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The aim of the present study was to analyze the efficacy and safety of tenofovir (TDF) treatment for up to 5 years in nucleos(t)ide-naïve chronic hepatitis B (CHB) patients, particularly those with a high viral load, a in real-life scenario. A total of 144 nucleos(t)ide-naïve CHB patients who received TDF monotherapy for at least 3 months were retrospectively analyzed. The primary endpoint measure was the achievement of virological response (VR; undetectable serum HBV DNA, <100 IU/ml). The secondary endpoints were alanine aminotransferase (ALT) normalization (ALT < upper limit of normal), hepatitis B e antigen (HBeAg) seroconversion and safety. The median follow-up period was 120 weeks (range, 12–264 weeks). In total, 144, 130, 114, 78, 67, 40 and 13 patients were followed up for at least 12, 24, 48, 96, 144, 192 and 240 weeks, respectively. An incremental trend was observed in the rate of VR: 73.1, 91.3, 98.1, 100, 100 and 100% of the patients exhibited VR at 24, 48, 96, 144, 192 and 240 weeks, respectively. Furthermore, 29 patients with hepatitis B virus (HBV) DNA ≥8 log10 IU/ml at baseline achieved VR during the follow-up period. The proportions of patients achieving normal ALT levels were 72.1, 78.6, 91.2, 95, 96 and 100%, at 24, 48, 96, 144, 192 and 240 weeks, respectively. The rate of HBeAg loss reached 35.6% at week 240. Among the 130 patients, HBV DNA was detectable [partial VR (PVR)] in 35 patients at 24 weeks of follow-up, and 30 of those 35 patients (85.7%) required >24 weeks of further TDF therapy to achieve VR. No serious adverse events were reported. In conclusion, long-term TDF treatment of nucleos(t)ide-naïve chronic hepatitis B patients, regardless of high viral load at baseline, was effective and safe in a real-life scenario. Adjustment of TDF monotherapy may be unnecessary in nucleos(t)ide-naïve patients with PVR at 24 weeks. [ABSTRACT FROM AUTHOR]

This retrospective cohort study aimed to analyse the risk of congenital anomalies (CAs) in infants conceived by infertile women through assisted reproductive technology (ART). A total of 9,013 clinical pregnancy cycles resulting in 9,101 live births between 2004 and 2014 were analysed. Congenital anomalies were evaluated and compared with spontaneous pregnancies in infertile women. A total of 9,101 infants were born following ART. Three subgroups were established: In vitro fertilisation fresh embryo transfer (IVF-ET), n=2,919, intracytoplasmic sperm injection fresh embryo transfer (ICSI), n=1,996 and frozen-thawed embryo transfer (FET), n=4,186. No significant differences in perinatal outcomes were observed between the three subgroups. A total of 105 (1.15%) infants were born with CAs. The birth defect rate was slightly higher in the IVF-ET subgroup compared with the other subgroups. Among infants in the IVF-ET and ICSI-ET subgroup, the probability of birth defects increased with increased maternal age (>35 years), male factors and diminished ovarian reserve. In the FET group, the risk of birth defects was significantly increased with multiple births and maternal age >35 years. The risk of congenital anomalies following ART was not significantly different compared with spontaneous conceptions within the infertile study population. The results of the present study may provide guidance for patients who are considering treatment for infertility in China. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effect of propofol on immunoglobulin (Ig)E-activated mast cell degranulation and explore the underlying mechanisms responsible. RBL-2H3 cells were treated with propofol for at a variety of concentrations and different amounts of time. Cell viability was assessed using an MTT assay and microRNA (miR)-221 expression was quantified using reverse transcription-quantitative polymerase chain reaction. RBL-2H3 cells were transfected with miR-221 mimic or a negative control and degranulation, including the release of β-hexosaminidase and histamine, was evaluated using an ELISA kit. The effect of miR-221 overexpression on the phosphorylation of protein kinase B (Akt) was detected using western blotting and extracellular Ca2+ influx was measured via afura-2 assay. The phosphoinositide 3-kinase(PI3K) inhibitor LY294002 was used to investigate the association between PI3K/Akt signaling and Ca2+ influx in the presence of propofol. The results demonstrated that propofol treatment suppressed RBL-2H3 cell proliferation in a dose- and time-dependent manner. Propofol inhibited miR-221 expression in a dose-dependent manner compared with the control group; however, the inhibitive effect was significantly abrogated following transfection with miR-221 mimics. Furthermore, β-hexosaminidase and histamine release, PI3K/Akt signaling and Ca2+ influx were decreased following propofol application. miR-221 overexpression markedly ameliorated the suppressive effect of propofol. Treatment with LY294002 reversed the propofol-induced decrement of Ca2+ influx on IgE-mediated RBL-2H3 cells, suggesting an association between PI3K/Akt signaling and Ca2+ influx. In conclusion, the results of the present study suggest that propofol treatment attenuates mast cell degranulation via inhibiting the miR-221/PI3K/Akt/Ca2+ pathway. These results indicate that propofol may have a potential therapeutic effect as a treatment for allergic diseases. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the impact of carbobenzoxy-Leu-Leu-leucinal (MG-132) on myocardial remodeling in rats with myocardial infarction (MI) and investigate the possible underlying mechanisms. The rat model of MI was established, followed by administration of MG-132 (MG group), pyrrolidine dithiocarbamic acid (PDTC group) or normal saline (MI group) for 28 days. The expression of nuclear factor-κB (NF-κB) p65, interleukin 1β (IL-1β) and matrix metalloproteinase 2 (MMP-2), as well as the total volume of collagen and the ratio of type I/III collagen were then detected. Total collagen, including type I and III collagen, and the ratio of type I/III collagen were significantly increased in MI rats compared with those in the sham group (P<0.01), while it was significantly decreased in the PDTC and MG groups compared with that in the MI group (P<0.01). A similar trend was identified for the expression of NF-κB, IL-1β and MMP-2, which was significantly increased in the MI group compared with that in the sham group (P<0.01), while it was significantly decreased in the MG and PDTC groups compared with that in the MI group (P<0.01). In conclusion, MG-132 was demonstrated to improve post-MI tissue remodeling, and the mechanism may be associated with the inhibition of NF-κB activation and the downregulation of inflammatory cytokines, such as IL-1β. [ABSTRACT FROM AUTHOR]

