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Search Results: 1 - 10 of 82208 matches for " Shih-Heng Chen "
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Biomechanical comparison of unilateral and bilateral pedicle screws fixation for transforaminal lumbar interbody fusion after decompressive surgery -- a finite element analysis
Shih-Hao Chen, Shang-Chih Lin, Wen-Chi Tsai, Chih-Wei Wang, Shih-Heng Chao
BMC Musculoskeletal Disorders , 2012, DOI: 10.1186/1471-2474-13-72
Abstract: A validated finite-element (FE) model of L1-S1 was established to implant three types of cages (TLIF with a single moon-shaped cage in the anterior or middle portion of vertebral bodies, and TLIF with a left diagonally placed ogival-shaped cage) from the left L4-5 level after unilateral decompressive surgery. Further, the effects of unilateral versus bilateral pedicle screw fixation (UPSF vs. BPSF) in each TLIF cage model was compared to analyze parameters, including stresses and ROM on the neighboring annulus, cage-vertebral interface and pedicle screws.All the TLIF cages positioned with BPSF showed similar ROM (<5%) at surgical and adjacent levels, except TLIF with an anterior cage in flexion (61% lower) and TLIF with a left diagonal cage in left lateral bending (33% lower) at surgical level. On the other hand, the TLIF cage models with left UPSF showed varying changes of ROM and annulus stress in extension, right lateral bending and right axial rotation at surgical level. In particular, the TLIF model with a diagonal cage, UPSF, and contralateral facet screw fixation stabilize segmental motion of the surgical level mostly in extension and contralaterally axial rotation. Prominent stress shielded to the contralateral annulus, cage-vertebral interface, and pedicle screw at surgical level. A supplementary facet screw fixation shared stresses around the neighboring tissues and revealed similar ROM and stress patterns to those models with BPSF.TLIF surgery is not favored for asymmetrical positioning of a diagonal cage and UPSF used in contralateral axial rotation or lateral bending. Supplementation of a contralateral facet screw is recommended for the TLIF construct.
Naloxone inhibits immune cell function by suppressing superoxide production through a direct interaction with gp91phox subunit of NADPH oxidase
Qingshan Wang, Hui Zhou, Huiming Gao, Shih-Heng Chen, Chun-Hsien Chu, Belinda Wilson, Jau-Shyong Hong
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-32
Abstract: Inhibition of NOX-2-derived superoxide by (-) and (+)-naloxone was measured in lipopolysaccharide (LPS)-treated midbrain neuron-glia cultures and phorbol myristate acetate (PMA)-stimulated neutrophil membranes by measuring the superoxide dismutase (SOD)-inhibitable reduction of tetrazolium salt (WST-1) or ferricytochrome c. Further, various ligand (3H-naloxone) binding assays were performed in wild type and gp91phox-/- neutrophils and transfected COS-7 and HEK293 cells. The translocation of cytosolic subunit p47phox to plasma membrane was assessed by western blot.Both (-) and (+)-naloxone equally inhibited LPS- and PMA-induced superoxide production with an IC50 of 1.96 and 2.52 μM, respectively. Competitive binding of 3H-naloxone with cold (-) and (+)-naloxone in microglia showed equal potency with an IC50 of 2.73 and 1.57 μM, respectively. 3H-Naloxone binding was elevated in COS-7 and HEK293 cells transfected with gp91phox; in contrast, reduced 3H-naloxone binding was found in neutrophils deficient in gp91phox or in the presence of a NOX2 inhibitor. The specificity and an increase in binding capacity of 3H-naloxone were further demonstrated by 1) an immunoprecipitation study using gp91phox antibody, and 2) activation of NOX2 by PMA. Finally, western blot studies showed that naloxone suppressed translocation of the cytosolic subunit p47phox to the membrane, leading to NOX2 inactivation.Strong evidence is provided indicating that NOX2 is a non-opioid novel binding site for naloxone, which is critical in mediating its inhibitory effect on microglia overactivation and superoxide production.Recent studies strongly support that neuroinflammation plays a critical role in the pathogenesis of various neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis, Huntington's disease and multiple system atrophy [1]. Microglia, the resident immune cells of the brain, are the major players in t
Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity
Dan Zhang, Xiaoming Hu, Li Qian, Shih-Heng Chen, Hui Zhou, Belinda Wilson, David S Miller, Jau-Shyong Hong
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-3
