well preserve the parent artery with excellent therapeutic results.

OBJECTIVE:To investigate the inhibitory effects mechanism of scallop skirt glycosaminoglycan(SS-GAG)on inju-ry in human umbilical vein endothelium cells (HUVEC). METHODS:In the test,there was a negative control group,a model group and the groups of SS-GAG at high,middle and low concentrations(mass concentrations of 200,100 and 50 mg/L respective-ly). The cells in latter 3 groups were cultured in SS-GAG at different mass concentrations for 12 h,and then in 50 μmol/L oxidized low-density lipoprotein(OX-LDL)for 24 h. MTT method was used to detect cell viability and the activity of lactic dehydrogenase (LDH),the flow cytometer to determine the level of reactive oxygen species (ROS),real-time fluorescence quantitative poly-merase chain reaction (RT-PCR) to detect mRNA expression of lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), and Western blot to detect NOX4 protein expression. RESULTS:Compared to the cells in the negative control group,those in the model group demonstrated lower viability,higher activity of LDH,higher level of ROS,and stronger expressions of LOX-1 mRNA and NOX4 protein. There was statistical significance (P<0.01). Compared to the cells in the model group,those in the groups of SS-GAG at high,middle and low concentrations showed higher viability,lower activity of LDH,lower level of ROS and weaker expressions of LOX-1 mRNA and NOX4 protein. There was statistical significance (P<0.01). CONCLUSIONS:SS-GAG can protect HUVEC to some degree by a mechanism which may be related to inhibiting ROS production via LOX-1/NOX4 pathway and relieving oxidative stress injury.

Seven compounds were isolated from fermentation extract of cave-derived Metarhizium anisopliae NHC-M3-2 by silica gel, semi-preparative HPLC and other chromatographic methods. Their structures were elucidated by UV, IR, MS and NMR methods as 2,3-dehydroindigotide G (1), (-)-regiolone (2), naphtho-γ-pyrone (3), indigotide G (4), indigotide B (5) destruxin A (6) and destruxin B (7). Compound 1 is a new glycoside naphthopyranone compound. The anti-hepatitis B virus (HBV) activity of these compounds was evaluated. The EC₅₀ and CC₅₀ of compound 3 against HBV were 4.5 μmol·L^-1 and 92.3 μmol·L^-1, respectively. This is the first report of the antiviral activity of compound 3.