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Li Dong,1 Yu-Min Zheng,2 Xiao-Guang Luo,3 Zhi-Yi He2 1Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, People’s Republic of China; 3Department of Neurology, The First Affiliated Hospital of South University of Science and Technology, The Second Clinical College of Jinan University, Shenzhen People’s Hospital, Shenzhen, People’s Republic of ChinaCorrespondence: Xiao-Guang LuoDepartment of Neurology, The First Affiliated Hospital of South University of Science and Technology, The Second Clinical College of Jinan University, Shenzhen People’s Hospital, Shenzhen, People’s Republic of ChinaEmail guanche537@126.comZhi-Yi HeDepartment of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, People’s Republic of ChinaEmail yizizhan40559@163.comBackground: Parkinson’s disease is a common neurodegenerative disease in the elderly. The incidence of various cancers in Parkinson’s disease patients is significantly lower than in healthy people. Parkinson’s disease patients are individuals with a high tendency for inflammation, whose peripheral immune system is represented in an activated state. We hypothesized that the hyperinflammatory predisposition of Parkinson’s disease patients is pathogenic.Methods: DBA/1 mice were used to simulate “highly inflammatory individuals”, and the carcinogen DEN was used to induce malignancy. Hematoxylin & eosin (H&E) staining was used to observe the formation of lung tumors. Apoptosis of neurons was observed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Immunohistochemistry and flow cytometry were used to observe CD4, CD28, major histocompatibility complex II (MHCII), cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), and programmed death 1 (PD-1). The ionized calcium binding adaptor molecule-1 (IBA-1) + inducible nitric oxide synthase (iNOS) was used to label M1 microglia, and IBA-1 + arginase 1 (Arg1) was used to label M2 microglia by immunofluorescence. The expression of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and anti-inflammatory cytokines IL-10 and IL-4 was detected by ELISA.Results: DBA/1 mice with high inflammatory tendency showed a continuous increase of peripheral inflammation, promoting intracranial inflammation, decreasing the tumor incidence and increasing the neurodegeneration under induction of malignant change. CD28 and CTLA-4/PD-1 reduced the T-cell-dominated inflammatory response, reduced the intracerebral inflammatory response, protected from neurodegeneration, and increased the incidence of tumor. Combination of CTLA-4 and PD-1 blocker can overactivate T cells, worsen peripheral and intracranial inflammation, reduce the incidence of tumor, cause damage to dopamine neurons, and promote the occurrence of neurodegeneration.Conclusion: High inflammatory tendency induced by malignant stimulation through the imbalance of CD28 and CTLA-4/PD-1 leads to dopamine neuron injury.Keywords: high inflammatory tendency, malignant stimulation, CD28, CTLA-4/PD-1, dopamine neuron injury

In this study, we investigated the beneficial effects of high endogenous levels of n-3 polyunsaturated fatty acids (PUFAs) on skeletal muscle repair and regeneration using a mouse cardiotoxin (CTX, 20 μM/200 μL) -induced gastrocnemius muscle injury model. Transgenic fat-1 mice expressing the Caenorhabditis elegans fat-1 gene, encoding n-3 fatty acid desaturase, showed higher n-3 PUFA levels and lower n-6/n-3 PUFA ratios in gastrocnemius muscle tissues. Hematoxylin and eosin and Masson’s trichrome staining of gastrocnemius sections revealed increased muscle fiber size and reduced fibrosis in fat-1 mice on days 7 and 14 after CTX injections. Gastrocnemius muscle tissues from fat-1 mice showed reduced inflammatory responses and increased muscle fiber regeneration reflecting enhanced activation of satellite cells on day 3 after cardiotoxin injections. Gastrocnemius muscle tissues from cardiotoxin-treated fat-1 mice showed reduced levels of pro-apoptotic proteins (Caspase 3 and Bax) and increased levels of anti-apoptotic proteins (Bcl-2 and Survivin). Moreover, eicosapentaenoic acid (EPA) reduced the incidence of apoptosis among cardiotoxin-treated C2C12 mouse myoblasts. These findings demonstrate that higher endogenous n-3 PUFA levels in fat-1 mice enhances skeletal muscle repair and regeneration following cardiotoxin-induced injury.

Background The global incidence and mortality rates of liver cancer, which is the second leading cause of cancer-related deaths worldwide, are increasing. However, information on its epidemiology and clinical prognosis is limited. This study aimed to characterize the epidemiology and prognostic factors of secondary liver cancer to aid in the pretreatment evaluation of the disease. Methods Patients diagnosed with secondary liver cancer between 2010 and 2014 in the Surveillance, Epidemiology, and End Results (SEER) database were retrospectively included. Kaplan-Meier analysis and Multivariate Cox regression analysis were performed to screen for significant factors associated with secondary liver cancer. Results A total of 85,738 secondary liver cancer patients were identified; in this population, the first primary site was the lung (25.9%), followed by the colorectum, pancreas, stomach, breast, and cecum. Patients with primary tumors of the colorectum, cecum and breast had longer median survival time. Advanced age, male gender, black race, poor differentiation or lack of differentiation, regional lymph node metastases, and presence of distant metastasis were associated with poor prognosis. Conclusions In this study, novel findings on the role of the primary site and synchronous distant metastasis to specific organs in patients with secondary liver cancer were described. These findings have significant implications in clinical diagnosis and treatment, and provide a better understanding of secondary liver cancer in the general population.

BackgroundThis study aimed to develop an artificial neural network (ANN) model for predicting synchronous organ-specific metastasis in lung cancer (LC) patients.MethodsA total of 62,151 patients who diagnosed as LC without data missing between 2010 and 2015 were identified from Surveillance, Epidemiology, and End Results (SEER) program. The ANN model was trained and tested on an 75/25 split of the dataset. The receiver operating characteristic (ROC) curves, area under the curve (AUC) and sensitivity were used to evaluate and compare the ANN model with the random forest model.ResultsFor distant metastasis in the whole cohort, the ANN model had metrics AUC = 0.759, accuracy = 0.669, sensitivity = 0.906, and specificity = 0.613, which was better than the random forest model. For organ-specific metastasis in the cohort with distant metastasis, the sensitivity in bone metastasis, brain metastasis and liver metastasis were 0.913, 0.906 and 0.925, respectively. The most important variable was separate tumor nodules with 100% importance. The second important variable was visceral pleural invasion for distant metastasis, while histology for organ-specific metastasis.ConclusionsOur study developed a “two-step” ANN model for predicting synchronous organ-specific metastasis in LC patients. This ANN model may provide clinicians with more personalized clinical decisions, contribute to rationalize metastasis screening, and reduce the burden on patients and the health care system.