Abstract: For the in vitro study, mesencephalic neuron-glia cultures and microglia-enriched cultures from mice deficient in the MAC1 receptor (MAC1-/-) and wild type controls were used to investigate the role of MAC1 receptor in Aβ-induced neurotoxicity and the role of phosphoinositide-3 kinase (PI3K) in the signal pathway between MAC1 receptor and PHOX. For the in vivo study, Aβ was injected into the substantia nigra of MAC1-/- mice and wild type mice to confirm the role of MAC1 receptor.We found that Aβ-induced activation of microglia, activation of PHOX, generation of superoxide and other reactive oxygen species, and loss of dopaminergic neurons were decreased in MAC1-/- cultures compared to MAC1+/+ cultures. In MAC1-/- mice, dopaminergic neuron loss in response to Aβ injection into the substantia nigra was reduced relative to MAC1+/+ mice. Thus, MAC1 receptor-mediated PHOX activation and increased superoxide production are associated with Aβ-induced neurotoxicity. PI3K activation was one downstream step in MAC1 signaling to PHOX and played an important role in Aβ-induced neurotoxicity. In microglia-enriched cultures from MAC1-/- mice, Aβ-induced activation of PI3K (phosphorylation of target proteins and PIP3 production) was reduced relative to MAC1+/+ cultures.Taken together, our data demonstrate that Aβ activates MAC1 receptor to increase the activity of PI3K, which in turn phosphorylates p47phox, triggers the translocation of cytosolic subunits of PHOX to microglia membrane, increases PHOX activation and the subsequent production of superoxide and causes neurotoxicity.β-Amyloid peptide (Aβ) has been reported to exist in numerous diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), age-related macular degeneration and Lewy body disease with dementia [1-3]. Immunohistochemical analysis reveals that Aβ deposits in the brain are surrounded by and infiltrated by activated microglia [4,5], suggesting that microglia are involved in the pathogenesis of amyloid-r
Interaction between Serotonin Transporter and Serotonin Receptor 1 B genes polymorphisms may be associated with antisocial alcoholism
Tzu-Yun Wang, Sheng-Yu Lee, Shiou-Lan Chen, Yun-Hsuan Chang, Shih-Heng Chen, Chun-Hsien Chu, San-Yuan Huang, Nian-Sheng Tzeng, Chen-Lin Wang, I Lee, Tzung Yeh, Yen Yang, Ru-Band Lu
Behavioral and Brain Functions , 2012, DOI: 10.1186/1744-9081-8-18
Abstract: We recruited 273 Han Chinese male inmates with antisocial personality disorder (ASPD) [antisocial alcoholism (AS-ALC) group (n?=?120) and antisocial non-alcoholism (AS-N-ALC) group (n?=?153)] and 191 healthy male controls from the community. Genotyping was done using PCR-RFLP.There were no significant differences in the genotypic frequency of the 5-HT1B G861C polymorphism between the 3 groups. Although AS-ALC group members more frequently carried the 5-HTTLPR S/S, S/LG, and LG/LG genotypes than controls, the difference became non-significant after controlling for the covarying effects of age. However, the 5-HTTLPR S/S, S/LG, and LG/LG genotypes may have interacted with the 5-HT1B G861C C/C polymorphism and increased the risk of becoming antisocial alcoholism.Our study suggests that neither the 5-HTTLPR gene nor the 5-HT1B G861C polymorphism alone is a risk factor for antisocial alcoholism in Taiwan’s Han Chinese population, but that the interaction between both genes may increase susceptibility to antisocial alcoholism.Alcoholism (also: alcohol dependence) is a complex, heterogeneous disorder that is influenced by multiple genes as well as sociocultural factors [1,2]. Twin studies have shown that genetic factors account for about 50-60% of the overall variance in alcoholism [3-5]. Many candidate genes have been studied; however, the results are controversial. Therefore, to reduce the heterogeneity of alcoholism by proper subtyping is important. In addition, a gene-to-gene interaction approach may be more revealing than a single-gene approach for studying alcoholism. By using appropriate subtypes of alcoholism and the gene-to gene interaction approach, the results may be more conclusive.Cloninger (1987) identified two subtypes of alcoholism. Type I alcoholism is characterized by late onset, more psychological dependence, and anxious/depressed personality traits. Individuals with type II alcoholism are characterized by early onset, a higher familial risk for alcoholis
Poorer sustained attention in bipolar I than bipolar II disorder
Chian-Huei Kung, Sheng-Yu Lee, Yun-Hsuan Chang, Jo Wu, Shiou-Lan Chen, Shih-Heng Chen, Chun-Hsien Chu, I-Hui Lee, Tzung-Lieh Yeh, Yen-Kuang Yang, Ru-Band Lu
Annals of General Psychiatry , 2010, DOI: 10.1186/1744-859x-9-8
Abstract: In all, 51 interepisode BP patients (22 with BP I and 29 with BP II) and 20 healthy controls participated in this study. The severity of psychiatric symptoms was assessed by the 17-item Hamilton Depression Rating Scale and the Young Mania Rating Scale. All participants undertook Conners' Continuous Performance Test II (CPT-II) to evaluate sustained attention.After controlling for the severity of symptoms, age and years of education, BP I patients had a significantly longer reaction times (F(2,68) = 7.648, P = 0.001), worse detectability (d') values (F(2,68) = 6.313, P = 0.003) and more commission errors (F(2,68) = 6.182, P = 0.004) than BP II patients and healthy controls. BP II patients and controls scored significantly higher than BP I patients for d' (F = 6.313, P = 0.003). No significant difference was found among the three groups in omission errors and no significant correlations were observed between CPT-II performance and clinical characteristics in the three groups.These findings suggested that impairments in sustained attention might be more representative of BP I than BP II after controlling for the severity of symptoms, age, years of education and reaction time on the attentional test. A longitudinal follow-up study design with a larger sample size might be needed to provide more information on chronological sustained attention deficit in BP patients, and to illustrate clearer differentiations between the three groups.The prevalence of bipolar disorder (BP) is estimated at 3.5% to 6.4% of the general population [1,2], and 30% to 50% of those in remission will not achieve premorbid psychosocial function levels [3]. Accordingly, evidence has shown that poor functional outcome is highly associated with cognitive impairment, and may persist through the remission period [4].However, most previous studies only focused on type I bipolar disorder (BP I) with regard to neuropsychological aspects, mainly because type II bipolar disorder (BP II) was often underdiagn