Azithromycin has been widely used for the treatment of Treponema pallidum. However, the drug resistance of T. pallidum for azithromycin is currently increasing. The aim of the present study was to analyze the association between gene subtypes of T. pallidum and drug resistance for azithromycin. The gene subtypes of T. pallidum were assayed by a polymerase chain reaction technique. Drug resistance of T. pallidum was analyzed using an antimicrobial susceptibility test. The results demonstrated that gene type tpr presented higher drug resistance compared with arp and tp0548 gene types of T. pallidum. Gene type tpr was identified as eight gene subtypes (14a/f, 14e/f, 12e/f, 12d/f, 6d/f, 11d/f, 14j/f and 8d/f) among 324 cases. It was identified that 23S rRNA A2058G mutation was observed in gene subtypes 14a/f, 14e/f and 12e/f. A2059G mutation occurred in the gene subtypes 8d/f, 12d/f, 6d/f, 11d/f and 14j/f. The proportions of azithromycin-resistant genotypes harboring either the A2058G or the A2059G mutation among the T. pallidum strains were 34.2 and 65.8%, respectively. The antimicrobial susceptibility test demonstrated that A2059G mutations exhibited a higher drug resistance for azithromycin compared with A2058G mutations. In conclusion, these results indicate that azithromycin resistance in T. pallidum is associated with gene subtype, which may contribute to the treatment of T. pallidum. [ABSTRACT FROM AUTHOR]

Dexmedetomidine is a highly-selective a adrenergic receptor agonist, widely used as an anesthesia adjuvant drug in clinic. Effects of dexmedetomidine on autophagy of hippocampal neurons and cognitive dysfunction in aged rats under sevoflurane anesthesia were investigated. Sixty healthy Sprague-Dawley (SD) rats aged 4-6 months of either sex, weighing 150-200 g were selected and randomly divided into control group (n=10), sevoflurane group (n=25) and dexmedetomidine + sevoflurane group (compound group, n=25). The control group was inhaled with 60% O2 for 6 h, the sevoflurane group was inhaled with 3.4-3.6% sevoflurane for 6 h, and the compound group was treated with intraperitoneal injection of 4 μg/kg dexmedetomidine 1 h before the inhalation of sevoflurane. Five rats were taken from each group 1 h before sevoflurane anesthesia (T1), immediately after anesthesia (T2), 12 h after anesthesia (T3) and 24 h after anesthesia (T4), respectively. The expression levels of microtubule-associated protein 1 light-chain 3-I (LC3-I), LC3-II and Beclin-1 were detected via western blotting, and the LC3-II/LC3-I value was calculated. Moreover, Morris water maze test was performed for the five rats in each group 5 weeks after anesthesia to detect the cognitive function; the escape latency, times across platform and swimming time in target quadrant were recorded. The levels of LC3-I, LC3-II and Beclin-1 in hippocampal neurons and LC3-II/LC3-I value in sevoflurane group at T2 were significantly higher than those at T1, and they reached the peak at T3, but were decreased at T4 (P<0.05); the levels of proteins and LC3-II/LC3-I value in compound group at T2 were significantly higher than those at T1 and reached the peak, and remained unchanged at T3-T4; besides, the level of proteins and LC3-II/LC3-I values in compound group at T2-T4 were obviously lower than those in sevoflurane group (P<0.05). In sevoflurane group, the escape latency was prolonged, the times across platform were reduced and the swimming time in target quadrant was shortened compared with those in control group (P<0.05); these parameters were significantly improved in compound group compared with those in sevoflurane group and control group (P<0.05). In conclusion, dexmedetomidine can improve the cognitive dysfunction in aged rats under sevoflurane anesthesia, which is related to the decreased autophagy of hippocampal neurons. [ABSTRACT FROM AUTHOR]