BackgroundStroke is the leading cause of mortality in China, with limited evidence of in-hospital burden obtained from nationwide surveys. We aimed to monitor and track the temporal trends and rural–urban disparities in cerebrovascular risk factors, management and outcomes from 2005 to 2015.MethodsWe used a two-stage random sampling survey to create a nationally representative sample of patients admitted for ischaemic stroke in 2005, 2010 and 2015. We sampled participating hospitals with an economic-geographical region-stratified random-sampling approach first and then obtained patients with a systematic sampling approach. We weighed our survey data to estimate the national-level results and assess changes from 2005 to 2015.ResultsWe analysed 28 277 ischaemic stroke admissions from 189 participating hospitals. From 2005 to 2015, the estimated national hospital admission rate for ischaemic stroke per 100 000 people increased (from 75.9 to 402.7, Ptrendtrendtrendtrend=0.046), and decreases in in-hospital mortality (0.7% in 2015 vs 1.8% in 2005; adjusted OR (aOR) 0.52; 95% CI 0.32 to 0.85) and the composite outcome of in-hospital mortality or DAMA (8.4% in 2015 vs 13.9% in 2005; aOR 0.65; 95% CI 0.47 to 0.89) were observed. Disparities between rural and urban hospitals narrowed; however, disparities persisted in in-hospital management (brain MRI: rural–urban difference from −14.4% to −11.2%; cerebrovascular assessment: from −20.3% to −16.7%; clopidogrel: from −2.1% to −10.3%; anticoagulant for atrial fibrillation: from −10.9% to −8.2%) and in-hospital outcomes (DAMA: from 2.7% to 5.0%; composite outcome of in-hospital mortality or DAMA: from 2.4% to 4.6%).ConclusionsFrom 2005 to 2015, improvements in hospital admission and in-hospital management for ischaemic stroke in China were found. A temporal improvement in DAMA and improvements in in-hospital mortality and the composite outcome of in-hospital mortality or DAMA were observed. Disparities between rural and urban hospitals generally narrowed but persisted.

Lung and systemic inflammation are associated with impaired lung function and increased mortality in patients with chronic obstructive pulmonary disease (COPD). Theophylline and glucocorticoids have been shown to have an anti-inflammatory effect in some respiratory diseases. However, corticosteroid insensitivity is a major barrier to the anti-inflammatory management of COPD. This study aimed to explore whether a combined treatment of theophylline and dexamethasone (Dex) could decrease cigarette smoke extract (CSE)-induced inflammation via prevention of a reduction in histone deacetylase 2 (HDAC2) expression and through inhibition of the PI3K/Akt pathway, which may be related to corticosteroid sensitivity. The half-maximal inhibitory concentration (IC(50)) of Dex (IC(50)-Dex) was used to as a marker of corticosteroid sensitivity. IC(50)-Dex was determined through observation of Dex inhibition of tumor necrosis factor-α (TNF-α)-induced interleukin (IL)-8 release. Using reverse transcription quantitative PCR and western blotting, U937 cells treated with CSE were assessed for HDAC2 expression levels and phosphorylation levels of Akt. Theophylline and Dex pre-treatment was shown to significantly reduce the CSE-induced release of IL-8 and TNF-α. The combination of theophylline and Dex pretreatment also reversed corticosteroid insensitivity in CSE-induced U937 cells and inhibited the PI3K/AKT pathway to a greater extent than theophylline treatment alone. CSE-treated U937 cells showed a reduction in HDAC2 mRNA and protein expression compared with the control group. However, this effect was reduced after pre-incubation with the combined therapy or theophylline alone. In conclusion, pretreatment with theophylline and Dex decreased CSE-induced inflammation via inhibition of the PI3K/Akt pathway and increase in HDAC2 protein expression.

Oxidized low-density lipoprotein receptor 1 (OLR1) is upregulated in neurons and participates in hypertension-induced neuronal apoptosis. OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke. Therefore, OLR1 is likely involved in the progress of intracerebral hemorrhage. In this study, we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model. OLR1 small interfering RNA (10 μL; 50 pmol/μL) was injected into the right basal ganglia to knock down OLR1. Twenty-four hours later, 0.5 U collagenase type VII was injected to induce intracerebral hemorrhage. We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma, neuron loss, inflammatory reaction, and oxidative stress in rat brain tissue. We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway. Therefore, silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage. These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.

Two common polymorphisms of the peroxisome proliferator-activated receptor gamma (PPARG) gene, rs1801282 and rs3856806, may be important candidate gene loci affecting the susceptibility to ischemic stroke. This case-control study sought to identify the relationship between these two single-nucleotide polymorphisms and ischemic stroke risk in a northern Chinese Han population. A total of 910 ischemic stroke participants were recruited from the First Hospital of China Medical University, Shenyang, China as a case group, of whom 895 completed the study. The 883 healthy controls were recruited from the Health Check Center of the First Hospital of China Medical University, Shenyang, China. All participants or family members provided informed consent. The study protocol was approved by the Ethics Committee of the First Hospital of China Medical University, China on February 20, 2012 (approval No. 2012-38-1). The protocol was registered with the Chinese Clinical Trial Registry (registration number: ChiCTR-COC-17013559). Plasma genomic DNA was extracted from all participants and analyzed for rs1801282 and rs3856806 single nucleotide polymorphisms using a SNaPshot Multiplex sequencing assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using unconditional logistic regression to estimate the association between ischemic stroke and a particular genotype. Results demonstrated that the G allele frequency of the PPARG gene rs1801282 locus was significantly higher in the case group than in the control group (P < 0.001). Individuals carrying the G allele had a 1.844 fold increased risk of ischemic stroke (OR = 1.844, 95% CI: 1.286–2.645, P < 0.001). Individuals carrying the rs3856806 T allele had a 1.366 fold increased risk of ischemic stroke (OR = 1.366, 95% CI: 1.077–1.733, P = 0.010). The distribution frequencies of the PPARG gene haplotypes rs1801282-rs3856806 in the control and case groups were determined. The frequency of distribution in the G-T haplotype case group was significantly higher than that in the control group. The risk of ischemic stroke increased to 2.953 times in individuals carrying the G-T haplotype (OR = 2.953, 95% CI: 2.082–4.190, P < 0.001). The rs1801282 G allele and rs3856806 T allele had a multiplicative interaction (OR = 3.404, 95% CI: 1.631–7.102, P < 0.001) and additive interaction (RERI = 41.705, 95% CI: 14.586–68.824, AP = 0.860; 95% CI: 0.779–0.940; S = 8.170, 95% CI: 3.772–17.697) on ischemic stroke risk, showing a synergistic effect. Of all ischemic stroke cases, 86% were attributed to the interaction of the G allele of rs1801282 and the T allele of rs3856806. The effect of the PPARG rs1801282 G allele on ischemic stroke risk was enhanced in the presence of the rs3856806 T allele (OR = 8.001 vs. 1.844). The effect of the rs3856806 T allele on ischemic stroke risk was also enhanced in the presence of the rs1801282 G allele (OR = 2.546 vs. 1.366). Our results confirmed that the G allele of the PPARG gene rs1801282 locus and the T allele of the rs3856806 locus may be independent risk factors for ischemic stroke in the Han population of northern China, with a synergistic effect between the two alleles.

Inverse Synthetic Aperture Radar has been proved to be a powerful tool in imaging moving targets in military and civilian applications. The target's movement with respect to the radar sensor provides the angular diversity required for range-Doppler ISAR imagery and image blur due to its motion error. For real targets such as plane, ship and tank have complicated motion components which are unknown to the radar. This paper is a brief review of universally used motion compensation techniques employed in ISAR for a clear and focused image.