A network flow approach to predict drug targets from microarray data, disease genes and interactome network - case study on prostate cancer
Shih-Heng Yeh, Hsiang-Yuan Yeh, Von-Wun Soo
Journal of Clinical Bioinformatics , 2012, DOI: 10.1186/2043-9113-2-1
Abstract: We integrate gene expression, disease genes and interaction networks to identify the effective drug targets which have a strong influence on disease genes using network flow approach. In the experiments, we adopt the microarray dataset containing 62 prostate cancer samples and 41 normal samples, 108 known prostate cancer genes and 322 approved drug targets treated in human extracted from DrugBank database to be candidate proteins as our test data. Using our method, we prioritize the candidate proteins and validate them to the known prostate cancer drug targets.We successfully identify potential drug targets which are strongly related to the well known drugs for prostate cancer treatment and also discover more potential drug targets which raise the attention to biologists at present. We denote that it is hard to discover drug targets based only on differential expression changes due to the fact that those genes used to be drug targets may not always have significant expression changes. Comparing to previous methods that depend on the network topology attributes, they turn out that the genes having potential as drug targets are weakly correlated to critical points in a network. In comparison with previous methods, our results have highest mean average precision and also rank the position of the truly drug targets higher. It thereby verifies the effectiveness of our method.Our method does not know the real ideal routes in the disease network but it tries to find the feasible flow to give a strong influence to the disease genes through possible paths. We successfully formulate the identification of drug target prediction as a maximum flow problem on biological networks and discover potential drug targets in an accurate manner.Cancer is extremely complex and it is viewed as a multi-stage disease caused by the accumulation of genetic alterations in tumor associated suppressor oncogenes [1]. It is a fundamental challenge in human health to understand disease mechanisms for
Gly1057Asp polymorphism of insulin receptor substrate-2 is associated with coronary artery disease in the Taiwanese population
Chan Shih-Hung,Chen Jyh-Hong,Li Yi-Heng,Tsai Liang-Miin
Journal of Biomedical Science , 2012, DOI: 10.1186/1423-0127-19-100
Abstract: Background Gly1057Asp polymorphism in insulin receptor substrate (IRS)-2 is related to insulin resistance and diabetes mellitus (DM), which both contribute to the pathogenesis of coronary artery disease (CAD). Hence, we hypothesize that Gly1057Asp polymorphism in IRS-2 is associated with CAD. Methods Patients receiving elective coronary angiography were enrolled. Significant stenosis is defined as a luminal diameter stenosis greater than 50%. Patients without significant stenosis were defined as group A, and those with significant stenosis in at least one major coronary artery were defined as group B. Genotypes were determined by polymerase chain reaction/restriction fragment length polymorphism. Chi-square test and multivariate logistic regression were used to evaluate the relationship between Gly1057Asp polymorphism in IRS-2 and CAD. The homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated as a representative of insulin resistance. Multiple linear regression was used to analyze the association between Gly1057Asp polymorphism in IRS-2 and the HOMA-IR index. Results There were 170 patients in group A and 284 patients in group B. The Gly allele frequencies were 54.7% for group A and 60.9% for group B (p = 0.077). The Gly/Gly + Gly/Asp genotype frequency was 74.1% for group A and 84.9% for group B (p = 0.007). After adjustments for conventional risk factors in multivariate logistic regression, the odds ratio for CAD in patients with the Gly/Gly + Gly/Asp genotype was 2.008 [95% confidence interval (95% CI) = 1.210-3.332, p = 0.007], using patients with the Asp/Asp genotype as a reference group. The concurrence of Gly1057Asp polymorphism in IRS-2 with DM is correlated with occurrence of CAD. In multivariate logistic regression, employing non-diabetics with the Asp/Asp genotype as a reference group, the odds ratio for CAD was 1.561 [95% CI = 0.517-4.713, p = 0.430] for diabetics with the Asp/Asp genotype, 1.922 [95% CI = 1.086-3.400, p = 0.025] for non-diabetics with the Gly/Gly + Gly/Asp genotype, and 3.629 [95% CI = 1.820-7.236, p < 0.001] for diabetics with the Gly/Gly + Gly/Asp genotype. There was no association between Gly1057Asp polymorphism in IRS-2 and HOMA-IR index. Conclusion Gly allele at codon 1057 in IRS-2 is correlated with an increased susceptibility to CAD in the Taiwanese population. There is a synergistic effect toward CAD between the pathogenicity of DM and that of the Gly allele.
