BioMedicine

Published by China Medical University
Online ISSN: 2211-8039
Publications
Interstitial deletions of the long arm of chromosome 3 have, to our knowledge, been reported in only eleven patients; detailed genotype- phenotype correlations are not well established. Here we describe a case with interstitial deletion involving 3q25.33 region. Dysmorphic features and developmental delay lead to clinical genetic and enzyme assessment. Low alpha-hexosaminidase level is also noted, which imply Mucopolysaccharidosis(MPS) IIIB.
 
PCR products of VEGF-460 gene C/T polymorphism present on 3% agarose gel. Lane 1 “CC” homozygote: the two BstUI cuttable bands were 155 bp and 20 bp. Lane 2 “TT” homozygote: “T” was BstUI uncuttable site, and the fragment was measured 175 bp. Lane 3 “TC” heterozygote.
Age-adjusted tests for genotypes of VEGF-460 gene polymorphism
Hypoxia and nitric oxide (NO) play important roles in the onset and progression of glaucoma. Vascular endothelial growth factor (VEGF) is one of the main factors responsive to hypoxia and NO. In this study, we investigated the association between the BstUI C/T VEGF gene polymorphism and primary open angle glaucoma (POAG). 60 POAG patients and 78 healthy volunteers were enrolled in this study. The most frequently observed polymorphism in the VEGF gene is BstUI C/T, which was located 460 nucleotides upstream of the gene. The polymorphism was observed using polymerase chain reaction-based restriction analysis. Significant differences were observed in the distribution of the polymorphism between control subjects and POAG patients (p = 0.003). C/C homozygotes are absent in the control group; therefore, this genotype represents a suitable genetic maker for POAG. Hypoxia and NO may be involved in the pathway whereby the VEGF-460 polymorphism regulates POAG. Furthermore, homozygous C/C VEGF genotype is a useful maker for Chinese POAG. Hypoxia and nitric oxide (NO) play important roles in the onset and progression of glaucoma. Vascular endothelial growth factor (VEGF) is one of the main factors responsive to hypoxia and NO. In this study, we investigated the association between the BstUI C/T VEGF gene polymorphism and primary open angle glaucoma (POAG). 60 POAG patients and 78 healthy volunteers were enrolled in this study. The most frequently observed polymorphism in the VEGF gene is BstUI C/T, which was located 460 nucleotides upstream of the gene. The polymorphism was observed using polymerase chain reaction-based restriction analysis. Significant differences were observed in the distribution of the polymorphism between control subjects and POAG patients (p = 0.003). C/C homozygotes are absent in the control group; therefore, this genotype represents a suitable genetic maker for POAG. Hypoxia and NO may be involved in the pathway whereby the VEGF-460 polymorphism regulates POAG. Furthermore, homozygous C/C VEGF genotype is a useful maker for Chinese POAG.
 
Demographic and clinical characteristics 
Cardiometabolic parameters and physical fitness 
Sleep parameter measurement 
Schizophrenic patients suffer from more metabolic or sleep problems. Little is known about risk factors. We recruited 17 patients with chronic schizophrenia from the rehabilitation center in a medical center in Taiwan and measured their demographic data, cognitive performance, and physical fitness, metabolic profiles and sleep parameters. They were divided into two groups according to clinical severity, then compared in terms of metabolic and sleep parameters. Those with more severe symptomatology had more metabolic abnormality and shorter slow wave sleep (SWS). Our findings suggest clinical symptoms as linked with heavier body weight, wider neck circumference, elevated blood pressure, and shorter SWS. Further studies are warranted to confirm the preliminary finding and to elucidate the underlying mechanism
 
Parkinson's disease (PD) is a degenerative disorder of the central nervous system that is characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta as well as motor impairment. Aggregation of α-synuclein in neuronal cells plays a key role in this disease. At present, therapeutics for PD provides moderate symptomatic benefits, but it is not able to delay the development of the disease. Current efforts toward the treatment of PD are to identify new drugs that slow or arrest the progressive course of PD by interfering with a disease-specific pathogenetic process in PD patients. Irisflorentin derived from the roots of Belamcanda chinensis (L.) DC. is an herb which has been used for the treatment of inflammatory disorders in traditional Chinese medicine. The purpose of the present study was to assess the potential for irisflorentin to ameliorate PD in Caenorhabditis elegans models. Our data reveal that irisflorentin prevents α-synuclein accumulation in the transgenic Caenorhabditis elegans model and also improves dopaminergic neuron degeneration, food-sensing behavior, and life-span in a 6-hydroxydopamine-induced Caenorhabditis elegans model, thus indicating its potential as a anti-parkinsonian drug candidate. Irisflorentin may exert its effects by promoting rpn-3 expression to enhance the activity of proteasomes and down-regulating egl-1 expression to block apoptosis pathways. These findings encourage further investigation on irisflorentin as a possible potent agent for PD treatment.
 
-Component analysis and antioxidative capacity of Auricularia Polytricha and Auricularia Auricula water
depicts growth and feed efficiency of animals fed a
Background: Amelioration effect of Auricularia polytricha water extract (AP) on hepatic injury in an animal model of NAFLD was investigated. Methods: Forty six-week-old Wistar rats were housed and thirty-two fed ten percent lard high-fat diet to induce NAFLD. After eight weeks of induction, animals were divided into five groups of eight rats each: normal control, high-fat diet, RN (reversion to a normal diet), 1× AP (normal diet plus 0.75% AP, w/w), and 2×AP (normal diet plus 1.5% AP). Animals were sacrificed four weeks later. Results: Rats receiving either 0.75% or 1.5% AP exhibited effective interruption of NAFLD progression, as evidenced by decreased lipid accumulation and elevated antioxidative status. Histological examination proved AP anti-inflammatory function and lower level of related markers for tumor necrosis factor-α and interleukin-6. Besides abundant polysaccharides against lipid accumulation, AP had a specific high level of phenolic compounds and tannins thus may be a potent anti-inflammatory and antioxidative agent. Conclusion: Findings suggest that under normal diet recovery, AP supplement may represent novel, protective material against NAFLD by attenuating inflammatory response, oxidative stress and lipid deposition.
 
Protective effects of Houttuynia cordata aqueous extract (HCAE) against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined. HCAE, at 1 or 2 g/L, was added into the drinking water for 4 weeks. Acute liver injury was induced by acetaminophen treatment intraperitoneally (350 mg/kg body weight). Acetaminophen treatment significantly depleted hepatic glutathione (GSH) content, increased hepatic malonyldialdehyde (MDA), reactive oxygen species (ROS) and oxidized glutathione (GSSG) levels, and decreased hepatic activity of glutathione peroxidase (GPX), catalase and superoxide dismutase (SOD) (p<0.05). The pre-intake of HCAE alleviated acetaminophen-induced oxidative stress by retaining GSH content, decreasing MDA, ROS and GSSG production, and maintaining activity of GPX, catalase and SOD in liver (p<0.05). The pre-intake of HCAE also significantly lowered acetaminophen-induced increase in cytochrome P450 2E1 activity (p<0.05). Acetaminophen treatment increased hepatic release of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein-1 (p<0.05). HCAE intake significantly diminished acetaminophen-induced elevation of these cytokines (p<0.05). These results support that HCAE could provide hepato-protection.
 