The present study aimed to investigate the effects of the phosphoinositide 3‑kinase (PI3K)/Akt signaling pathway on the Wnt/β‑catenin signaling pathway in rats with focal cerebral ischemia‑reperfusion injury. A total of 96 rat focal cerebral ischemia‑reperfusion models, established according to a modified version of Longa's method, were randomly divided into four groups: Sham‑operated (S), cerebral ischemia‑reperfusion injury (I), cerebral ischemia‑reperfusion + basic fibroblast growth factor (bFGF) post‑processing and, finally, cerebral ischemia‑reperfusion + bFGF post‑processing + PI3K inhibitor LY294002 (LY). Each group consisted of 24 rats and each group was divided into four subgroups according to the indicated reperfusion times of 12, 24, 48 and 72 h. The morphological changes of the cortical tissue and the cellular apoptosis were determined using hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling method, respectively. The expression levels of phosphorylated (p‑)Akt, glycogen synthase kinase‑3β (GSK‑3β) mRNA and β‑catenin in the cortical tissue were detected at different time‑points. The number of apoptotic cells and the expression levels of p‑Akt, GSK‑3β mRNA and β‑catenin in the I and LY groups were significantly higher compared with those in the S group (P

Rapid allele-specific PCR primer was designed base on Cytb 155 A/T single nucleotide polymorphism, DNA was extracted by alkaline lysis and the PCR reaction systems including denatured and annealing temperature and cycle numbers were optimized. The results were performed to authenticate Ranae Oviductus and its 4 adulterants. When 100×SYBR Green I was added in the PCR product at 90 ℃ denatured 3 s, 62 ℃ annealing 20 s and 32 cycle. Ranae Oviductus visualized strong green fluorescence under 365 nm UV lamp whereas adulterants appeared negative. The whole process can be completed in 40 minutes．The established method provides the technical support for authentication of the Ranae Oviductus.

Given that cyclooxygenase-2 (COX-2) plays a crucial role during cerebral ischemia and Apobec-1 is a critical regulator of COX-2 mRNA stabilization in gastrointestinal settings, the correlation of COX-2 and Apobec-1 was investigated in neurogenic cells and rat model of cerebral ischemia. After neurogenic SH-SY5Y, NG108-15 and PC12 cells were exposed to oxygen-glucose deprivation, cell viability, LDH leakage and Apobec-1 expression were determined. The effect of Apobec-1 overexpression on injury severity of oxygen-glucose deprivation, COX-2 expression, C-to-U editing of COX-2 mRNA were measured in vitro. Then the correlation of Apobec-1 level and injury severity was analyzed in cells with oxygen-glucose deprivation and in rats with middle cerebral artery occlusion. Apobec-1 expression was elevated along with upregulation of COX-2 and injury severity of oxygen-glucose deprivation in the three cell lines. Apobec-1 overexpression aggravated injury of oxygen-glucose deprivation in vitro and could be correlated to injury severity in vivo. Meanwhile, Apobec-1 increased COX-2 expression and COX-2 mRNA stabilization in neurogenic cells, and failed to catalyze C-to-U editing of COX-2 mRNA. Apobec-1 could upregulate COX-2 expression in neurogenic cells by stabilizing COX-2 mRNA, and might aggravate injury of oxygen-glucose deprivation in neurogenic cells as well as in rats with cerebral ischemia.

Background: Macrolide antibiotics have anti-inflammatory effects which are utilized for the treatment of chronic inflammatory airway diseases. Recently, their anti-inflammatory effects have been proposed to be beneficial in patients with chronic obstructive pulmonary disease (COPD). Objectives: Since the molecular mechanisms of anti-inflammatory effects are associated with inhibition of activator protein 1 (AP-1) and nuclear factor (NF)-ĸB, and both are reported to be involved in the expression of γ-glutamylcysteine synthetase (γ-GCS), we set out to determine if these drugs influence the oxidant-antioxidant balance in human bronchial epithelial (HBE) cells. Methods: 16HBE cells were preincubated with erythromycin (EM) at different concentrations and times and then exposed to hydrogen peroxide (0.01 mM). Levels of interleukin (IL)-8 and glutathione (GSH), and activity of γ-GCS and γ-GCS heavy subunit (γ-GCS-HS) protein production were assayed. AP-1 and NF-ĸB binding to the 5′-flanking region of IL-8 and γ-GCS-HS genes was assessed by electrophoretic mobility-shift assay. Results: The increase in IL-8 levels and activity of AP-1 induced by H2O2 were abrogated by preincubation of the cells with EM (5 µg/ml) for 36 h. We also showed that preincubation with EM for 48 h inhibited H2O2-induced GSH levels, γ-GCS activity and expression of γ-GCS-HS, and decreased AP-1 binding to the γ-GCS-HS 5′-flanking region. Conclusions: The confirmation of antioxidants maintaining enzyme suppression by EM raised concerns on whether this drug could disrupt the oxidant/ antioxidant balance during long-term use. These data provide important insights into the treatment of inflammatory lung diseases with macrolide antibiotics.

The time dependence of Sm2+ fluorescence in orthorhombic BaCl2 was investigated between 77 and 300 K. The thermal quenching mechanism of the 4f–4f emissions of Sm2+ was examined. The position of the lowest level of Sm2+ 4f55d states was calculated from the temperature dependence of 5D1 lifetime by the two-step quenching model and was estimated in good approximation from the emission and excitation peaks by the electron–phonon coupling theory. A growing process of 5D0–7F0 emission and a double-decay process of 5d–4f emission were observed in the time-resolved fluorescence. They show clearly the population transfer among the Sm2+ excited states via thermal transition.

Phorbol myristate acetate (PMA), as a potent tumor promoter, may induce microglial senescence. The present study investigated the effect of PMA infection on microglial senescence. From 58 male Sprague‑Dawley rats, 10 were randomly selected and divided into a PMA injection group, containing five rats (0.5 µg/µl PMA) and a control group, containing five rats (commensurable 0.9% saline). Immunofluorescent staining of Iba‑1 and enzyme‑linked immunosorbent assay analyses of the expression levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑1 β were performed in these two groups. The remaining 48 rats were randomly divided into the following three groups, each containing 16 rats: Repeated injection control group (commensurable normal saline, once a week for 4 weeks), single PMA injection group (0.5 µg/µl PMA, once in the first week) and repeated injection PMA group (0.5 µg/µl PMA, once a week for 4 weeks). The expression levels of p21, detected using double immunofluorescence staining with Iba‑1, and β‑galactosidase, via double immunohistochemical staining of Iba‑1, were examined in these three groups. The results indicated that a single injection of PMA did not change the microglial morphology and had no significant effects on the expression levels of TNF‑α and IL‑1β, compared with the control group (P>0.05). Following four repeated injections of PMA, the microglia in the substantia nigra presented with features of senescence, characterized by increased expression levels of β-galactosidase (P

Systemic sclerosis (SSc) is a connective tissue disease characterized by fibrosis of the skin and internal organs. Th17 cells and interleukin-17 (also called IL-17A) have been found to be increased in peripheral blood and skin in patients with SSc. IL-21 is a potent inducer of Th17 differentiation that is produced by activated T cells, and whose relationship with Th17 cells in SSc is unclear. Here, using a bleomycin (BLM)-induced mouse model of skin fibrosis, we detected the frequency of CD4+/IL-17+ (Th17) cells, CD4+/IL-21+ T cells and IL-21+ Th17 cells in peripheral blood, skin and lungs, as well as the serum content of IL-17A and IL-21. In addition, we assessed the differentiation of CD4+ T cells cultured from these mice into Th17 cells in response to treatment with IL-21. Compared with the control mice, Th17 cell counts and IL-17A levels were significantly increased and correlated with inflammatory and fibrotic indices in the skin and lungs of the BLM-induced fibrosis mice. Moreover, serum levels of CD4+/IL-21+ T cells, IL-21+ Th17 cells, and IL-21 were significantly increased in these mice, and correlated positively with serum levels of Th17 cells. In vitro experiments showed that IL-21 treated CD4+ T cells derived from BLM-induced mice differentiated into Th17 cells. Our results indicate that Th17 cells and IL-17A contributes to inflammatory and fibrotic processes in the skin and lungs in a BLM-induced mouse model of SSc. Moreover, the expansion of the Th17 cell population may be subsequent to IL-21 promotion of the differentiation of CD4+ T cells in these mice.