The aim of the present study was to elucidate the mechanism of amygdalin treatment on reducing liver fibrosis by investigating its role in regulating the expression level of platelet‑derived growth factor (PDGF), insulin‑like growth factor (IGF) and PDGF receptor (PDGFR) in the hepatic stellate cell (HSC)‑T6 line. HSC‑T6 cells were used as an in vitro model and randomly assigned into four groups: control, high‑dose amygdalin, mid‑dose amygdalin and low‑dose amygdalin. Following amygdalin treatment, compared with the control, a high dose of amygdalin significantly suppressed the mRNA expression of PDGF and IGF (each P<0.05), whereas moderate and low doses showed no significant effect, relatively low doses of amygdalin are not sufficient to transfer signals to its receptor. The high‑dose amygdalin and low‑dose amygdalin displayed suppressed protein expression of PDGF at 24, 48 and 72 h, with the high‑dose group exhibiting the most marked suppression at all three time points. By reducing the transcription of PDGF and IGF mRNA and the expression of PDGF protein, amygdalin decreased the synthesis and release of PDGF and IGF, thereby reducing the influence of PDGF and IGF on HSCs, thus protecting the liver from fibrosis. [ABSTRACT FROM AUTHOR]

For several thousand years, Ganoderma lucidum (Ling-Zhi in Chinese and Reishi in Japanese) has been widely used as a traditional medication for the prevention and treatment of various diseases in Asia. Its major biologically active components, ganoderic acids (GAs), exhibit significant medicinal value due to their anti-inflammatory effects. Dysregulation of microglial function may cause seizures or promote epileptogenesis through release of proinflammatory cytokines, including interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α. At present, only little information is available on the effects of GAs on microglia-mediated inflammation in vitro and/or in vivo. The present study aimed to investigate the role of GA-A on microglia-mediated inflammation in vitro. In addition, the effect of GA-A on lipopolysaccharide (LPS)-evoked alterations in mitochondrial metabolic activity of microglia was evaluated. The results of the present study demonstrated that GA-A significantly decreased LPS-induced IL-1β, IL-6 and TNF-α release from mouse-derived primary cortical microglial cells in a concentration-dependent manner. GA-A treatment reduced LPS-induced expression of nuclear factor (NF)-κB (p65) and its inhibitor, demonstrating that non-toxic suppression of IL-1β, IL-6 and TNF-α production by GA-A is, at least in part, due to suppression of the NF-κB signaling pathway. In addition, the LPS-induced stimulation of mitochondrial activity of microglial cells was abolished by co-treatment with GA-A. Thus, GA-A treatment may be a potential therapeutic strategy for epilepsy prevention by suppressing microglia-derived proinflammatory mediators. [ABSTRACT FROM AUTHOR]

Endometriosis (EM) is associated with oxidative stress. Advanced oxidation protein products (AOPPs) are novel markers of oxidative stress, which serve an important role as an inflammatory mediator in various chronic diseases. In order to examine the role of AOPPs in infertile women with EM, the present study analyzed the levels of AOPPs, estradiol (E2) and progesterone (P4) in the follicular fluid (FF) of 89 women with or without EM undergoing in vitro fertilization (IVF). The AOPP concentration in the FF of the EM group was significantly higher when compared with that of the control group (51.5±22.4 vs. 41.8±18.3 µmol/l; P<0.05). However, the FF P4 levels and blastocyst rate were significantly lower in the EM group compared with the control group (P4:1,249.6±465.4 vs. 1,752.7±565.4 ng/ml, P<0.05; blastocyst rate: 0.511±0.322 vs. 0.662±0.278; P<0.05). The AOPP concentration and P4 level in the FF presented a significant negative correlation in the EM and control groups, as well as in the total cohort of patients (EM group: r=-0.406, P=0.006; control group: r=-0.315, P=0.035; total: r=-0.421, P<0.001). In addition, there was a significant negative correlation between the FF AOPP concentrations and blastocyst rate in the EM group and in the total cohort (EM group: r=-0.376, P=0.012; total: r=-0.367, P<0.001). In conclusion, these results suggested that AOPPs may be a potentially effective marker for predicting the oocyte quality and outcomes of IVF in infertile women with EM. [ABSTRACT FROM AUTHOR]