-The demography of the enrolled patients.
Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae are the common pathogens that colonize in the nasopharynx of children. Polymicrobial interactions are thought to play an important role in different sites throughout the human body. However, there are currently very few studies that investigate the interactions between S. aureus, S. pneumoniae, and H. influenzae in the nasopharynx. We retrospectively analyzed the adenoid tissue culture from 269 children who received adenoidectomy. S. aureus, S. pneumoniae, and H. influenzae constituted the major microorganisms which were cultured from these adenoidectomies, at 23.4%, 21.6%, and 18.2%, respectively. S. pneumoniae and H. influenzae were the most prevalent in the preschool-aged children (3 < age ≤ 6), whereas S. aureus was more prevalent in infants and toddlers (age ≤ 3) and school-aged children (age > 6). Bacterial interference was found between S. aureus and S. pneumoniae and between S. aureus and H. influenzae, whereas there was an association found between S. pneumoniae and H. influenzae. The synergism and antagonism among these three species are investigated in the following paper, with the possible mechanisms involved in these interactions also discussed.
 
Single-nucleotide polymorphisms (SNPs) of the LRP1B gene used in this study. Genomic location of SNPs present on chromosome 2q22.1.
Single-nucleotide polymorphisms (SNPs) of the LRP1B gene used in this study. Genomic location of SNPs present on chromosome 2q22.1. 
Background: Kawasaki disease (KD) is an acute and systemic vasculitis. Its complications in coronary artery aneurysms (CAA) make KD one of the leading causes of acquired cardiovascular diseases in childhood. Low density lipoprotein receptor-related protein 1B (LRP1B) is abundantly expressed in the medial layer of coronary arteries and involved in endothelium inflammations. Purpose: We aimed to identify the role of LRP1B in CAA formation during KD progression. Methods: we investigated genetic variations in LRP1B in a Taiwanese cohort of 258 KD patients (83 with CAA and 175 without CAA complications). We used univariate and multivariate regression analyses to identify the associations between LRP1B genetic variations and KD patients. Results: CAA formation in KD was significantly associated with the LRP1B (rs6707826) genetic variant (p = 0.007). By using multivariate regression analysis, significant correlations were observed between KD with CAA complications and the presence of the TT+TG genotypes for the LRP1B rs6707826 single-nucleotide polymorphism (full model: odds ratio = 2.82; 95% CI = 1.33–5.78). Conclusion: Our results suggest that genetic polymorphism of LRP1B gene may be used as a genetic marker for the diagnosis and prognosis of the CAA formation in KD and contribute to genetic profiling studies for personalized medicine.
 
Background: Human skin keratinocyte (HaCaT) cells served to examine effects of asiatic acid (AA) at 1, 2, 4 and 8 μM against advanced glycative endproduct (AGE)-modified bovine serum albumin (BSA) induced glycative stress. Results: AGE-BSA treatment reduced cell viability; and increased reactive oxygen species, nitric oxide, protein carbonyl, interleukin (IL)-1beta and tumor necrosis factor-alpha levels in HaCaT cells. Yet AA pretreatments decreased these oxidative and inflammatory factors, dose-dependently lowering nitric oxide synthase activity and expression. AGE-BSA raised activity and expression of caspase-3 and caspase-8. AA pretreatments at 2-8 μM decreased activity and expression of these two caspases. AGE-BSA declined collagen I expression, but enhanced matrix metalloproteinase (MMP)-1, MMP-8 and MMP-9 protein expression. AA pretreatments at 2-8 μM maintained collagen I expression, and reduced three MMPs expression. AGE-BSA also up-regulated RAGE (receptor of AGE), p-p38 and p-JNK expression. AA pretreatments at 2-8 μM suppressed RAGE expression, and at 1-8 μM down-regulated p-p38 and p-JNK expression. Conclusion: Asiatic acid, via its anti-glycative activity, could protect skin. Thus, this compound could be developed as an external agent and applied for personalized medicine.
 
A hypothetical model for interaction networks obtained with identified proteins in EGFP-expressing H9c2 cells. The proteins identified were imported into the EMBL Search Tool for the Retrieval of Interacting Proteins (STRING) database, and an interaction map generated was used to construct the hypothetical mechanism for EGCG-induced fluorescence changes in EGFP-expressing H9c2 cells with or without H2O2 pretreatment [30].
Ischemic heart disease is the leading cause of death worldwide. An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway. Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury. Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed. Proteomics analyses widely used to identify the protein targets for many cardiovascular diseases have advanced the discovery of the signaling mechanism for GTPs-mediated cardio-protection. This review focuses on putative triggers, mediators, and end effectors for the GTPs-mediated cardio-protection signaling pathways engaged in myocardial ischemia crisis, allowing a promising natural product to be used for ameliorating oxidative stress associated with ischemic heart diseases.
 
Platelet hyperactivity often occursd in hypertensive patients and is a key factor in the development of cardiovascular diseases including thrombosis and atherosclerosis. Nifedipine, an L-type calcium channel blocker, is widely used for hypertension and coronary heart disease therapy. In addition, nifedipine is known to exhibit an antiplatelet activity, but the underlying mechanisms involved remain unclear. Several transcription factors such as peroxisome proliferator-activated receptors (PPARs) and nuclear factor kappa B (NF-κB) exist in platelets and have an ability to regulate platelet aggregation through a non-genomic mechanism. The present article focuses on describing the mechanisms of the antiplatelet activity of nifedipine via PPAR activation. It has been demonstrated that nifedipine treatment increases the activity and intracellular amount of PPAR-β/-γ in activated platelets. Moreover, the antiplatelet activity of nifedipine is mediated by PPAR-β/-γ-dependent upon the up-regulation of the PI3K/AKT/NO/cyclic GMP/PKG pathway, and inhibition of protein kinase Cα (PKCα) activity via an interaction between PPAR-β/-γ and PKCα. Furthermore, suppressing NF-κB activation by nifedipine through enhanced association of PPAR-β/-γ with NF-κB has also been observed in collagen-stimulated platelets. Blocking PPAR-β/-γ activity or increasing NF-κB activation greatly reverses the antiplatelet activity and inhibition of intracellular Ca(2+) mobilization, PKCα activity, and surface glycoprotein IIb/IIIa expression caused by nifedipine. Thus, PPAR-β/-γ- dependent suppression of NF-κB activation also contributes to the antiplatelet activity of nifedipine. Consistently, administration of nifedipine markedly reduces fluorescein sodium-induced vessel thrombus formation in mice, which is considerably inhibited when the PPAR-β/-γ antagonists are administrated simultaneously. Collectively, these results provide important information regarding the mechanism by which nifedipine inhibits platelet aggregation and thrombus formation through activation of PPAR-β/-γ- mediated signaling pathways. These findings highlight that PPARs are novel therapeutic targets for preventing and treating platelet-hyperactivity-related vascular diseases.
 
Overview of the xenograft mice model with ACM or ACME feeding procedure. Parental HNSCC cells (5 × 105 cells) were subcutaneously implanted into the back of nude mice to develop tumor to a size about 0.1 cm3. At day 7 after cells implantation, tumor-bearing nude mice were fed with lyophilized particles or ethanolic extracts diet (3 times per week) for 21 day by tube feeding, respectively.
Gross appearance of organs and body weight measurement during the ACME feeding model. Gross appearance of organs of mice followed by lyophilized particles or ethanolic extracts treatment after 28 day of tumor development. (B) Measurement of body weight of tumor-bearing nude mice (n = 4) during the course of the lyophilized particles feeding or ethanolic extracts feeding.
Head and neck cancer (HNC) is one of the most common forms of cancer in Taiwan. In addition, head and neck cancer cells (HNCs) are highly tumorigenic and resistant to conventional therapy. Therefore, development of new therapeutic regimens that are adjuvant to conventional treatments would benefit future head and neck cancer therapy. In this study, we found that the lyophilized particles and ethanolic extracts of Antrodia cinnamomea mycelia inhibited the tumor growth of HNCs by xenograft assay in vivo. Moreover, administration of lyophilized particles or ethanolic extracts to nude mice did not cause significant side effects. Our study revealed that the Antrodia cinnamomea mycelia extract (ACME) efficiently inhibited the tumorigenicity of HNCs without causing organ failure. Furthermore, it showed that ACME may work as a novel drug candidate for alternative treatments for head and neck cancer.
 
