bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acupuncture for primary dysmenorrhoea: a systematic review
Authors: Cho S‐H , Hwang E‐W 
Published: February 2010

Please cite this paper as: Cho S‐H, Hwang E‐W. Acupuncture for primary dysmenorrhoea: a systematic review. BJOG 2010;117:509–521.Background  The effectiveness of acupuncture in primary dysmenorrhoea is not fully understood.Objectives  To assess the effectiveness of acupuncture for the symptomatic treatment of primary dysmenorrhoea from randomised controlled trials (RCTs).Search strategy  Nineteen electronic databases, including English, Korean, Japanese and Chinese databases, were systematically searched for RCTs investigating acupuncture for primary dysmenorrhoea up to July 2008 with no language restrictions.Selection criteria  All RCTs that evaluated the effects of acupuncture compared with controls were included. Studies that assessed the effect of moxibustion or body acupressure were excluded.Data collection and analysis  The study abstraction and quality assessment of all studies were undertaken following the detailed descriptions of these categories as described in the Cochrane Handbook for Systematic Reviews of Interventions.Main results  Twenty‐seven RCTs were systematically reviewed. Only nine of the 27 trials clearly described their methods of randomisation and none of the trials stated the methods of allocation concealment. Compared with pharmacological treatment or herbal medicine, acupuncture was associated with a significant reduction in pain. Three studies reported reduced pain within groups from baseline; however, two RCTs did not find a significant difference between acupuncture and sham acupuncture.Author’s conclusions  The review found promising evidence in the form of RCTs for the use of acupuncture in the treatment of primary dysmenorrhoea compared with pharmacological treatment or herbal medicine. However, the results were limited by methodological flaws. The evidence for the effectiveness of acupuncture for the treatment of primary dysmenorrhoea is not convincing compared with sham acupuncture. Further rigorous nonpenetrating placebo‐controlled RCTs are warranted.
Abnormal post‐translational and extracellular processing of brevican in plaque‐bearing mice over‐expressing APPsw
Authors: Ajmo Joanne M. , Bailey Lauren A. , Howell Matthew D. , Cortez Lisa K. , Pennypacker Keith R. , Mehta Hina N. , Morgan Dave , Gordon Marcia N. , Gottschall Paul E. 
Published: February 2010

J. Neurochem. (2010) 113, 784–795.AbstractAggregation of amyloid‐β (Aβ) in the forebrain of Alzheimer’s disease (AD) subjects may disturb the molecular organization of the extracellular microenvironment that modulates neural and synaptic plasticity. Proteoglycans are major components of this extracellular environment. To test the hypothesis that Aβ, or another amyloid precursor protein (APP) dependent mechanism modifies the accumulation and/or turnover of extracellular proteoglycans, we examined whether the expression and processing of brevican, an abundant extracellular, chondroitin sulfate (CS)‐bearing proteoglycan, were altered in brains of Aβ‐depositing transgenic mice (APPsw – APP gene bearing the Swedish mutation) as a model of AD. The molecular size of CS chains attached to brevican was smaller in hippocampal tissue from APPsw mice bearing Aβ deposits compared to non‐transgenic mice, likely because of changes in the CS chains. Also, the abundance of the major proteolytic fragment of brevican was markedly diminished in extracts from several telencephalic regions of APPsw mice compared to non‐transgenic mice, yet these immunoreactive fragments appeared to accumulate adjacent to the plaque edge. These results suggest that Aβ or APP exert inhibitory effects on proteolytic cleavage mechanisms responsible for synthesis and turnover of proteoglycans. As proteoglycans stabilize synaptic structure and inhibit molecular plasticity, defective brevican processing observed in Aβ‐bearing mice and potentially end‐stage human AD, may contribute to deficient neural plasticity.
Human neuroblastoma cells with MYCN amplification are selectively resistant to oxidative stress by transcriptionally up‐regulating glutamate cysteine ligase
Authors: De Tudela Miguel Veas‐Perez , Delgado‐Esteban María , Cuende Julia , Bolaños Juan P. , Almeida Angeles 
Published: February 2010