The clinical efficacy of ulinastatin (UTI) combined with continuous renal replacement therapy (CRRT) in the treatment after early cardiopulmonary resuscitation (CPR) was evaluated. A total of 70 patients who were successfully treated with CPR in Ganzhou People's Hospital from October 2016 to March 2017 were selected as the subjects. The patients were randomly divided into control group (35 cases, conventional treatment) and UTI combined with CRRT group (35 cases, UTI + CRRT). The whole blood of patients was collected at 0, 3, 6 and 12 h after CPR. Reverse transcription-polymerase chain reaction assay was used to detect the changes of tolllike receptor 4 (TLR4) gene in mRNA levels between the two groups, i-STAT system 300 was used to analyze pH level, SO2, HCO3 - and lactic acid (LAC) concentration; Abbott AXSYM system was used to detect the expression of cardiac troponin I (cTnI) in serum; the concentration of plasma malondialdehyde (MDA) was examined by a special kit; interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in patients was determined by enzyme-linked immunosorbent assay. The effect of UTI combined with CRRT in the early stage of CPR was analyzed. The levels of TLR4, cTnI, TNF-α, IL-6 and MDA in the plasma of patients in both groups were significantly increased (P<0.05), but the expression level in UTI + CRRT group was lower than that in control group (P<0.05). Compared with the control group, the HCO3 - decreased significantly (P<0.05) in the UTI + CRRT group at 3 h, while the pH and SO2 did not change significantly. UTI + CRRT could significantly shorten the average recovery time of consciousness and the average recovery time of consciousness and spontaneous respiration in patients treated with CPR (P<0.05). Moreover, the score of APACHE II was significantly lower than that of control group (P<0.05). UTI combined with CRRT treatment can significantly improve the patient's condition after early CPR. [ABSTRACT FROM AUTHOR]

There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning. [ABSTRACT FROM AUTHOR]

Pulmonary mucormycosis, a relatively rare pulmonary fungal disease, is difficult to diagnose and lacks effective treatment. The present study reports the case of a 64-year-old patient who was treated successfully for pulmonary mucormycosis in Xuan Wu Hospital. The patient presented with low-grade fever and a productive cough that persisted for 1 month with no evident cause, and also suffered from diabetes mellitus. Prior antibiotic treatment with levofloxacin had been ineffective. Culture of mucus obtained by bronchoscopy resulted in a diagnosis of pulmonary mucormycosis. The patient received a cumulative dose of 1,355 mg amphotericin B over 2 months and presented a full recovery. [ABSTRACT FROM AUTHOR]

Breast cancer, which is the second leading cause of cancer-associated mortality in women worldwide, develops from breast tissue. Chemotherapy is the most commonly used therapy to treat breast cancer. However, a number of natural plant-derived products have been suggested as alternative therapies to treat different types of cancer, such as breast cancer. The aim of the present study was to determine the anti-tumor effects of ursolic acid and its effect on apoptosis and inflammation in breast cancer cells. The anti-cancer effects of ursolic acid were evaluated in vitro using flow cytometry, western blotting and reverse transcription-quantitative polymerase chain reaction. The results suggest that ursolic acid inhibits the viability of breast cancer cells by inducing autophagy and apoptosis without inducing cell death. Cellular migration assays demonstrated that ursolic acid was able to suppress the invasive ability of breast cancer cells (P<0.05). In addition, the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway was downregulated following ursolic acid administration (P<0.05), leading to an upregulation of glycogen synthase kinase activity (P<0.05) and downregulation of B-cell lymphoma 2 (P<0.05), subsequently causing autophagy and apoptosis via cyclin-D1 inhibition and caspase-3 stimulation (P<0.05). Furthermore, the inflammatory response of breast cancer cells was assessed by measuring levels of nuclear factor (NF)-κB. Ursolic acid was found to downregulate NF-κB in breast cancer cells, thus inhibiting inflammation and preventing the progression of breast cancer (P<0.05). To the best of our knowledge, the present study is the first to assess the effect of ursolic acid on breast cancer cells through PI3K/AKT-regulated GSK and caspase-3 accompanied by NF-κB signaling pathways. The results of the present study regarding the potential underlying molecular mechanisms of ursolic acid may be used to develop novel therapeutic strategies for breast cancer treatment. [ABSTRACT FROM AUTHOR]