Objective To clarify the relationship between the quantitatively assessed cube-copying test (CCT) and clinical profiles of cognitive and motor ability in Chinese patients with Parkinson disease (PD). Methods We gave the Montreal Cognitive Assessment (MoCA), which includes the CCT, to evaluate the cognitive function of 102 outpatients with PD. We also gave the Unified Parkinson's Disease Rating Scale (UPDRS) II and III and the Hoehn-Yahr scale to evaluate the patients' motor function and disease severity, respectively. We used Maeshima's method for quantitative assessment of the CCT, and calculated CCT errors by adding incomplete connections and plane-drawing errors. We divided the patients into 2 groups based on normal (no errors) versus abnormal (≥1 errors) CCT scores. Results We found 34 patients with normal scores and 68 with abnormal scores. The 2 groups had significant differences in age of onset, MoCA score, UPDRS II and III scores, and cognitive deterioration rate. CCT errors correlated inversely with cognitive domains except for orientation. Executive function was most commonly affected in both groups. We found correlations between numbers of CCT errors and left-limb movement, fine hand movement, postural instability and gait disorders, UPDRS II and III scores, and cognitive and motor deterioration rates. Conclusions The quantitatively assessed CCT may be useful in estimating cognitive and motor dysfunction in patients with PD, and in monitoring disease progression.

The relation between the LRRK2 mutation and its effect on Parkinson’s disease (PD) has always caught a lot attention. Recent studies found that the G2385R polymorphism of LRRK2 may increase the risk of PD in Asian populations. Here we tried to clarify the relationship between the LRRK2 G2385R variant and the clinical profiles including motor complication in Chinese PD patients. We identified the LRRK2 variant in the Chinese Han population in northern China and evaluated the relationship between the G2385R variant and clinical profiles through comparison between 36 carriers and 139 non-carriers. We found that G2385R carriers scored significantly higher in motor fluctuation and dyskinesia than non-carriers. Logistic regression analysis showed that the G2385R variant was an independent risk factor for motor fluctuation in females (odds ratio = 12.538, 95 % CI 2.216–70.942, P = 0.004), and a Chi-squared test showed that the frequency of dyskinesia tended to be higher in the carrier group compared to the non-carrier group (16 vs. 4.4 %, P = 0.050, OR = 4.127, 95 % CI 1.074–15.864). These findings indicate that the variant was closely related to the occurrence of motor complication. Additionally, the G2385R variant was significantly related to the early-onset of PD in female carriers (20.0 vs. 1.5 %, odds ratio = 16.25, 95 % CI 1.557–169.618, P = 0.020). Our study found that the G2385R variant was significantly associated with motor complications and that this variant was an independent risk factor for motor fluctuation in females. These findings provide the necessary preliminary data to better understand the unique profile of PD G2385R variant carriers.

To investigate the impact of treatment with low dose roxithromycin on clinical symptoms and CT scores in patients with stable bronchiectasis.Fifty patients with bronchiectasis in stable condition were randomly assigned to a control group and a treatment group. Patients in the control group received ambroxol hydrochloride tablet 90 mg 3 times a day. Patients in the treatment group received roxithromycin disperse tablet 0.15 g every day and ambroxol hydrochloride tablet 90 mg 3 times a day. The course of treatment lasted for 6 months. Quality of life was assessed using St. George's respiratory questionnaire (SGRQ). The British Medical Research Council (MRC) dyspnea scale was used to assess the degree of dyspnea. The score for CT evaluation of the thorax, quality of life and SGRQ were performed for all patients before and after the treatment.After 6 months, the scores for quality of life (48 ± 13) were lower compared to that (58 ± 15) before treatment in the control group; however, the scores for bronchial wall thickening of bronchiectasis (1.8 ± 0.5) were higher than that (1.8 ± 0.4) before study. The scores for the extent of bronchiectasis (2.7 ± 1.6), the bronchial wall thickening of bronchiectasis (1.3 ± 0.4) and the global CT score (6.7 ± 2.5) were reduced after treatment as compared to those before treatment [(4.8 ± 2.3), (1.8 ± 0.5), (9.5 ± 3.3)] in the treatment group, (all P0.01). The degree of dyspnea (1.3 ± 0.4) and quality of life (42 ± 12) were lower than those before treatment [(1.89 ± 0.45), (56 ± 15)] in the treatment group. Furthermore, the scores for extent of bronchiectasis (2.7 ± 1.6), the scores for the bronchial wall thickening of bronchiectasis (1.3 ± 0.4) and the global CT score (6.7 ± 2.5) in the treatment group were significantly improved as compared with those [(4.8 ± 2.0), (1.8 ± 0.5), (9.7 ± 3.6)] in the control group respectively after treatment. At the same time, the degree of dyspnea (1.3 ± 0.4) in the treatment group was significantly improved as compared with that (1.7 ± 0.4) in the control group after treatment.The scores for the bronchial wall thickening of bronchiectasis were increased in patients with stable bronchiectasis. Low dose roxithromycin combined with ambroxol hydrochloride significantly improved degree of dyspnea, reduced scores for extent of bronchiectasis, scores for the bronchial wall thickening of bronchiectasis and the global CT score as compared to treatment with ambroxol hydrochloride alone in patients with bronchiectasis in stable condition.

Pulmonary sparganosis mansoni is rare in humans and bronchial sparganosis mansoni has not been reported. We reported a patient with a soft-tissue mass in the right hilum area on a chest computed tomography (CT) scan that was suspected of being lung cancer. Bronchoscopy identified sparganum larvae. Bronchial sparganosis mansoni accompanied by abnormal hyperplasia was diagnosed by histopathology. We introduced our experience and reviewed the clinical characteristics of three pulmonary sparganosis mansoni cases and three pleural cavity sparganosis mansoni cases that have been reported.