Background: Purple laver ((Porphyra dentate) is a popular edible seaweed in Asia. This study examined protective effects of extract from purple laver extract (PLE) in diabetic mice. Methods: Content of carotenoids and anthocyanins in PLE was analyzed. PLE at 0.5 and 1% was supplied for 7 weeks. Results: PLE was rich in anthocyanins. PLE intake at 0.5 and 1% lowered plasma glucose level (P<0.05); only at 1% raised plasma insulin level, and decreased plasma triglyceride and total cholesterol levels (P<0.05). PLE treatments at 1% lowered hepatic triglyceride and total cholesterol (P<0.05); it reduced renal reactive oxygen species level (P<0.05); retained renal glutathione level, maintaining renal glutathione peroxidase and catalase activities (P<0.05). Conclusion: Porphyra dentate aqueous extract could attenuate diabetic progression via anti-oxidative and lipid lowering effects. This seaweed could be considered as potent healthy food, and used for personalized medicine.
 
Key ingredients for upgrading health care include bolstering and appraising professional medical education. Health examination as a crucial element of health care that we must incorporate into medical education. This research evaluates medical students' awareness of national health examinations. Two surveys, focused on health examination knowledge and perspective, were conducted for first- to fourthyear medical students, results analyzed by descriptive statistics, t-test and ANOVA. Research subjects scored maximum 11 (of possible 15): i.e., 76.2% accuracy for health examination knowledge questions and held positive views on seven (58%) perspective-related questions. Self-directed learning courses do provide a positive effect on students' learning. Respondents' varying backgrounds had insignificant impact on overall results, but in-depth analysis for each individual question does reveal differences among several backgrounds. Medical students' overall awareness level for health examination is above average in comparison to the general public. This research result can provide a basis to improve the related professional programs, courses and teachings or used as a reference for modifications on future classes. The above observations were discussed based on the medical education system in Taiwan.
 
Background/Introduction: Wild bitter gourd (Momordica charantia L. var. abbreviate Seringe) common vegetable in Asia, is used in traditional medicine to treat various diseases, including inflammation. Extant literature indicates that wild bitter gourds have components that activate PPARα and PPARγ. This research probed influence of adding wild bitter gourd to diets on inflammation responses in mice with sepsis. Purpose: This study evaluated influence of eating wild bitter gourd on inflammation responses in mice with sepsis. Methods: We injected intraperitoneal LPS to induce sepsis. Male BALB/c mice were divided normal, sepsis, positive control, and three experimental groups. The latter ate diets with low (1%), moderate (2%), and high (10%) ratios of wild bitter gourd lyophilized powder. Before mice were sacrificed, with the exception of the normal group, intraperitoneal injection of LPS induced sepsis in each group; positive control group was injected with LPS after PDTC. Results: This experiment revealed weights in groups with added wild bitter gourd starkly lower than those of the remaining groups. Blood lipids (TG, cholesterol, and NEFA) were also lower in comparison to the sepsis group, and blood glucose concentrations recovered and approached normal levels. Blood biochemistry values related to inflammation reactions indicated GOT, GPT, C-RP, and NO concentrations of groups with wild bitter gourd added all lower than that of the sepsis group. Secretion levels of the spleen pro-inflammatory cytokines IL-1, IL-6, and TNF-α tallied significantly lower in comparison to the sepsis group, whereas secretion levels of IL-10 anti-inflammatory cytokine increased. Expression level of proteins NF-κB, iNOS, and COX-2 were inhibited significantly. Conclusion: Wild bitter gourd in diets promoted lipid metabolism, improved low blood glucose in sepsis, and attenuated inflammatory stress. These findings suggested that this plant food might provide medical benefits for certain persons.
 
Microsatellites appear widely in genomes of diverse species. Variants of repeat number of microsatellites often correlate with risks of genetic disorder or severity of diseases. Using cross-species comparison, the proposed system comprehensively verifies microsatellites of specific genes related to 16 genetic disorders. Genomic information retrieved from 14 frequently used model organisms in biomedical study was thoroughly analyzed, emphasizing conserved and diverse traits. Features of microsatellite sequences among different organisms, including appearing frequency, position, pattern and distribution, could be determined automatically for stating genetically functional conservation and evolutionary correlation. This research found that among mammals and fishes, the microsatellite sequences are conserved in the genes of epidermal growth factor receptor, ataxia telangiectasia mutated and androgen receptor corresponding to cancers, ataxia telangiectasia and hepatocellular carcinoma, respectively. Still, except fruit fly conserved CAG repeats in Huntington and Spinocerebellar ataxia type 2 genes, no microsatellites were conserved in those genes linked to neurological/neurodegenerative disorders among mammal and fish species. In comparison of mammalian species, microsatellite biomarkers identified from 17 genetic disorder-related genes revealed high repeat conservation, especially in human, gorilla and macaque. Obviously, this comparative analysis illustrates microsatellite repeats affecting genetic disorders, highly correlated to evolutionary distance of species. Chief contribution of this in silico research lies in assisting biologists to identify disease-related microsatellite biomarkers and employ appropriate model organisms for further biomedical studies relying on microsatellite conservation information. Database http://ssrtc.cs.ntou.edu.tw is for academic use.
 
Aim: Cell cycle regulator cyclin D1 (CCND1) is a pivotal regulator for G1/S phase transition, playing a critical part in initiation of carcinogenesis. Triple negative breast cancer comprises a very heterogeneous group of cancer cells, but little is known about what is wrong in the genome of these patients. This study investigated contribution of CCND1 genotype to individual triple negative breast cancer susceptibility. Materials: In all, 2464 native Taiwan subjects consist of 1232 breast cancer cases and 1232 controls were enrolled in a hospital-based, case-control study. CCND1 A870G (rs9344) genotyping was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Risk-stratified analyses correlated genotype and age-related characteristics of breast cancer subgroups. Results: No significant difference was found between patient and control groups in distribution of genotypic and allelic frequencies in CCND1 genotype, yet CCND1 A870G (rs9344) GG genotype was far less prevalent in breast cancer patients younger than 55 years (OR=0.62, 95%CI=0.43–0.89, P=0.0362), with first menarche earlier than 12.2 years (OR=0.61, 95% CI=0.42–0.87, P=0.0241), with menopause earlier than 49.0 years (OR=0.57, 95%CI=0.39–0.82, P=0.0093), or showing triple-negative breast cancer (OR=0.28, 95%CI=0.13–0.62, P=0.0006). Such valuable findings suggest CCND1 A870G (rs9344) as a predictive marker for triple negative breast cancer in Taiwanese women; the authors sincerely hope these help us fight the toughest subtype in clinical management.
 
With advances in molecular biologic and genomic technology, detailed molecular mechanisms for development of castration-resistant prostate cancer (CRPC) have surfaced. Metastatic prostate cancer (PCa) no longer represents an end stage, with many emerging therapeutic agents approved as effective in prolonging survival of patients from either pre- or post-docetaxel stage. Given tumor heterogeneity in patients, a one-size-fits-all theory for curative therapy remains questionable. With the support of evidence from continuing clinical trials, each treatment modality has gradually been found suitable for selective best-fit patients: e.g., new androgen synthesis inhibitor arbiraterone, androgen receptor signaling inhibitor enzalutamide, sipuleucel-T immunotherapy, new taxane carbazitaxel, calcium-mimetic radium-223 radiopharmaceutical agent. Moreover, several emerging immunomodulating agents and circulating tumor cell enumeration and analysis showed promise in animal or early phase clinical trials. While the era of personalized therapy for CRPC patients is still in infancy, optimal therapeutic agents and their sequencing loom not far in the future.
 