The objective of this study was to investigate the effects of leukotriene B4 (LTB4) on the expression of interleukin-32 (IL-32) interferon-γ (IFN-γ) and chemokine monocyte chemoattractant protein (MCP-1) and macrophage inhibitory protein (MIP-1α) in rheumatoid arthritis (RA). The rat model of RA collagen induced-arthritis (CIA) was established. The levels of LTB4, interleukin-32, IFN-γ and chemokines MCP-1 and MIP-1α in CIA rats were detected by ELISA. After the rat synovial cells were isolated and treated with different concentrations of LTB4, the effect of LTB4 the expression of IL-32, IFN-γ and chemokines MCP-1 and MIP-1α mRNA in synovial cells was detected by real-time quantitative PCR, the effect of LTB4 on protein expression was detected by immunoblotting. The effects of different concentrations of LTB4 on the viability and apoptosis of synovial cells were detected by LDH and cell proliferation reagent WST-1. Compared with the control group, the levels of LTB4, IL-32, IFN-γ and chemokines MCP-1 and MIP-1α were significantly increased in the serum of the CIA group. After treatment of CIA rat synovial cells with different concentrations of LTB4, the expression of IL-32, IFN-γ and chemokines MCP-1 and MIP-1α mRNA and protein were increased with significant differences among groups. WST-1 and flow cytometry showed that LTB4 had significant toxic effects on synovial cells and promoted apoptosis. In conclusion, LTB4 promotes the expression of interleukin-32, IFN-γ and chemokines MCP-1 and MIP-1α in synovial cells and facilitates apoptosis of synovial cells. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the effect of orally administered simvastatin on lumbar vertebral bone mass and intervertebral disc (IVD) degeneration in ovariectomized (OVX) rats. A total of 30 female Sprague-Dawley (SD) rats were subjected to either bilateral ovariectomy (n=20) or sham surgery (n=10). After 12 weeks, the OVX rats were orally administered either saline vehicle (OVX + V group; n=10), or 5 mg/kg/day simvastatin (OVX + SIM group; n=10). Following 12 weeks of treatment, necropsy was conducted and bone mineral density (BMD) was determined in the L5-6 vertebrae. Furthermore, the microstructure and biomechanical properties of the L3 vertebrae were detected by micro-computed tomography and compression testing, respectively. The L5-6 vertebrae were analyzed by measurement of IVD height, observation of histological changes by van Gieson staining, and evaluation of collagen-II (col-II), aggrecan (AGG) and collagen I (col-I) expression by immunohistochemical analysis. Rats in the OVX+V group had lower BMD, bone volume/trabecular volume ratio, maximum load and elastic modulus than the sham group. Rats in the OVX + SIM group had higher BMD and biomechanical strength values than the rats in the OVX+V group. Histological analysis showed that the OVX + V and OVX + SIM groups exhibited significantly higher disc degeneration scores and significantly lower IVD height than the sham group. Immunohistochemical analysis revealed lower expression levels of col-II and AGG, but higher levels of col-I in the annulus fibrosis and endplate in OVX+V rats compared with the sham group. The OVX + SIM group exhibited levels of col-II, AGG and col-I expression comparable with those of OVX+V rats, with the exception of an upregulation of col-II expression in the annulus fibrosis. These data demonstrate that simvastatin treatment partially prevented bone loss and the deterioration of biomechanical properties of lumbar vertebrae, but not the progression of IVD degeneration in OVX rats. [ABSTRACT FROM AUTHOR]

The expression of cell factors of schizophrenia and the effect of the modified electric convulsive treatment (MECT) were studied. In total, 156 patients with schizophrenia were selected, and divided into the drug group (70 cases) and the drug combined with MECT group (combined group) (86 cases) according to the treatment methods. In addition, 70 cases of healthy volunteers (control group) were selected according to the closest matching method based on 1:1 of age and gender. The drug treatment, consisted of anti-psychotic drugs, such as risperidone 2-8, quetiapine 300-750, ziprasidone 80-160 or aripiprazole 10-30 mg/day, and for the control group, we used the electric spasm therapeutic instrument, Thymatron®IV Systems up to 6 times, 3 times a week. The levels of interleukin (IL)-10, IL-4, IL-6 and IL-1 were detected before and after treatment by ELISA. The positive and negative symptom scale (PANSS) was used to evaluate the efficiency. Before the treatment, IL-1 and IL-6 levels of drug and combined groups were significantly higher than those of the control group (P<0.05), while IL-4 and IL-10 had no difference with the control group. There was no significant difference of each factor between the drug and combined groups. After treatment, IL-1, IL-6 and IL-10 of the drug group did not change compared to the levels before treatment, but IL-4 increased significantly; IL-1 and IL-10 of the combined group did not change, while IL-4 and IL-6 increased significantly; IL-1, IL-4 and IL-6 of the drug and combined groups were significantly (P<0.05) higher than those in the control group, but not IL-10. IL-1, IL-4 and IL-6 levels of the combined group were significantly higher (P<0.05) than those of the drug group. After treatment, the PANSS scores of the two groups decreased and the combined group decreased more significantly (P<0.05). The reduction rate of the combined group was significantly higher (P<0.05) than that of the drug group. The total efficiency of the combined group was significantly higher than that of the drug group, and after comparing these levels, there was statistical significance (P<0.05). IL-1, IL-4, IL-6 and IL-10 levels of the drug and combined groups before treatment were not associated with PANSS scores and the variation of IL-1, IL-4, IL-6 and IL-10 of the drug and combined groups had no correlation with the reduction rate of the PANSS. The results showed that, cell factors of schizophrenia had an abnormal expression, and medication and MECT can affect the expression level. In addition, MECT can improve the effect in the treatment of schizophrenia, but had no obvious correlation with the change of cell factors. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the clinical, biochemical and genetic mutation characteristics of two cases of late-onset glutaric aciduria type I (GA-I) in Uighur. The clinical data and glutaryl-CoA dehydrogenase (GCDH) genetic test results of two cases of late-onset GA-I in Uighur were collected and analyzed, and reviewed with relevant literature. One patient with late-onset GA-I primarily exhibited clinical intermittent headache, while the other patient was asymptomatic. The urinary organic acid analysis detected a large number of glutaric acid and 3-hydroxy glutaric acid, 3-hydroxy-propionic acid. One patient exhibited white matter degeneration in cranial magnetic resonance imaging (MRI) and the other patient showed no abnormality. The two patients both exhibited c. 1204C >T, p.R402W, heterozygous mutation, and c. 532G >A, p.G178R, heterozygous mutation. Besides central nervous system infectious diseases, patients with clinical headache, cranial MRI-suggested bilateral temporal lobe arachnoid cyst and abnormal signals in the basal ganglia should be highly suspected as late-onset GA-I. Early diagnosis and correct treatment are key to improve its prognosis. [ABSTRACT FROM AUTHOR]