To evaluate the changes of CD(4)(+)IL-17(+) T (Th17) and CD(4)(+)Foxp3(+) regulatory T (Treg) cells in peripheral blood and bronchoalveolar lavage fluid (BALF), and therefore to explore the role of Th17 and Treg in cigarette smoke-induced airway inflammation/COPD in rats.Forty male Wistar rats were randomly divided into 4 groups: a 12 wk smoke-exposure group, a 24 wk smoke-exposure group, a 12 wk control group and a 24 wk control group (n = 10 each). Cells in BALF were collected and analyzed by absolute and differential cell counts. IL-17 and IL-6 levels in serum and BALF were tested by enzyme linked immunosorbent assay (ELISA). The proportion of CD(4)(+)IL-17(+) T and CD(4)(+)Foxp3(+) Treg in peripheral blood and BALF were determined by flow cytometry. The mRNA expressions of IL-17 and Foxp3 were measured by real-time PCR. Comparisons of the data between different groups were performed using one-way ANOVA, and SNK and Games-Howell test were used for comparison between 2 groups.Levels of IL-17 were remarkable increased in the 12 wk smoke-exposure group and the 24 wk smoke-exposure group in serum [(52.6 ± 1.8) ng/L, (75.4 ± 6.0) ng/L] and BALF [(78.1 ± 5.8) ng/L, (95.0 ± 6.8) ng/L] compared with the 12 wk control group [(40.0 ± 3.2)ng/L, (54.5 ± 4.6) ng/L] and the 24 wk control group [(36.7 ± 3.2) ng/L, (53.9 ± 3.7) ng/L], all P0.05. IL-6 in serum was significantly increased in the 24 wk smoke-exposure group [(31.4 ± 2.1) ng/L] compared with the 24 wk control group [(11.5 ± 0.5) ng/L], and it was increased in the 12 wk and the 24 wk smoke-exposure group [(33.3 ± 2.3) ng/L, (44.6 ± 3.0) ng/L] compared with the 12 wk and the 24 wk control group [(15.6 ± 1.8) ng/L, (18.0 ± 1.9) ng/L] in BALF. Ratio of Th17 was higher in the 12 wk and the 24 wk smoke-exposure groups in peripheral blood [(1.81 ± 0.19)%, (3.74 ± 0.55)%] and BALF [(7.84 ± 0.28)%, (8.01 ± 0.39)%] compared with the12 wk [(0.97 ± 0.08)%, (5.64 ± 0.54)%] and the 24 wk control group [(1.08 ± 0.10)%, (5.95 ± 0.48)%]. Ratio of Treg in BALF was higher in the smoke-exposure groups [(8.81 ± 0.49)%, (11.98 ± 0.72)%] compared with the control groups [(4.34 ± 0.28)%, (5.21 ± 0.42)%]. The level of IL-17 mRNA was increased in the 12 wk and the 24 wk smoke-exposure group in peripheral blood (25.7 ± 2.0, 33.9 ± 1.5) and in BALF (22.2 ± 1.8, 34.7 ± 4.2) compared with the 12 wk (11.3 ± 2.6, 11.6 ± 2.4) and the 24 wk (11.1 ± 2.0, 13.5 ± 3.4) control groups. Foxp3 mRNA was increased in the smoke-exposure groups (24.4 ± 2.7, 30.3 ± 2.7) compared with the control groups (12.7 ± 2.7, 14.6 ± 3.8). Th17 in smoke-exposure groups was positively correlated with counts of total cells and macrophages (r = 0.512, 0.543, all P0.05).An elevated expression of Th17 and Treg cells and an increase of inflammatory cytokines were evident in airway inflammation of cigarette smoke-exposed rats, suggesting that Treg was involved in the immunological regulation and Th17 was associated with the persistent inflammation in cigarette smoke-induced airway inflammation in rats.

To study the pathological characteristics of intra-acinar pulmonary artery inflammation and its correlation with smoking index and disease progression in smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).Patients requiring lung resection for peripheral lung cancer were divided into group A (nonsmokers with normal lung function, n = 10), group B (smokers with normal lung function, n = 13), and group C (smokers with stable COPD, n = 10). The lung tissue far away from tumor were resected to compare the pathological changes of intra-acinar pulmonary arteries and infiltration level of inflammatory cell in pulmonary non-muscularized arteries (NMA), pulmonary partially muscularized arteries (PMA) and muscularized arteries (MA) among the three groups. The correlation analysis was made among infiltration level, smoking index, percentage of predicted value of forced expiratory volume in one second (FEV(1)%Pred), six-minute-walk distance (6MWD) and BODE index.(1) Both group B and group C showed the intima and media thickness of MA was significantly higher, the lumen area of MA was narrower and the proportion of MA was higher, and collagenous fiber of MA adventitial proliferated and area increased in group C (P0.05 or P0.01). (2) In group B and group C, the percentage of the intra-acinar pulmonary arteries that contained leukocytes, T lymphocytes, CD(8)(+)T lymphocytes and the number of these positive cells infiltrating the intra-acinar pulmonary arteries were increased, especially an increased number of CD(8)(+)T lymphocytes infiltrating in the arterial adventitia as compared with group A, moreover there were significant difference between group C and group B (P0.05 or P0.01). In group B and group C, the degree of these positive cells infiltrating NMA, PMA and MA presented a decreasing sequence (P0.05 or P0.01). Among the intima, media and adventitia of MA, the infiltration of these positive cells was the highest in the adventitia. Among group A, group B and group C, infiltration degree of CD(4)(+)T lymphocyte, B lymphocyte, macrophage and neutrophil demonstrated no significant difference, also among NMA, PMA and MA (P0.05). (3) The number of leukocytes, T lymphocytes, CD(8)(+)T lymphocytes infiltrating MA showed a positive correlation with the thickness of MA (r = 0.563, 0.627, 0.589, P0.01, respectively) and smoking index (r = 0.551, 0.665, 0.600, P0.01, respectively), moreover the degree of these cells infiltrating MA demonstrated negative correlation with FEV(1)%Pred (r = -0.763, -0.703, -0.767, P0.01, respectively). Also infiltrating degree of T lymphocytes and CD(8)(+)T lymphocytes was positively correlated with BODE (r = 0.390, 0.476, P0.05, respectively). Furthermore the infiltrating degree of CD(8)(+)T lymphocytes had negative correlation with 6MWD (r = -0.356, P0.05).(1) Pulmonary arterial inflammation appears in smokers with normal lung function and smokers with COPD patients. It involves in all types of intra-acinar pulmonary arteries especially NMA and infiltrates whole layer of MA with a characteristic of CD(8)(+)T lymphocytes infiltrating in the adventitia of intra-acinar pulmonary arteries. (2) Pulmonary inflammation is closely correlated to cigarette smoking and clinical parameters such as BODE index, FEV(1)% pred and 6MWD. It is one of the key factors affecting the progression of COPD.