During the last twenty years, mounting studies have supported the hypothesis that there is a genetic component that plays an important role in clinically observed variability in individual tissue/organ toxicity after radiotherapy. We propose the term "Personalized Radiogenomics" for the translational study of individual genetic variations that may associate with or contribute to the responses of tissues to radiation therapy used in the treatment of all types of cancer. The missions of personalized radiogenomic research are 1) to reveal the related genes, proteins, and biological pathways responsible for non-tumor or tumor tissue toxicity resulting from radiotherapy that could be targeted with radio-sensitizing and/or radio-protective agents, and 2) to identify specific genetic markers that can be used in risk prediction and evaluation models before and after clinical cancer surgery. For the members of the Terry Fox Cancer Research Lab in China Medical University and Hospital, the long-term goal is to develop SNP-based risk models that can be used to stratify patients to more precisely tailored radiotherapy protocols. Worldwide, the field has evolved over the last two decades in parallel with rapid advances in genetic and genomic technology, moving step by step from narrowly focused candidate gene studies to large-scale, collaborative genome-wide association studies. This article will summarize the candidate gene association studies published so far from the Terry Fox Cancer Research Lab as well as worldwide on the risk of radiation-related cancers and highlight some wholegenome association studies showing feasibility in fulfilling the dream of personalized radiogenomic cancer therapy.
 
Enhancer of Zeste homlog 2 (EZH2) is a catalytic subunit of epigenetic regulator Polycomb repressive complex 2 (PRC2), which trimethylates Lys 27 of histone H3, leading to silencing of the target genes that are involved in a variety of biological processes including tumor progression and stem cell maintenance. However, in addition to its canonical PRC2-dependent transcriptional repression function, EZH2 also acts as a gene activator in a noncanonical PRC2-independent manner. Overexpression of EZH2 has been detected in diverse cancers, and is associated with tumor malignancy. Moreover, activating mutations and inactivating mutations of EZH2 are also associated with certain types of cancer. Given EZH2's multi-faceted function and role in cancer, context-specific strategy for targeting EZH2/EZH2-mediated signaling could serve as future targeted therapy/personalized medicine for human cancer.
 
Retinoic acid which belongs to the retinoid class of chemical compounds is an important metabolite of vitamin A in diets. It is currently understood that retinoic acid plays important roles in cell development and differentiation as well as cancer treatment. Lung, prostate, breast, ovarian, bladder, oral, and skin cancers have been demonstrated to be suppressed by retinoic acid. Our results also show that low doses and high doses of retinoic acid may respectively cause cell cycle arrest and apoptosis of cancer cells. Also, the common cell cycle inhibiting protein, p27, and the new cell cycle regulator, Cdk5, are involved in retinoic acid's effects. These results provide new evidence indicating that the molecular mechanisms of/in retinoic acid may control cancer cells' fates. Since high doses of retinoic acid may lead to cytotoxicity, it is probably best utilized as a potential supplement in one's daily diet to prevent or suppress cancer progression. In this review, we have collected numerous references demonstrating the findings of retinoic acid in melanoma, hepatoma, lung cancer, breast cancer, and prostate cancer. We hope these observations will shed light on the future investigation of retinoic acid in cancer prevention and therapy.
 
A) Pedigree of PKC/PKD Taiwanese family: persons designated by sex, disease status (filled symbols represent patients, open symbols normal persons). Index case indicated by arrow. (B) Sequencing results of mutation in PRRT2 gene of index case. Arrow indicates one-base C inserted at nucleotide 650 (c.650insC), causing protein translation shift and stopping after seventh residue.
Paroxysmal kinesigenic dyskinesia (PKD), a rare paroxysmal movement disorder often misdiagnosed as epilepsy, is characterized by recurrent, brief dyskinesia attacks triggered by sudden voluntary movement. Pathophysiological mechanism of PKD remains not well understood. Ion channelopathy has been suggested, since the disease responds well to ion channel blockers. Mutations in proline-rich transmembrane protein 2 (PRRT2) were recently identified in patients with familial PKD. To extend these genetic reports, we studied a family with clinical manifestations of familial PKD responding well to low dose carbamazepine. Therapeutic dose ranged from 1.5 to 2.0 mg/ kg/day, below that in seizure control. One insertion mutation c.649_650insC (p.P217fsX7) was identified in three patients of the family. This study avers PRRT2's high sensitivity for PKD phenotype. Identification of genes underlying pathogenesis will enhance diagnosis and treatment. Function of PRRT2 and its role in PKD warrant further investigation.
 
Integrons, mobile genetic units, capture and incorporate antibiotic resistance gene cassette by site-specific recombination. Class 1 integrons are widespread and associated with dispersion of antibiotic resistance among Gram-negative bacteria. The expression of gene cassette in Class 1 can vary, based on the Pc promoter but seldom from another promoter hiding downstream of Pc, called P2. To probe distribution and prevalence of gene cassette promoter variants, we analyzed 169 S. Choleraesuis and 191 S. Typhimurium isolates from humans and animals, finding 95.27% occurrence of integrin among S. Choleraesuis, 83.25% among S. Typhimurium. PCR-RFLP analysis identified four promoters (PcS+P2, PcWTGN-10+P2, PcH1+P2, and PcWTGN-10+P2-GGG) in said integron-positive isolates; major types in S. Choleraesuis and S. Typhimurium were PcS+P2 and PcWTGN-10+P2, respectively. Likewise, β-galactosidase assay rated promoter strength of variants by transcriptional fusion constructs to show extended -10 promoter (TGn/-10 promoter) in Pc and three-nucleotide insertion (GGG) between -35 and -10 region of P2 improving promoter strength of gene cassette.
 
Scan modes of tandem mass spectrometry. (1) Product ion scan: select Q1 precursor ion and scan Q3 production. (2) Selected ion monitoring: select precursor ion in Q1 and monitor one or more fragment ions in Q3. (3) Neutral loss scan: scan all ions in Q1 and select ions with neutral loss in Q3. (4) Precursor ion scan: scan precursor ion in Q1 and select certain fragment ion in Q3, all collision induced dissociation carried out in Q2.
-Selected representative studies of Mass spectrometry-based proteomics in Chest Medicine.
Mass spectrometry (MS) is currently the most promising tool for studying proteomics to investigate largescale proteins in a specific proteome. Emerging MS-based proteomics is widely applied to decipher complex proteome for discovering potential biomarkers. Given its growing usage in clinical medicine for biomarker discovery to predict, diagnose and confer prognosis, MS-based proteomics can benefit study of personalized medicine. In this review we introduce some fundamental MS theory and MS-based quantitative proteomic approaches as well as several representative clinical MS-based proteomics issues in Chest Medicine, Gerontology, and Nephrology.
 
Background: Naringin is a major antioxidant in Citrus fruits and herbs. To clarify molecular forms distributed to various tissues, we investigated tissue distribution of naringin and relevant metabolites in rats after repeated dosing. Methods: Male Sprague-Dawley rats were orally administered naringin (210 mg/kg) twice daily for eight days. At 6 h post the 17th dose, various tissues including liver, kidney, heart, spleen and brain were collected and analyzed by HPLC method before and after hydrolysis with β-glucuronidase and sulfatase, individually. Results: The free forms of naringin and naringenin were not detected in all the tissues assayed. Liver contained the highest concentration of naringenin sulfates, followed by spleen, heart, brain and kidney. Naringenin glucuronides were present in liver and kidney, but not in spleen, brain and heart. Conclusion: The bioavailability of naringenin glucuronides and sulfates supported its application for personalized medicine.
 