Atherosclerosis, the major cause of cardiovascular disease, is accompanied by a chronic inflammatory response during the disease. Triptolide (TPL) is an active natural compound that has been demonstrated to possess anti-inflammatory activities in various cell types. However, the effects of TPL on atherosclerosis have not yet been studied. The goal of the present study was to determine the effects of TPL on apolipoprotein E knock-out (ApoE-/-) mice fed with a high-fat diet and to analyze the changes in lipid metabolism and inflammatory cytokines to clarify the underlying molecular mechanisms. Firstly, the genotypes of ApoE-/- mice and corresponding wild-type mice were identified using polymerase chain reaction. The ApoE-/- mice were randomly divided into four groups: ApoE-/- model mice, and ApoE-/- mice treated with 25, 50 or 100 μg/kg TPL every twice day. Wild-type mice with the same genetic background constituted the fifth group. The mice in each group were given a high-fat diet from week 8 after birth until week 20. Total cholesterol and total triglyceride levels were determined at 16 and 20 weeks. The results demonstrated that the levels of total cholesterol and total triglyceride in the plasma were highly increased in ApoE-/- mice models, compared with those of wild-type mice, and the ApoE-/- mice treated with TPL had decreased levels of total cholesterol and total triglyceride in plasma, which exhibited a dose-dependent reduction as the dose of TPL increased. Moreover, the effects of TPL on the production of inflammatory cytokines in macrophages were determined by ELISA. The results demonstrated that the macrophages from ApoE-/- mice produced high levels of the inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and IL-8. However, following treatment with TPL doses of 25, 50 and 100 μg/kg, the cytokine levels were significantly decreased in a dose-dependent manner. Additionally, proteins associated with lipid metabolism were tested by western blotting. The results showed that the expression of anti-ATP-binding cassette transporter A1 in the macrophages of ApoE-/- mice was increased following treatment with TPL. However, the expression levels of LXRα were not markedly changed following treatment of the mice with different doses of TPL. These results suggest that TPL inhibited the progression of atherosclerosis not only by inhibiting the chronic inflammatory response, but also by regulating lipid metabolism, which may provide new insights useful in the clinical therapy of atherosclerosis. [ABSTRACT FROM AUTHOR]

In patients undergoing off-pump coronary artery bypass surgery (OPCAB), it is important to attenuate myocardium injury during the surgery. The present study aimed to observe the cardioprotection induced by sevoflurane induction and maintenance compared with propofol intravenous anesthesia, and to detect its potential protection against acute myocardial injury with sensitive biomarkers. In total, 36 patients undergoing OPCAB were randomly assigned into two groups, receiving sevoflurane (n=18) or propofol (n=18) as the induction and maintenance anesthetic agent. The depth of anesthesia in the two groups was kept at a bispectral index value of 40-50. Physiological and hemodynamic parameters were recorded during the surgery. Cardiac troponin-I (cTnI), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and two microRNAs (miR-499 and miR-208b) were also measured during and subsequent to surgery. Nno statistically significant differences were observed in the physiological and hemodynamic parameters between the two groups prior to surgery. Following surgery, the cardiac output and stroke volume improved significantly in the sevoflurane group (P<0.05). In addition, patients in the sevoflurane group had lower miR-499 (P<0.05) and miR-208b (P<0.01) levels at 12 h after surgery when compared with the propofol group. However, no significant differences in cTnI, CK-MB and LDH levels were observed following surgery between the two groups. In conclusion, volatile induction and maintenance with sevoflurane resulted in some extent of cardiac function improvement in patients undergoing OPCAB. Cardioprotection by sevoflurane is suggested by reduced cardiac injury compared with propofol, and indicated by the sensitive biomarkers, circulating miR-499 and miR-208b. [ABSTRACT FROM AUTHOR]