To evaluate the expression of Tc17 in a cigarette smoke-induced mice model of emphysema. To explore the probable mechanisms about how Tc17 cells to elevate in lungs of mice.Forty male Balb/c mice were randomly divided into four groups, including control group (12 weeks, C12), control group (24 weeks, C24), smoke-exposure group (12 weeks, S12) and smoke-exposure group (24 weeks, S24), 10 mice each group, Emphysema of mice was observed by HE pigmentation. Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The proportion of CD(8)(+)IL-17(+)Tc17, CD(8)(+)IL-17(+) CC chemokine receptor type 6 (CCR6)(+) and 6CCR6(+)Tc17 cells in lungs of mice was determined by flow cytometry. The mRNA expressions of retinoid-related orphan nuclear receptor (RORγt) and IL-17 were evaluated by real-time PCR. The levels of IL-1β, IL-6, IL-23, transforming growth factor β (TGFβ) and CC chemokine ligand 20(CCL20) were tested by ELISA. Correlations among these indexes were analyzed.Lm and DI were significantly higher in S12 and S24 than in C12 and C24, S24 in particular (t value 4.378 - 15.188, all P0.05). The percentages of Tc17 in S12 and S24 [(9.28 ± 1.12)%, (13.13 ± 3.56)%] was significantly increased as compared with that in C12 and C24 [(2.40 ± 0.60)%, (2.64 ± 0.96)%], S24 in particular. The mRNA levels of RORγt and IL-17 in S12 and S24 were higher than in C12 and C24, S12 and S24 in particular. There was significant difference (all P0.05). The frequency of Tc17 cells had a positive correlation with Lm and DI (r value were 0.734 and 0.884 respectively, P0.01). The percentages of CD(8)(+)IL-17(+)CCR6(+)T cells and CCR6(+)Tc17 were significantly elevated in S12 and S24 compared to C12 and C24, S24 in particular (all P0.05). There was positive correlation between Tc17 cell ratio and CCL20 levels (r = 0.899, P0.01). The levels of IL-1β, IL-6, IL-23 and TGFβ in S12 and S24 were significantly increased as compared with that in C12 and C24. There was significant difference (all P0.05). Meanwhile, the frequency of Tc17 cells had a positive correlation with IL-1β, IL-6, IL-23, and TGFβ.An up-regulation of proportions Tc17 in lungs of cigarette smoke-induced emphysema mice were detected. The CCR6/CCL20 axis and the increased IL-1β, IL-6, IL-23 and TGFβ probably contributed to this up-regulation.

To evaluate the expression of Th17 cell in a cigarette smoke-induced mice model of emphysema and explore the probable mechanisms of its elevation.Forty male Balb/c mice were randomly divided into 4 groups: control group for 12 weeks (C12), control group for 24 weeks (C24), smoke-exposure group for 12 weeks (S12) and smoke-exposure group for 24 weeks (S24)(n = 10 each). Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The percentages of Th17, Th1, Th17/Th1, CD4(+)IL-17(+)CCR6(+)T and CCR6(+)Th17 cells were determined by tetra-color flow cytometry while the levels of interleukin (IL)-1β, IL-6, IL-23, transforming growth factor (TGF)-β, interferon (IFN)-γ and CC chemokine ligand (CCL)-20 assayed by enzyme-linked immunosorbent assay (ELISA).The values of Lm [(39 ± 4) µm, (47 ± 7) µm] and DI [(39.1 ± 1.6), (45.2 ± 3.1)] were significantly higher in S12 and S24 than those in C12 [(33 ± 3) µm, (28.2 ± 1.6)] and C24 [(32 ± 4) µm, (28.9 ± 2.1)], particularly in C24 (all P0.05). The percentages of Th17 cell [(3.27 ± 1.12), (7.19 ± 2.24)], Th17/Th1 cell [(0.61 ± 0.30), (1.82 ± 0.52)] and Th1 cell [(10.02 ± 3.68), (26.21 ± 6.04)] in the lungs of S12 and S24 significantly increased than those in C12 [(1.80 ± 0.75), (0.27 ± 0.12), (3.75 ± 1.72)] and C24 [(1.99 ± 0.59), (0.28 ± 0.11), (4.16 ± 1.32)], particularly in C24 (all P0.01). The percentages of Th17, Th17/Th1 and Th1 cells in the lungs of S12 and S24 had a positive correlation with Lm and DI (all P0.01). The percentages of CD4(+)IL-17(+)CCR-6(+)T cell [(0.69 ± 0.34), (1.11 ± 0.48)] and CCR6(+)Th17 cell [(12.23 ± 2.13), (18.65 ± 1.17)] were significantly elevated in S12 and S24 compared to those in C12 [(0.22 ± 0.18), (6.55 ± 2.13)] and C24 [(0.25 ± 0.17), (7.29 ± 1.57)], particularly in C24 (all P0.05). Furthermore, a positive correlation between CCR6(+)Th17 cell and emphysematous lesions was also found (all P0.05). The levels of IL-1β, IL-6, IL-23, TGF-β, IFN-γ and CCL20 significantly increased in S12 and S24 as compared with those of C12 and C24 (all P0.05). Meanwhile, the percentage of Th17 cell had a positive correlation with IL-1β, IL-6, IL-23, TGF-β, IFN-γ and CCL20.There is an up-regulated expression of Th17 in lungs of cigarette smoke-induced emphysema mice. The CCR6/CCL20 axis and the elevated levels of IL-1β, IL-6, IL-23, TGF-β and IFN-γ may be related with the above effect.

The echo wave of complex target consists by the waves of scatter centers, that is the reason for angle glint. The waves of different scatters have certain phase differences, and these phase differences can influence radar's angle measurement precision and target's RCS wave. By using the relationship, it can suppress angle glint according to the target's RCS at the moment. Simulation and real data validations show that the phase of scatters can help to suppress angle glint.

Background We performed a meta-analysis to evaluate the role of 18 F-fluorodeoxyglucos -e positron emission tomography/computed tomography ( 18 FDG-PET/CT) in detecting mediastinal nodal metastasis in patients with non-small cell lung cancer (NSCLC). Methods Studies about 18 FDG-PET/CT for detecting mediastinal nodal metastasis in patient with NSCLC were systematically searched in the MEDLINE, EMBASE, and EBM Review databases from January 1, 2000 to July 26, 2011. A software called "Meta-Disc" was used to obtain pooled estimates of sensitivity, specificity, positive likelihood ratio (PLR), and negative likelihood ratio (NLR), respectively. We also calculated summary receiver operating characteristic (SROC) curves, and the Q* index. Results 20 articles fulfilled all inclusion criteria (3028 eligible patients). The pooled sensitivity, and specificity with 95% confidence interval for PET/CT on a per-patient analysis were 0.719 (0.683–0.753), and 0.898 (0.882–0.912). Corresponding values for PET/CT on a per-nodal-station analysis were 0.610 (0.582–0.636), 0.924 (0.918–0.930). The Q* index estimates under SROC were 0.8464 and 0.8067, respectively. Conclusions 18 FDG-PET/CT had more specificity but less sensitivity for mediastinal nodal metastasis in patients with NSCLC.