Type 2 diabetes (T2D) is a global public health concern, its prevalence in Asia, especially Taiwan, rising every year. The risk of developing T2D and diabetes complications is not only controlled by environmental but also by genetic factors. Genetic association studies have shown polymorphisms at specific loci may help identify individuals at greatest risk and response to oral antidiabetic drugs. This review probes effect of genetic profiling on T2D and its complications, using our study population as examples. Also, pharmacogenetics and pharmacogenomics of oral anitdiabetic drug will be explored.
 
Ectodermal dysplasia (ED) syndrome comprises a large, heterogeneous group of inherited disorders that are defined by primary defects in the development of 2 or more tissues derived from the embryonic ectoderm. The tissues primarily involved are the skin and its appendages (including hair follicles, eccrine glands, sebaceous glands, nails) and teeth. The clinical features include sparse hair, abnormal or missing teeth, and an inability to sweat due to lack of sweat glands. One such case report of ectodermal dysplasia is presented here.
 
Sequences of novel mutations observed from patients’ EXT1 gene. Arrows indicate mutation sites. (A) A one-base C deleted at nucleotide 447 (c.447delC), (B) G to A substitution at nucleotide 2034 (c.2034T>G) resulting in p.Tyr678X
Multiple hereditary exostoses (MHE) is characterized by multiple benign projections of bone capped by cartilage, most numerous in metaphyses of long bones. HME are usually inherited in autosomal dominant mode, chief genes EXT1 and EXT2. Two MHE patients were identified from clinic and enrolled in genetic study, complete coding regions of EXT1 and EXT2, including intron/exon boundaries, sequenced via DNA samples drawn from participants. DNA sequencing revealed mutant EXT1 gene in both cases, within which frame-shift mutation c.447delC (p.Ser149fsX156) in exon1 and nonsense mutation c.2034T>G (p.Tyr678X) in exon10, emerged. Neither mutation was detected in control group. Our results extended the spectrum of EXT1 mutations, revealing similar incidence of EXT1 and EXT2 in Taiwanese MHE patients.
 
Idiopathic membranous nephropathy (MN) is one common cause of idiopathic nephrotic syndrome in adults; 25% of MN patients proceed to end-stage renal disease. In adults, membranous nephropathy is a lead cause of nephrotic syndrome, with about 75% of the cases idiopathic. Secondary causes include autoimmune disease, infection, drugs and malignancy. Three hypotheses about pathogenesis have surfaced: preformed immune complex, in situ immune complex formation, and auto-antibody against podocyte membrane antigen. Pathogenesis does involve immune complex formation with later deposition in sub-epithelial sites, but definite mechanism is still unknown. Several genes were recently proven associated with primary membranous nephropathy in Taiwan: IL-6, NPHS1, TLR-4, TLR-9, STAT4, and MYH9 . These may provide a useful tool for diagnosis and prognosis. This article reviews epidemiology and lends new information on KIRREL2 (rs443186 and rs447707) polymorphisms as underlying causes of MN; polymorphisms revealed by this study warrant further investigation.
 
Stimulation of a sensitive locus with needle tip during MTrP injection to elicit pain, referred pain or local twitch response.
Contraction knot in the endplate zone of a taut band with shortening of sarcomeres, but relatively elongated sarcomeres outside the endplate zone, to increase tension of the taut band.
Simons’ integrated hypothesis of myofascial trigger point.
Hong’ rapid multiple needle insertion technique, including careful palpation of MTrP to direct the injection needle (A), and a special way of holding and controlling syringe with the palm firmly contact with patient’s body (B).
Myofascial trigger point (MTrP) is a major cause of muscle pain, characterized with a hyperirritable spot due to accumulation of sensitized nociceptors in skeletal muscle fibers. Many needling therapy techniques for MTrP inactivation exist. Based on prior human and animal studies, multiple insertions can almost completely eliminate the MTrP pain forthwith. It is an attempt to stimulate many sensitive loci (nociceptors) in the MTrP region to induce sharp pain, referred pain or local twitch response. Suggested mechanisms of needling analgesia include effects related to immune, hormonal or nervous system. Compared to slow-acting biochemical effects involving immune or hormonal system, neurological effects can act faster to provide immediate and complete pain relief. Most likely mechanism of multiple needle insertion therapy for MTrP inactivation is to encounter sensitive nociceptors with the high-pressure stimulation of a sharp needle tip to activate a descending pain inhibitory system. This technique is strongly recommended for myofasical pain therapy in order to resume patient's normal life rapidly, thus saving medical and social resources.
 
Structure of boswellic acid. 
Hepatic protein expression of TLR-3, TLR-4, MyD88, NF-κB p50, NF-κB p65, JNK and p-JNK in mice with BA intake at 0, 0.05 or 0.1% for 4 weeks, and followed by APAP treatment. Normal groups had neither BA nor APAP treatment. BA groups had 0.1% BA intake without APAP treatment. A representative image is shown for each group. Values are mean ± SD, n = 10. a-d Means among bars without a common letter differ, P < 0.05. 
Effects of BA upon hepatic inflammation, determined by H&E stain, in mice with BA at 0, 0.05 or 0.1% for 4 weeks, and followed by APAP treatment. Normal groups had neither BA nor APAP treatments. BA groups had 0.1% BA intake without APAP treatment. Ishak inflammation score was used to quantify the injury area. Values are mean ± SD, n = 10. A representative image is shown for each group. Magnification: 200×. 
Protective effects of boswellic acid (BA) against acetaminophen (APAP)-induced hepatotoxicity in Balb/ cA mice were examined. BA, at 0.05 or 0.1%, was supplied for 4 weeks. Acute liver injury was induced by APAP treatment. Results showed that BA intake increased hepatic BA bioavailability. APAP treatment decreased glutathione (GSH) level, increased reactive oxygen species (ROS) and oxidized glutathione (GSSG) production; and lowered activity and protein expression of glutathione reductase (GR) and heme oxygenase (HO)-1 in liver. BA intake at both doses alleviated subsequent APAP-induced oxidative stress by retaining GSH content, decreasing ROS and GSSG formations, reserving activity and expression of GR and HO-1 in liver, and lowering hepatic cytochrome P450 2E1 activity and expression. APAP treatment enhanced hepatic levels of interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1. BA pre-intake diminished APAP-induced release of those inflammatory cytokines and chemokines. APAP up-regulated hepatic protein expression of toll-like receptor (TLR)-3, TLR-4, MyD88, nuclear factor kappa B (NF-κB) p50, NF-κB p65 and JNK. BA pre-intake at both doses suppressed the expression of NF-κB p65 and p-JNK, and only at 0.1% down-regulated hepatic TLR-3, TLR-4 and MyD88 expression. APAP led to obvious foci of inflammatory cell infiltration in liver, determined by H&E stain. BA intake at both doses attenuated hepatic inflammatory infiltration. These findings support that boswellic acid is a potent hepato-protective agent.
 