The aim of the present study was to evaluate the clinical efficacy of peritoneal dialysis (PD) in patients with severe lupus nephritis (LN) complicated with organ dysfunction. In total, 13 severe LN patients complicated with multiple-organ dysfunction, who underwent PD treatment between November 2003 and September 2010, were enrolled in the study. Six patients received methylprednisolone pulse therapy due to lupus activity and progressive renal failure. These patients were complicated with severe edema, cardiac insufficiency and severe hypoalbuminemia. PD was applied to the patients, followed by the administration of immunosuppressants. Patients were followed-up to review the parameters of renal function, the immunological indexes and the systemic lupus erythematosus disease activity index. The results indicated that the general state of health was markedly improved following PD treatment, with edema abatement and improvement of heart function and physical strength. Serum creatinine levels significantly decreased from 6.3±1.6 to 2.6±1.0 mg/dl. A total of 10 cases ceased PD treatment during the follow-up, while three cases continued PD to the end of the follow-up period. The levels of albumin and hemoglobin exhibited a marked increase from 29.7±5.7 to 35.2±5.5 g/l and 8.7±1.8 to 9.8±1.8 g/l, respectively. There was one case of peritonitis, one case of peritoneal leakage and two cases of pneumonia. Therefore, PD may be a successful treatment method for severe LN patients complicated with essential organ dysfunction. PD not only improved the symptoms of edema and heart failure, but also played an important role in preserving residual renal function and improving the nutritional state of the patients. Thus, PD can be considered as a treatment option for patients with severe LN associated with acute kidney injury, however, selecting a suitable immunosuppressant during PD treatment is essential. [ABSTRACT FROM AUTHOR]

The purpose of this study was to explore the feasibility of continuous remote monitoring, and the induction and termination of malignant ventricular arrhythmias (VAs) by a novel implantable electronic cardiovascular device (IECD) system in rabbits with myocardial infarction (MI). The IECD was implanted and MI was induced by ligation of the left anterior descending coronary artery in 20 adult rabbits. Internet-based remote electrocardiogram (ECG) monitoring and ventricular stimulation were conducted in remote locations with internet access. The voltage amplitudes of the stimulation signals were recorded synchronously by remote and surface ECG. Programmed stimulation with regular stimuli and regular stimuli with an added extra stimulus were performed prior to and following the MI surgery to induce and terminate VAs. IECD implantation and MI surgery, as well as qualified remote and bidirectional signal communications between the implanted IECD and extracorporeal system, were successfully achieved in 18 rabbits. The voltage of the stimulation signals recorded by the remote and surface ECGs showed a good correlation with the stimulation current (remote ECG, r=0.972 and surface ECG, r=0.988; P<0.001). Sustained ventricular tachycardia (VT) was induced in five rabbits (5/20, 25%) prior to MI induction and in 12 rabbits (12/16, 75%) following MI induction. Of the 17 induced VTs, 16 were successfully terminated by remote ventricular stimulation. The novel IECD system provides qualified remote wireless ECG monitoring and possesses the potential to induce and terminate VAs by remote ventricular pacing in this rabbit model of MI. Thus, this model of MI may be used to test the efficacy of novel drugs and devices for the management of VAs. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the clinical characteristics of and treatment strategies for interstitial pneumonia induced by gefitinib in patients with advanced non-small cell lung cancer (NSCLC). The detailed clinical data of one patient with NSCLC and gefitinib-induced interstitial pneumonia were compiled and a review of relevant previous studies was performed. Based on this case report and the review, the clinical characteristics, mechanisms and treatment strategies of this rare disease were analyzed. The analyses showed that older, male patients with a long smoking history, high smoking index and adenocarcinoma (particularly bronchoalveolar carcinoma) were more likely to suffer from interstitial pneumonia while taking gefitinib. The onset time of interstitial pneumonia was 1-2 months subsequent to gefitinib administration. The clinical manifestations included chest tightness, shortness of breath, progressive dyspnea, severe hypoxemia and respiratory failure. Diffuse infiltration and alveolar interstitial shadows were observed on the chest tomography scan. In such circumstances, a timely judgment is required, in addition to the withdrawal of gefitinib treatment and the administration of high-dose glucocorticoids, as well as oxygen inhalation and anti-infective therapies, in order to relieve the symptoms. In conclusion, following the onset of gefitinib-induced interstitial pneumonia, the discontinuation of gefitinib is likely to alleviate the suffering of the majority of patients. Early interstitial pneumonia is not an absolute index for the permanent discontinuation of gefitinib treatment. It is necessary to comprehensively consider the benefits and hazards of gefitinib for the patients. [ABSTRACT FROM AUTHOR]