To evaluate the expression and the role of Th17 in cigarette smoke-induced lung inflammation and emphysema in mice.Forty male BALB/c mice were randomly divided into 4 groups, including a control group C12, a control group C24, a smoke-exposure 12 week group (S12) and a smoke-exposure 24 week group S24 (n = 10 each). Morphological changes were evaluated by mean linear intercepts and destructive index (DI). The proportion of CD(4)(+)IL-17(+)Th17, CD(4)(+)IFN-γ(+)Th1, CD(4)(+)IL-17(+)IFN-γ(+)T(Th17/Th1), CD(8)(+)IFN-γ(+)Tc1, CD(8)(+)IL-21R(+) and CD(4)(+)IL-17(+)IL-21(+) T cells in lungs of mice was determined by flow cytometry. The mRNA expressions of RORγt and IL-17 were evaluated by real-time PCR.Mean linear intercepts and DI were significantly higher in S12 and S24 groups [(39 ± 4) µm, (47 ± 7) µm], (39.1 ± 1.6, 45.2 ± 3.1) as compared to C12 [(32 ± 4) µm, 28.2 ± 1.6] and C24 groups [(33 ± 3) µm, 28.9 ± 2.1], all P0.05. The percentage of Th17 of S12 and S24 groups [(3.3 ± 1.1)%, (7.2 ± 2.2)%] was significantly increased as compared with that of C12 and C24 groups [(1.8 ± 0.8)%, (2.0 ± 0.6)%], all P0.05. The mRNA levels of RORγt [(25 ± 4), (35 ± 3)] and IL-17 [(26 ± 3), (36 ± 3)] in S12 and S24 groups were higher than in C12 [(10 ± 5), (13 ± 5)] and C24 groups [(11 ± 7), (8 ± 6)], all P0.05. The percentage of Th1, Th17/Th1 and Tc1 cells of S12 and S24 groups [(10.0 ± 3.7)%, (26.2 ± 6.0)%], [(0.61 ± 0.30)%, (1.82 ± 0.52)%], [(17.0 ± 4.5)%, (26.8 ± 8.5)%] was significantly increased as compared with that of C12 [(3.8 ± 1.7)%, (0.27 ± 0.17)%, (4.8 ± 1.9)%] and C24 groups [(4.2 ± 1.3)%, (0.28 ± 0.11)%, (5.2 ± 1.0)%], all P0.05. Moreover, the frequency of Th17 cells had a positive correlation with Th1, Tc1 cells and emphysematous lesions (r = 0.519 - 0.797, all P0.01). In addition, a positive correlation between Th17/Th1 cells and emphysematous lesions was also found (r = 0.742, 0.802, all P0.01). The percentage of CD(4)(+)IL-17(+)IL-21(+) T cells was significantly increased in S12 and S24 groups [(0.19 ± 0.04)%, (0.55 ± 0.24)%] compared to controls [(0.07 ± 0.03)%, (0.08 ± 0.03)%], all P0.05. Meanwhile, as compared with that of the controls [(1.22 ± 0.31), (1.34 ± 0.18)], the percentage of CD(8)(+)IL-21R(+) T cells was also increased in S12 and S24 groups [(2.94 ± 1.26), (4.12 ± 2.26)], but there were no differences among smoke-exposure groups (P0.05). The frequency of CD(4)(+)IL-17(+)IL-21(+) T cells had a positive correlation with Th1, Tc1 cells and emphysematous lesions (r = 0.694 - 0.754, all P0.05). And the frequency of CD(8)(+)IL-21R(+) T cells also had a positive correlation with emphysematous lesions (r = 0.516, 0.725, all P0.05).Cigarette smoke increased the expression and the activity of Th17 in mice. Th17 may play a potential (active) role in the development of lung inflammation through IL-21/IL-21R pathway.

Background and Aim: The dual action of microglia in neurodegenerating diseases has been controversial for some time. Recent studies indicate that microglia senescence might be the key determinant. When microglia age, they function abnormally and fail to respond correctly to stimuli, which eventually promotes neurodegeneration. Accumulating evidence has shown a close relationship between inflammation and aging. Since neuroinflammation is characterized by microglia activation, we assessed if the repeated activation of microglia would lead to senescence. Method: The microglia cell line BV2 was repeatedly stimulated every 48 h with lipopolysaccharide (LPS; 10 ng/ml) and senescence was evaluated by β-galactosidase staining and the presence of senescence-associated heterochromatic foci as well as by cell cycle arrest detection by flow cytometry. The senescence-associated protein p53 was also detected by Western blot. Results: β-Galactosidase staining was barely detectable in control cells, while it tended to increase with repeated LPS stimulation and was positive in most cells after stimulation with LPS 6 times. Similarly, senescence-associated heterochromatic foci were most prominent in cells repeatedly stimulated with LPS, while almost undetectable in control cells or cells receiving a single stimulation. p53 expression was highest in the cells that received LPS stimulation 6 times, and the largest number of cells arrested in the G0/G1 phase was observed in this same group. Conclusion: Microglial cells tend to undergo senescence after repeated activation, implying that microglia senescence may start after multiple inflammatory challenges.

Aim at the problem of glint in amplitude-comparison monopulse radar, the text uses the target's RCS weights method to suppress glint. For the effect of the method, besides using the simulation of extended target, the text uses real data of amplitude-comparison monopulse radar to validate the algorithm, and explains the adjust when way used for real data, finally demonstrates the suppressing effect and advances the practicable way for use.

Background/Aims: Cognitive impairment (CI) is common in Parkinson’s disease (PD), and the cognitive deterioration rate (CDR) is heterogeneous among PD patients. However, very few studies have reported on the association of PD features and risk factors with rapid CDR. The Montreal Cognitive Assessment (MoCA) is considered to be a sensitive and reliable approach to detect mild CI. In the present study, we sought to define and compare the cognitive profiles and clinical features of PD patients with slow or rapid CDRs, and then to identify the PD risk factors associated with rapid CDR. Methods: A cross-sectional study of cognitive rate was performed using the MoCA in a cohort of 73 PD patients and 41 controls matched for age, sex and education level. Results: The rapid CDR group was characterized by older age (58.8 years in slow CDR vs. 64.1 in rapid CDR; p = 0.02), later age at disease onset (52.7 vs. 61.7 years; p < 0.001), a faster deterioration rate of movement symptoms (UPDRS III increment of 12.8 vs. 5.9/year; p < 0.001), a higher rate in multiple-domain CI (38.9 vs. 10.8%), and generally lower MoCA subscores for the Clock Drawing Test, attention, verbal fluency and abstraction. According to the univariate logistic regression model, onset age, movement deterioration rate, multiple domains CI and executive function CI were risk factors for rapid CDR. However, only the movement deterioration rate (p = 0.01) and onset age (p = 0.05) remained independent predictors for rapid CDR according to the multivariate logistic regression model. Conclusions: The CI deterioration in a subset of PD patients appears to progress more rapidly. Identifying those PD patients may not only help to predict the development of PD dementia, but also facilitate therapeutic intervention at early disease stages.

To study the pathological characteristics of interleukin-16 (IL-16) and CXC chemokine receptor 3(CXCR3) in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: group NS (nonsmokers with normal lung function, n = 10); group S (smokers with normal lung function, n = 13); group COPD (smokers with stable COPD, n = 10). The clinical datas including blood gas analysis, pulmonary function, BMI, smoking index, BODE index, six-minute-walk distance (6MWD), Medical Research Council dyspnea scale (MRC), St. George Respiratory Questionnaire (SGRQ) were recorded in all subjects before the operation. We applied technique of hematoxylin-eosin staining to observe pathomorphological changes of the pulmonary arteries. The concentration of IL-16 in lung tissues were measured by ELISA. Muscularized arteries were examined with immunohistochemical methods to identify T-lymphocytes (CD(3)), CD(4) T-lymphocytes, CD(8) T-lymphocytes, IL-16, CXCR3. The correlation of IL-16 and CXCR3 in muscularized arteries in smokers with stable COPD were analysed.(1) The group COPD showed the highest concentration of IL-16 in lung tissue (P0.01). The concentration of IL-16 in group S was higher than group NS (P0.05). (2) Both in group S and group COPD, the percentage of the muscularized arteries that contained CXCR3 and IL-16 were increased as compared with group NS (P0.01). Moreover there were statistical significance have been observed between group COPD and group S (P0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD(3)(+)T-lymphocytes, CD(8)(+)T-lymphocytes, CXCR3 (r = 0.639, 0.803, 0.696; P0.05 or P0.01), smoking index, BODE index (r = 0.737, 0.704; P0.05). There was inverse relationship between the content of IL-16 in the muscularized arteries in group COPD and forced expiratory volume in one second% predicted (FEV(1)% Pred) and 6MWD (r = -0.803, -0.787; P0.01). We also found the intensity of CXCR3 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD(3)(+) T-lymphocytes, CD(8)(+)T-lymphocytes (r = 0.650, 0.767; P0.05), smoking index, BODE index (r = 0.650, 0.767; P0.05). There was inverse relationship between the content of CXCR3 in the muscularized arteries in group COPD and FEV(1)% Pred and 6MWD (r = -0.778, -0.774; P0.01).(1) Both in group S and group COPD, IL-16 and CXCR3 were mainly expressed in lymphocytes which were correlated with CD(8)(+)T-lymphocytes infiltrating the muscularized arteries. There were some suggestion that IL-16 probably recruited CD(8)(+)T-lymphocytes into muscularized arteries by enhancing the expression of CXCR3. (2) The intensity of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function that suggested pulmonary arterial inflammation might be one of the key factors associated with the progression of COPD, and inhibiting the pulmonary artery inflammation played an important role in prevention and cure of COPD.