The 11,12-epoxy-eicosatrienoic acid (11,12-EET) is formed from arachidonic acid (AA) by cytochrome P450 2J2 (CYP 2J2) epoxygenase and function as an effector in blood vessels. Human endothelial progenitor cells (hEPCs), a preceding cell source for endothelial cells (ECs), involve in the vascular tissue repairing by postnatal neovasculogenesis. However, the effect of 11, 12-EET on hEPCs and neovasculogenesis is not well known. In the current study, we examined the function of 11, 12-EET in hEPCs-mediated neovasculogenesis by using tubular formation analysis, Western Blotting assay, immunofluorescence staining, flow cytometry analysis and zymogram analysis. The results suggest that 11, 12-EET significantly induces neovasculogenesis through the phosphorylation of phosphoinositide 3-kinase (PI3-K)/Akt, endothelial-nitric oxide synthase (e-NOS) and extracellular signal-regulated kinase 1/2 (ERK 1/2) signaling pathways. 11, 12-EET up-regulates the expression of cyclin D1, cyclin-dependent kinase 4 (CDK4) and nuclear factor kappa B (NF-κB) proteins. Moreover, 11, 12-EET augments the expression of VE-cadherin and CD31 proteins in hEPCs. 11, 12-EET also augmented Rac1/Rho A signaling cascades, cell migration and an up-regulation of matrix metalloproteinase (MMP) -2 and -9 proteins. These results demonstrate that 11, 12-EET exerts a significant function in the neovasculogenesis of hEPCs.
 
Flow diagram of study selection.
Oxygen therapy in the care of COVID-19 patients.
Introduction: As the COVID-19 pandemic ravages the world, nursing resources, and capacities play an essential role in disease management. This literature review focuses on the central issues related to the nursing care of patients affected by COVID-19. Material and methods: This literature review was conducted with an extensive search of databases, including PubMed, Web of Science (WOS), and Scopus, using the keywords "COVID19", "2019-nCoV disease", "2019 novel coronavirus infection", "Nurse", "NursingCare", and" Nursing management." The span of the literature search was between December 01, 2020, and January 12, 2021. A total of 28 original and English-language articles were selected for inclusion in the review. Results: Nursing interventions such as monitoring, oxygen therapy, and the use of Extra Corporeal Membrane Oxygenation (ECMO) in the care of COVID-19 patients, caring for ICU patients with COVID-19, rehabilitation of COVID-19 patients, nurses' experiences and barriers in the care of patients with COVID-19, and also the ethical challenges in the care of patients with COVID-19, were found to be valuable in managing COVID-19 patients. Conclusion: Nurses have a pivotal role to play in the care of patients with COVID-19. Therefore, providing comprehensive and quality nursing care supported by experience and research is necessary to successfully reduce the length of hospital stay and decrease the morbidity and mortality rates of COVID-19.
 
COVID-19 pandemic has been a global outbreak of coronavirus (SARS-CoV-2 virus) since 2019. Taiwan Chingguan Yihau (NRICM101) is the first traditional Chinese medicine (TCM) classic herbal formula and is widely used for COVID-19 patients in Taiwan and more than 50 nations. This study is to investigate in silico target fishing for the components of NRICM101 and to explore whether NRICM101 inhibits cytokines-induced normal human lung cell injury in vitro. Our results showed that network prediction of NRICM101 by a high throughput target screening platform showed that NRICM101 has multiple functions that may affect cytokine regulation to prevent human lung cell injury. In addition, NRICM101 revealed protective effects against TNF-a/IL-1b-induced normal human lung HEL 299 cell injury through JNK and p38MAPK kinase signaling. Next-generation sequencing (NGS) analysis of NRICM101 on TNF-a/IL-1b-injured HEL 299 cells indicated that inflammatory pathway, cell movement of macrophages, cellular infiltration by macrophages, and Th1/Th2 immuno-regulation pathways were included. Thus, NRICM101 is a therapeutic agent, and it can improve COVID-19 syndrome to confer beneficial effects through multiple targeting and multiple mechanisms.
 
Objective: The objective of the study was to evaluate the prevalences and trends of multimorbidity and polypharmacy in older adults in Taiwan. Methods: An observational study was performed using the 2000-2013 database of the Taiwan National Health Insurance Program (analysis in 2018). Participants ≥65 years were included in the study. Multimorbidity was defined as participants having two or more chronic diseases annually. Polypharmacy was defined as the average daily number of prescribed medications ≥5. Results: The prevalences of multimorbidity were 42.4% in 2000 and 56% in 2013. The prevalences of polypharmacy were 22.9% in 2000 and 32.1% in 2013. Conclusions: From 2000 to 2013, multimorbidity and polypharmacy were prevalent among older adults in Taiwan. Public health efforts to intervene the primary prevention for chronic diseases should be considered in older adults.
 
− In hospital adverse events after DBS operation.
Generally regarding as a safe treatment for Parkinson's disease (PD) for the past 20 years, deep brain stimulation (DBS) is also an example of precision medicine where surgeons need to titrate individual patient's stimulating electrodes one by one down to the scale of micrometer for the maximum therapeutic effect. In order to prevent operation induced psychiatric complications and minimize any other potential side effects, we have followed 103 patients received this treatment provided by a single surgeon in the same medical institution from 2004 to 2017. We identified each patient complaint from nursing care records and complication data from medical charts during the perioperative hospitalization period to see if any of them correlate statistical significantly with the DBS lead placement procedure. Top five frequent complaints including fever, constipation, nausea, headache, wound pain. The majority of post-operative complaints turned out to be the same as general post-operative / post-anesthesia side effects rather than the DBS operation itself. However, a few rare but critical complications such as post-operative intracranial hemorrhage (ICH), postoperative epidural hematoma (EDH) were identified as well. These patients' subsequent treatments and prognosis were documented for revising the operating procedure in the future. Our retrospective study reconfirmed that DBS is indeed a relatively safe procedure and improve the life quality of PD patients in general. Hopefully, the through preoperative preparation and careful surgical approach will safeguard the patient's prognosis.
 
PCR result visualized in gel electrophoresis.
Electropherogram showing single nucleotide variation in rs69994. (a) Electropherogram of SNP A allele. (b) Electropherogram of C allele. (c) Electropherogram of T allele.
Characteristic between Case and Control Group.
Allele Distribution of VEGF -2578C/A Polymorphism Gene.
Background: Diabetic retinopathy (DR) is one of the complications in diabetes mellitus (DM) which caused by microvascular-damage in the retina due to long termmetabolic changes in diabetes. To date, there has been much research targeted on the determinant of genetic identification in DR patients. In DR, Vascular Endothelial Growth Factor (VEGF) gene is accountable for breaking down the blood-retinal barrier and implicated in the role of neovascularization. It is thought that the polymorphism of VEGF -2578C/A (rs699947) contributed to the development of diabetic retinopathy in type 2 DM. Aim: To determine whether the polymorphisms of VEGF-2578C/A are the risk factors for DR in type 2 DM patients in Bali, Indonesia. Methods: This study is a case-control model comparing 33 cases DR patients in type-2 diabetes mellitus and 35 cases of non-DR as controls in Balinese ethnic. Polymorphisms of VEGF-2578C/A were examined by PCR analysis and DNA sequencing on rs699947 to identify any variation in A/C/T allele distribution. Chi-square test was used to analyze the data and determine the relation of polymorphism and DR. Results: This research showed the genetic variation existence in VEGF-2578C/A polymorphism significantly (p = 0,000) with C allele was higher in the DR group, in contrast, A and T allele were greater in the non-DR group compared to DR group. The result showed that C allele in VEGF-2578 contributed as a risk factor (OR = 13.05; 95% CI = 2.69-63.18; p = 0.001) for DR in type-2 DM (T2DM) patients in Bali, Indonesia. Conclusion: Polymorphism of VEGF-2578C/A (rs699947) allele distribution can be concluded as a risk factor of DR within T2DM patients in Bali, Indonesia. This study may also be used to expand the knowledge in managing DR patients at an earlier stage to avoid further complications.
 