The present study aimed to evaluate the effects of an individualized, low-dose multi-drug immunosuppressive regimen for the treatment of immunoglobulin A nephropathy (IgAN). A preliminary investigation of the course of IgAN following immunosuppressive treatment was conducted based on repeat renal biopsies. Clinical and pathological data of 17 patients with IgAN who received repeat renal biopsies were analyzed retrospectively. In addition to basic treatment, 16 patients regularly received an individualized low-dose immunosuppressive regimen according to their clinical manifestations and pathological patterns following the first biopsy. Clinical parameters, including 24-h urinary protein excretion and levels of serum albumin, uric acid and total cholesterol were collected. Glomerular deposits of IgA and C3, as well as the activity and chronicity indexes of renal lesions were evaluated by semi-quantitative methods. The 24-h urinary protein excretion of the patients decreased significantly from the first biopsy (2.53±2.17 g/day) to the repeated biopsy (0.26±0.55 g/day) (P<0.001). Deposits of IgA and C3 in the glomerulus were persistent, but were reduced in quantity at the second biopsy. Although active renal lesions were observed in the majority of patients, the activity index decreased significantly from 3.18±1.33 prior to therapy to 2.47±0.80 following therapy (P<0.05), while the chronicity index did not change significantly (2.59±2.00 versus 2.76±1.89, respectively). The individualized, low-dose multi-drug immunosuppressive regimen used in the present study significantly minimized proteinuria, stabilized renal function and alleviated histological lesions in patients with IgAN without causing overt adverse effects during the short-term follow-up. In addition to proteinuria, renal pathological changes should be appraised when considering the withdrawal of immunosuppressants from IgAN treatment. [ABSTRACT FROM AUTHOR]

Basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) have been shown to be involved in a spectrum of cellular processes. In a previous study, we constructed a novel multigenic vector that contained two separate transcription units, each consisting of a strong promoter and an efficient polyadenylation signal. The two promoters were chosen for their ability to work simultaneously. Dual gene transfer of bFGF and PDGF in a single plasmid resulted in a significant increase in collateral blood vessel formation in a rabbit model of hind limb ischemia. The aim of the present study was to investigate the effect of this dual gene transfer strategy in a rat model of acute myocardial infarction (AMI). AMI was induced in rats by ligation of the left anterior descending coronary artery. The animals were randomly divided into four groups and treated with the following therapeutic strategies: Empty plasmid (control), plasmid encoding bFGF (PL-bFGF), plasmid encoding PDGF (PL-PDGF) or plasmid encoding bFGF and PDGF (PL-F-P). Echocardiography and histological examinations were performed 28 days subsequent to gene transfer. Dual gene therapy with bFGF and PDGF resulted in a significant angiogenic effect accompanied by vessel maturation, along with a significant reduction in infarct size and improvement in cardiac function. In a rat model of AMI, single plasmid-mediated dual gene therapy with bFGF and PDGF decreased infarct size and improved cardiac function due to the formation of functionally and morphologically mature vasculature. These results are relevant to the ongoing clinical trials involving the use of single plasmid-mediated angiogenic factors for the treatment of myocardial ischemic disease. [ABSTRACT FROM AUTHOR]

Cardiac electrophysiological heterogeneity related to the washout of acetylcholine (ACh) remains incompletely characterized. The aim of this study was to examine whether positive cardiac inotropic action is associated with electrophysiological heterogeneity between the atrium and the ventricle after ACh perfusion and washout. Epicardial monophasic action potentials (MAPs) from the right ventricle and right atrium, as well as cardiac contractility, were recorded from isolated Langendorff-perfused rabbit hearts using MAP electrodes and a force transducer. The results indicated that rebound positive inotropic actions were induced by ACh washout with adrenaline preconditioning. This effect was accompanied by an increase in MAP amplitude (MAPA) in the right ventricle but not the right atrium. These findings indicate that cholinergic muscarinic stimulation may lead to positive cardiac inotropic action followed by changes in regional electrophysiological heterogeneity between the atrial and ventricular myocardium. Therefore, we hypothesize that electrophysiological heterogeneity is an underlying cause of arrhythmogenesis as well as hemodynamic disturbance elicited by sudden termination of vagus stimulation. [ABSTRACT FROM AUTHOR]