Spermatic Cord Metastasis of Primary Hepatocellular Carcinoma Presenting as an Inguinal Mass: A Case Report
Heng-Chieh Chiang,Pao-Hwa Chen,Hung-Jen Shih
ISRN Oncology , 2011, DOI: 10.5402/2011/612753
Smoking, Alcohol, and Betel Quid and Oral Cancer: A Prospective Cohort Study
Wen-Jiun Lin,Rong-San Jiang,Shang-Heng Wu,Fun-Jou Chen,Shih-An Liu
Journal of Oncology , 2011, DOI: 10.1155/2011/525976
Abstract: We aimed to investigate the association between smoking, alcoholic consumption, and betel quid chewing with oral cancer in a prospective manner. All male patients age ≥18 years who visited our clinic received an oral mucosa inspection. Basic data including personal habits were also obtained. A multivariate logistic regression model was utilized to determine relevant risk factors for developing oral cavity cancer. A total of 10,657 participants were enrolled in this study. Abnormal findings were found in 514 participants (4.8%). Three hundred forty-four participants received biopsy, and 230 patients were proven to have oral cancer. The results of multivariate logistic regression found that those who smoked, consumed alcohol, and chewed betel quid on a regular basis were most likely to develop cancer (odds ratio: 46.87, 95% confidence interval: 31.84–69.00). Therefore, habitual cigarette smokers, alcohol consumers, and betel quid chewers have a higher risk of contracting oral cancer and should receive oral screening regularly so potential oral cancer can be detected as early as possible. 1. Introduction Smoking is one of the most important risk factors for developing oral cancers [1, 2]. Oral cancer is currently a major global health issue [3]. In developing countries, oral cavity cancer is estimated to be the third most common malignancy after cancer of the cervix and stomach [4]. Oral cancer has also been one of the top 10 causes of death from cancer since 1991 in Taiwan and the death toll for oral cancer in males has been rising at a surprising rate [5]. No significant advancement in the treatment of oral cancer has been found in recent years. Although better combinations of multidiscipline approach have improved the quality of life in oral cancer patients, the overall 5-year survival rate has not improved much over the past decades [6]. Therefore, primary prevention such as cessation of tobacco smoking and alcohols drinking along with early detection is necessary control procedures to improve the prognosis of oral cancer [7]. Other risk factors have been reported to be closely associated with oral cancers including alcoholic consumption, betel quid chewing [8], poor oral health [9], and human papilloma virus infection [10]. The incidence of oral cancer among patients who had the habit of tobacco smoking was 8.4 fold higher than that among patients who did not [8]. Another study also found the smokers had a 6.41-fold increase in the risk of contracting oral cancer [11]. However, few prospective cohort studies for the risk factors of developing oral
Comparison of Word Length Distributions in Spoken and Written Chinese  [PDF]
Heng Chen
Open Access Library Journal (OALib Journal) , 2018, DOI: 10.4236/oalib.1104660
In this study we apply Zipf-Alecseev’s function to word length distributions of Chinese prose and dialogue texts. Since there are two potential measurement units of Chinese word length, we applied Zipf-Alecseev’s function to both of them. The results show that all the word length distributions fit Zipf-Alecseev’s function, no matter the word length is measured in characters or components. The parameters a and b in Zipf-Alecseev’s function y = cxa bln(x) show no difference in different text styles (which are prose and dialogue in our case). However, the parameters are different when word length is measured in different units (character and component respectively). This indicates that the Zipf-Alecseev’s function is sensitive to word length measurement units, but not text styles.
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