Background: Breast cancer (BC) is known as the most prevalent type of cancer among women. Trastuzumab, as an anticancer drug, has been used broadly in human epidermal growth factor receptor 2 (HER-2) positive (+) BC patients. Moreover, accumulating evidence has demonstrated that microRNAs is involved in the pathogenesis BC. Hence, we aimed to investigate the effect of trastuzumab on the expression levels of microRNA-26a in HER-2 positive BC patients. Methods: This study was conducted among HER-2 + and HER-2 Negative (-) BC patients. Serum expression of microRNA-26a was detected by real-time PCR. Then, we assessed the correlations of microRNA-26a levels with multiple clinico-pathological characteristics of BC. Results: In HER-2 + patients, the microRNA-26a expression significantly increased after treatment with Docetaxel/Trastuzumab in comparison to before the treatment levels (p.value = 0.01). However, this overexpression in HER-2-patients after treatment with Docetaxel was not significant compared to the levels before the treatment (p.value = 0.14). In addition, the expression of microRNA -26a has significantly increased in HER-2 + patients who were ≤48 years old and premenopausal after the treatment with Docetaxel/Trastuzumab when compared to the levels before the treatment (p.value = 0.039 vs. 0.031, respectively). Furthermore, there was a significant correlation between the expression of microRNA -26a and the tumor size, stage, estrogen receptor (ER) and progesterone receptor (PR) status in the HER-2 + group before and after the treatment (p.value = 0.043, 0.042, 0.049 and 0.034 respectively). Conclusions: Trastuzumab led to overexpression of microRNA-26a in HER-2 + BC patients. It seems that the detecting microRNA -26a expression levels, during or after the trastuzumab therapy could be a useful biomarker for monitoring the therapeutic response in HER-2 + BC patients. However, further studies on large populations of women with HER-2+ BC are needed to explore this possible novel biomarker, in more detail, within various clinical contexts.
 
-Positive staining (magnification, ×100) for P53 in (A) psoriasis and (B) lichen simplex chronicus.
-Positive staining (magnification, ×100) for Ki-67 in (A) psoriasis and (B) lichen simplex chronicus.
The baseline characteristics of the patients included in psoriasis and psoriasiform dermatitis groups.
Comparison of the diagnostic markers between psoriasis and psoriasiform dermatitis patients.
Background: Psoriasis is the prime example of psoriasiform tissue pattern and should be differentiated from other psoriasiform dermatoses both clinically and histopathologically. Aim: To evaluate immunohistochemical expression of P53, Ki-67, and CD34 in psoriasis and psoriasiform dermatitis for diagnostic purposes. Methods: An analytical cross-sectional study was performed on the paraffin blocks of 60 psoriasis and 31 psoriasiform dermatitis patients between 2014 and 2017. The selected formalin-fixed paraffin-embedded tissues from each biopsy specimen were cut into 4-micron sections. Initial sections were stained by hematoxylin and eosin staining. Primary antihuman antibodies against P53, Ki-67, and CD34 were applied. Positive control samples for biomarkers were received from former strongly positive samples of papillary endothelial hyperplasia, high grade lymphoma, and breast ductal carcinoma for CD34, Ki-67, and P53, respectively. Results: Out of 60 psoriasis patients, 56.7% were men, with the mean age of 36.8 years. From 31 psoriasiform patients, 45.2% were men, with the mean age of 37.5 years. Both groups were matched in terms of sex and age. The mean staining of three markers was more significant in psoriasiform dermatitis than psoriasis. Conclusion: In spite of some other researches, the present study showed expression of P53, Ki-67, and CD34 biomarkers were significantly higher in psoriasiform dermatitis than psoriasis.
 
Background: Konjac glucomannan polysaccharide (KGM), inulin oligosaccharide (inulin) and their mixture has been shown to modulate the gut-associated lymphoid tissue immunity. Aims: The present study was mainly to determine effects of a low-level (2% w/w) KGM and inulin and their combination on dextran sodium sulfate (DSS)-induced colitis. We also determine the potential mechanisms mediating these effects of dietary fibers. Methods: C57BL/6J mice (6 weeks of age, eight per group) were randomly assigned to consume one of the following diets: control (DSS group) or control diet supplemented with 2% (w/w) of KGM (KGM group), 2% (w/w) of inulin oligosaccharide (inulin group) or KGM+Inulin (1%, w/w each (K+I group)) for 29 days, combined with the DSS drinking water (2% w/v) treatment on days 21-26. Another group served as vehicle was fed the control diet and given regular drinking water throughout the study. Fresh feces were collected on days 26-29. Mice were killed on day 30 after fasting. Segments of distal colon were processed for histological procedure. The remaining colonic tissues were processed to determine the colonic gene expressions of cytokines, tight junction proteins and antioxidant enzymes. Results: The present study indicated that DSS resulted in colonic dysplasia, severe leukocyte infiltration and enhanced gene expressions of pro-inflammatory cytokines. All fiber treatments ameliorated these indices of colitis. DSS treatment reduced the colonic gene expressions of tight junction proteins and antioxidant enzymes, which were ameliorated or normalized with fiber supplementation. In addition, all fiber treatments prevented the DSS-induced alterations in the fecal microbiota and short-chain acid levels. Conclusion: Supplementation of low-level, 2% (w/w), of KGM polysaccharide, inulin oligosaccharide and K + I reduced the DSS-induced colitis and mucosal barrier dysfunction, which was likely to be mediated by the prebiotic effects.
 
Hepatocellular carcinoma (HCC) is a disease usually diagnosed in its advanced-stage, and is frequently not amenable to curative surgical treatment. Also, HCC is resistant to chemotherapy and less vulnerable to radiation therapy compared to normal hepatic parenchyma. Both of these facts render the efficacy of adjuvant and palliative treatments problematic. Selective internal radiation therapy (SIRT) with 90Y-bearing microspheres is characterized by preferentially delivering substantially high doses of radiation to a liver tumor dose simultaneously limiting the damage to its non-tumorous cells, providing an opportunity for effective local tumor control and even tumor regression therapy. The current article reviews the specific characters, dosimetry, possible applications, and special considerations toward the pre-existing radiation therapy of 90Y microsphere SIRT in treating HCC.
 
Background: Desmodium gangeticum (L.)DC., which belongs to the Leguminosae family, has been used in Taiwan and other subtropical countries as an external medicine to remove blood stasis, activate blood circulation, and reduce inflammation. It has been reported to have antioxidant effects and improve inflammatory responses in rats stimulated by pro-inflammatory agents and induced gastric ulcers in experimental animals over the past few decades. This plant has also been used to treat parasitic infections, but there are no reports regarding its effects on lung cancer. Therefore, this study attempted to investigate its water crude extract (in abbreviation DG) on lung cancer cells. Methods: A549 human lung cancer cells were tested for survival using MTT, trypan blue, and propidium iodide. The effects of various concentrations of the crude extract of D. gangeticum (DG) (0.125~1 mg/ml) on the cell cycle and apoptosis of A549 cells were analyzed by flow cytometry and Western blotting methods. Results: DG can inhibit the growth of A549 human lung cancer cells in a concentration- and time-dependent manner. DG arrested A549 cells in the G1 phase by increasing the proteins expression of p21, p27, cyclin D1, and cyclin E. Additionally, DG decreased the expression of cyclin A, B1, and Cdc 2 (CDK1) proteins. Conclusions: DG demonstrated the anti-lung cancer activity by arresting the cell cycle in G1 via increasing the p21, p27, cyclin D1, cyclin E, and decreasing Cdc2, cyclin A, and B1 proteins expression in A549 human lung cancer cells.
 