Background CYP4F2 is a member of the cytochrome P450 enzymes and is responsible for metabolizing arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE); 20-HETE plays a role in the regulation of vascular tone in the cerebral, coronary, and renal circulation. The present study aimed to evaluate whether or not the CYP4F2 gene polymorphism V433M (rs2108622) is involved in ischemic stroke in the Northern Chinese Han population. Methods In a case–control study, the participants included 302 (193 males and 109 females) patients with ischemic stroke and 350 (212 males and 138 females) healthy subjects. The V433M polymorphism of the CYP4F2 gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) with the restriction enzyme PvuII. Results The frequencies of the GG genotype and the G allele were higher in participants with ischemic stroke than in the control group ( P = 0.018). Multiple logistic regression analysis revealed the significance of the rs2108622 in males after adjustment for confounding factors. No difference was found in all participants and females. Conclusion The GG genotype and G allele were associated with ischemic stroke in the male Northern Chinese Han population.

A meta-analysis was conducted to assess the relationship between serum homocysteine, vitamin B(12), and folate levels in patients with multiple sclerosis (MS). The DerSimonian and Laird Q test was used to evaluate the degree of heterogeneity between studies and a funnel plot was used to assess publication bias. The pooled effect size (standardized mean difference [SMD]) between patients with MS and control patients) from a random effects model was 0.84 (95% confidence interval: 0.18, 1.49) for homocysteine and -0.25 (-0.45, -0.04) for vitamin B(12), and from a fixed effects model was 0.98 (0.80, 1.16) for homocysteine and -0.25 (-0.41, -0.09) for vitamin B(12). Both nutrients were statistically significant, but the SMD for folate was not. Patients with MS were found to have raised homocysteine levels but low B(12) levels, which might contribute to the pathogenesis of MS.

To study the differences in the clinical and laboratory characteristics of disseminated penicilliosis marneffei (PSM) in patients with and without human immunodeficiency virus (HIV) infection.The clinical data of 33 patients with PSM in our hospital from 2002 to 2007 were retrospectively analyzed. The patients were divided into 2 groups, an HIV infection group (n = 22) and a non-HIV infection group (n = 11). The data of the 2 groups were compared.The common features in the 2 groups included that, the majority of the patients were manual laborers with a low educational level, and the most common clinical characteristics were fever, multiple organ involvement especially the lung, skin, digestive system, and generalized lymphadenopathy. Different characteristics between the 2 groups included, (1) In the non-HIV infection group, the duration of the disease was longer (median: 45 vs 180 d, P0.01), with more underlying diseases (5/11) and higher misdiagnosis rate (7/11) as compared to those of the HIV infection group; (2) High, persistent fever, acute dyspnea and molluscum of the skin were more common in the HIV infection group, but intermittent fever, subcutaneous nodules and abscess were the features of the non-HIV infection group. Generalized lymphadenopathy (10/11), bone ache (5/11) and chest pain (7/11) were also more common in the non-HIV infection group (10/22, 2/22, 0/22, respectively in the HIV infection group, P0.05; (3) The total white cell counts were mostly increased in the non-HIV infection group (9/11), but were mostly in the normal range (15/22) or decreased (7/22) in the HIV infection group (P = 0.000). The total white cell count, the neutrophil and the lymphocyte counts in the non-HIV infection group were significantly higher than those in the HIV infection group (median: 18.6 x 10(9)/L vs 4.71 x 10(9)/L; 14.24 x 10(9)/L vs 4.16 x 10(9)/L; 2.08 x 10(9)/L vs 0.42 x 10(9)/L, P0.01, respectively; (4) The blood CD(4)/CD(8) ratio was normal or higher than 0.5 in the non-HIV infection group, but was, less than 0.5 in the HIV infection group (P = 0.000); (5) The positive rate of blood culture (18/18) or bone marrow culture (14/20) was significantly higher in the HIV infection group than those in the non-HIV infection group (7/10, 2/8, P0.05, respectively); (6) Diffuse parenchymal and interstitial changes were the main manifestations of chest radiology in the 2 groups. High-density consolidation and pleuritis were common in the non-HIV infection group, and osteolysis occurred only in the non-HIV infection group (n = 4, P0.05); (7) The prognosis was better in the non-HIV infection group (P0.05).Fever, multiple organ dysfunction and poor prognosis are common clinical characteristics of PSM in the 2 groups, but there are significantly different characteristics between the 2 groups in underlying diseases, clinical presentations, disease progress and some laboratory studies.

To study the effects of erythromycin on Hydrogen peroxide (H2O2)-induced interleukin-8 synthesis and regulation of glutathione in human bronchial epithelial cells.Human bronchial epithelial (16HBE) growth curve was recorded by MTT, cells were divided into three groups (1) control (incubation for 24, 36, 48) (2) H2O2 (Pre-incubation for 24, 36, 48 h before adding H2O2 (3) H2O2 + EM (Pre-incubation EM for 24, 36, 48 h before adding H2O2). IL-8 levels were measured in culture supernatants by ELISA, activation of transcription factor NF-kappaB and AP-1 in HBE was evaluated by Electrophoretic mobility shift assay (EMSA). Intracellular GSH and Gamma-GCS concentrations were measured by spectrophotometric assay, gamma-GCS-HS protein were determined by Western blot.Erythromycin (1 microg/ml, 10 microg/ml) and H2O2 (0.01 mM, 0.1 mM) have no effects on cell growth, Preincubation with EM (5 microg/ml) for 36 h and 48 h significantly inhibit H2O2 (0.01 mmol/L) induced increase of IL-8 levels in HBE supernatants, in the mean time decrease the expression of NF-kB and AP-1. Preincubation with EM (5 microg/ml) for 48 h significantly inhibit H2O2 (0.01 mmol/L) induced increase of gamma-GCS levels, gamma-GCS-HS protein expression and AP-1 binding of gamma-GCS-HS promoter in HBE. However GSH and gamma-GCS-HS protein expression in EM + H2O2 group significantly higher than those in control group.Erythromycin inhibits oxidant-mediated IL-8 levels through down-regulation of NF-kB and AP-1 binding in HBE, which can further influence the synthesis of GSH and expression gamma-GCS in HBE.