The accurate diagnosis of pediatric acute abdominal pain is one of the most challenging tasks in the emergency department (ED) due to its unclear clinical presentation and non-specific findings in physical examinations, laboratory data, and plain radiographs. The objective of this study was to evaluate the impact of abdominal multidetector computed tomography (MDCT) performed in the ED on pediatric patients presenting with acute abdominal pain. A retrospective chart review of children aged <18 years with acute abdominal pain who visited the emergency department and underwent MDCT between September 2004 and June 2007 was conducted. Patients with a history of trauma were excluded. A total of 156 patients with acute abdominal pain (85 males and 71 females, age 1-17 years; mean age 10.9 ± 4.6 years) who underwent abdominal MDCT in the pediatric ED during this 3-year period were enrolled in the study. One hundred and eighteen patients with suspected appendicitis underwent abdominal MDCT. Sixty four (54.2%) of them had appendicitis, which was proven by histopathology. The sensitivity of abdominal MDCT for appendicitis was found to be 98.5% and the specificity was 84.9%. In this study, the other two common causes of nontraumatic abdominal emergencies were gastrointestinal tract (GI) infections and ovarian cysts. The most common etiology of abdominal pain in children that requires imaging with abdominal MDCT is appendicitis. MDCT has become a preferred and invaluable imaging modality in evaluating uncertain cases of pediatric acute abdominal pain in ED, in particular for suspected appendicitis, neoplasms, and gastrointestinal abnormalities.
 
Background: Astragalus fascicolifolius manna is used to treat different diseases. Because pregnant women tend to use Astragalus. fascicolifolius and Iranian traditional medicine emphasizes the abortifacient potential of this plant, this study aimed to investigate Astragalus fascicolifolius manna abortifacient property and effects on estrogen, progesterone, LH and FSH levels in BALB/c mice. Method: This experimental study was conducted with 70 female BALB/c mice assigned to seven groups: Nonpregnant, untreated; nonpregnant, Astragalus. fascicolifolius extract (400 mg/kg)-treated; pregnant, Astragalus. fascicolifolius extract (400, 800 and 1200 mg/kg)-treated; and two pregnant control groups. On 18 and 19 days of pregnancy, cesarean section performed on mice, resorbed embryos counted; then Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), estrogen and progesterone levels were measured by the ELISA. Results: Astragalus. fascicolifolius extract caused a significant increase abortion in mice. The levels of progesterone, FSH and LH were significantly different among the groups such that mean progesterone level was lower and mean LH and FSH levels were higher in the Astragalus. fascicolifolius extract-treated groups than the pregnant, untreated group. Conclusion: This extract has abortifacient properties and this plant can be used cautiously in pregnancy. Decreasing progesterone, increasing FSH and LH feedback in response to decreased progesterone by this extract is one of the potential mechanisms involved in abortion.
 
Incidence density of pyogenic liver abscesses stratified by sex, age, and follow-up period between herpes zoster group and non-herpes zoster group.
Objective The purpose of the paper was to explore the relationship between herpes zoster and pyogenic liver abscesses in Taiwan. Methods This was a nationwide cohort study. Using the database of the Taiwan National Health Insurance Program, there were 33049 subjects aged 20-84 years who were newly diagnosed with herpes zoster from 1998 to 2010 that were selected for our study, and they were our herpes zoster group. 131707 randomly selected subjects without herpes zoster were our non-herpes zoster group. Both groups were matched by sex, age, other comorbidities, and the index year of their herpes zoster diagnosis. The incidence of pyogenic liver abscesses at the end of 2011 was then estimated. The multivariable Cox proportional hazard regression model was used to estimate the hazard ratio and 95% confidence interval for pyogenic liver abscesses associated with herpes zoster and other comorbidities. Results The overall incidence rate was 1.38-fold higher in the herpes zoster group than in the non-herpes zoster group (4.47 vs. 3.25 per 10000 person-years, 95% confidence interval 1.32, 1.44). After controlling for potential confounding factors, the adjusted hazard ratio of pyogenic liver abscesses was 1.34 in the herpes zoster group (95% confidence interval 1.05, 1.72) when compared with the non-herpes zoster group. Sex (in this case male), age, presence of biliary stones, chronic kidney diseases, chronic liver diseases, cancers, and diabetes mellitus were also significantly associated with pyogenic liver abscesses. Conclusions Patients with herpes zoster are associated with an increased hazard of developing pyogenic liver abscesses.
 
Flow chart showing the selection process for the study's subjects. 
Background and aim: Few systematic studies focus on the association between weight loss and pyogenic liver abscesses. The objective of the study was to assess the association between weight loss and pyogenic liver abscesses in adults in Taiwan. Methods: This population-based cohort study utilized the database of the Taiwan National Health Insurance Program. Totally, 8453 subjects aged 20 to 84 years with newly diagnosed weight loss between 2000 and 2012 were assigned as the weight loss group, and 33777 randomly selected subjects without weight loss were assigned as the non-weight loss group. Both the weight loss and the non-weight loss groups were matched according to sex, age, and comorbidities. The incidence of pyogenic liver abscesses at the end of 2013 was measured in both groups. Results: A multivariable Cox proportional hazards regression model was done and presented evidence that the adjusted HR of pyogenic liver abscess was 2.47 (95 %CI 1.21, 5.02) for those subjects with weight loss and without comorbidities, as compared with those subjects without weight loss and without comorbidities. Among the weight loss group, 5% developed pyogenic liver abscesses within 3 months. Conclusion: Weight loss is associated with pyogenic liver abscesses in adults. Yet weight loss might not be an early clinical symptom of undiagnosed pyogenic liver abscesses.
 
Flow chart showing the selection of cases with pyogenic liver abscesses and controls for the study. 
− Risk of developing pyogenic liver abscesses associated with cumulative dosage of current use of oral corticosteroids category. 
Background and aim: There are no epidemiological studies focusing on the association between oral corticosteroid use and pyogenic liver abscesses. The aim of the study was to assess whether oral corticosteroid use is associated with increased odds of pyogenic liver abscesses in adults in Taiwan. Methods: This retrospective population-based case-control study was conducted to analyze the database of the Taiwan National Health Insurance Program from 2000 to 2013. Subjects aged 20 to 84 years with their first episode of pyogenic liver abscesses were assigned as the cases (n = 881). Randomly selected subjects without pyogenic liver abscesses aged 20 to 84 years were selected as the controls (n = 3207). A multivariable logistic regression model was used to assess the odds ratio and 95% confidence interval for the correlation of oral corticosteroid use with pyogenic liver abscesses. Results: After regulating for confounders, the adjusted odds ratio of pyogenic liver abscesses was 1.40 for subjects currently using oral corticosteroids (95% confidence interval 1.14, 1.70), compared with subjects who never used them. Upon further analysis, the adjusted odds ratio of pyogenic liver abscesses was 1.03 for subjects with current use of oral corticosteroids when increasing dosage for every one mg (95% CI 1.01, 1.06). Conclusion: Although the findings are not unexpected, they are important because they suggest that current use of oral corticosteroids is significantly associated with increased odds of developing pyogenic liver abscesses in adults in Taiwan, with a dose-dependent effect.
 
Top-cited authors
Viswanadha Vijaya Padma
  • Bharathiar University
Santhini Elango
  • The South India Textile Research Association (SITRA)
Chih-Yang Huang
  • China Medical University (ROC)
Fuu-Jen Tsai
  • China Medical University Hospital
P Muralidhar Reddy
  • Osmania University