J. Neurochem. (2010) 113, 819–825.AbstractNeuroblastoma is a sympathetic nervous system tumour whose degree of malignancy, prognosis and therapy resistance has been associated with the amplification of MYCN oncogene. However, the molecular pathway responsible for such resistance is unknown. To contribute addressing this issue, in this study, we have compared the vulnerability of four human neuroblastoma cell lines differentially amplifying MYCN, namely SK‐N‐BE‐2 and IMR‐32 (MYCN‐amplified cells) and SH‐SY5Y and SK‐N‐SH (MCYN‐non‐amplified cells), to H2O2‐mediated apoptotic death. We found that the high resistance of the MYCN‐amplified neuroblastoma cells against oxidative damage can be accounted for by their greater expression of both the mRNA and protein of the catalytic subunit of glutamate‐cysteine ligase (GCLcat), the rate‐limiting step in GSH biosynthesis. Furthermore, we found that MYCN directly binds to an E‐box containing GCLcat promoter and that over‐expression of MYCN in MYCN‐non‐amplified cells stimulated GCLcat expression and provided resistance to oxidative damage; whereas knock down of MYCN in MYCN‐amplified cells decreased GCLcat expression and sensitized them to oxidative damage. Finally, GCLcat knock down enhanced the vulnerability of MYCN‐amplified cells to oxidative damage. These results demonstrate that regulation of GCLcat by MYCN accounts for the survival of neuroblastoma cells against oxidative damage, and suggest that GCL should be considered a potential therapeutic target for the treatment of MYCN‐amplified neuroblastoma.
Cartilage Tissue Engineering With Demineralized Bone Matrix Gelatin and Fibrin Glue Hybrid Scaffold: An In Vitro Study
Authors: Wang Zheng‐Hui , He Xi‐Jing , Yang Zhuang‐Qun , Tu Jun‐Bo 
Published: February 2010

AbstractTo develop a cartilage‐like tissue with hybrid scaffolds of demineralized bone matrix gelatin (BMG) and fibrin, rabbit chondrocytes were cultured on hybrid fibrin/BMG scaffolds in vitro. BMG scaffolds were carefully soaked in a chondrocyte–fibrin suspension, which was polymerized by submerging the constructs into thrombin–calcium chloride solution. Engineered cartilage‐like tissue grown on the scaffolds was characterized by histology, immunolocalization, scanning electron microscopy, biochemical assays, and analysis of gene expression at different time points of the in vitro culture. The presence of proteoglycan in the fibrin/BMG hybrid constructs was confirmed by positive toluidine blue and alcian blue staining. Collagen type II exhibited intense immunopositivity at the pericellular matrices. Chondrogenic properties were further demonstrated by the expression of gene‐encoded cartilage‐specific markers, collagen type II, and aggrecan core protein. The glycosaminoglycan production and hydroxyproline content of tissue grown on the fibrin/BMG hybrid scaffolds were higher than that of the BMG group. In conclusion, the fibrin/BMG hybrid scaffolds may serve as a potential cell delivery vehicle and a structural basis for cartilage tissue engineering.
Prognostic Factors for Adult Patients Receiving Extracorporeal Membrane Oxygenation as Mechanical Circulatory Support—A 14‐Year Experience at a Medical Center
Authors: Lan Chinchun , Tsai Pi‐Ru , Chen Yih‐Sharng , Ko Wen‐Je 
Published: February 2010

AbstractExtracorporeal membrane oxygenation (ECMO) is a resource‐consuming and highly invasive treatment. There were 1100 ECMO cases at the National Taiwan University Hospital between August 1994 and November 2008. Of these, 607 were adults (>18 years old) who received ECMO as mechanical circulatory support. In this study, patient characteristics and complications during the ECMO course were evaluated for their correlation with prognosis. The following factors were significantly different between survivors and nonsurvivors: age, coronary artery disease, diabetes mellitus, brain death, stroke during ECMO, the need for dialysis during ECMO, pre‐ECMO infection, hypoglycemia, acidosis, alkalosis, the need for a distal perfusion catheter, and the amount of red blood cells transfused. Six independent predictors of mortality were identified: age, stroke, the need for dialysis during ECMO, pre‐ECMO infection, hypoglycemia, and alkalosis. Our institution has comparatively extensive experience with adult patients, which may be quite different from other medical centers with respect to distribution of patient age. The findings should lead to better utilization of ECMO for adult patients in the future.
Polyurethane Scaffolds Seeded With Genetically Engineered Skeletal Myoblasts: A Promising Tool to Regenerate Myocardial Function
Authors: Blumenthal Britta , Golsong Peter , Poppe Annika , Heilmann Claudia , Schlensak Christian , Beyersdorf Friedhelm , Siepe Matthias 
Published: February 2010

AbstractIn animal models, intramyocardial injection of primary skeletal myoblasts is supposed to promote tissue regeneration and to improve cardiac function after myocardial infarction. The usage of genetically engineered myoblasts overexpressing the paracrine factors involved in tissue repair is believed to enhance these effects. However, cell therapy via injection is always accompanied by a high death rate of the injected cells. Here, we describe the construction of a growth factor‐producing myoblast‐seeded scaffold to overcome this limitation. Skeletal myoblasts were isolated and expanded from newborn Lewis rats. Cells were seeded on polyurethane (PU) scaffolds (Artelon) and transfected with DNA of VEGF‐A, HGF, SDF‐1, or Akt1 using the lipid‐based Metafectene Pro method. Overexpression was verified by ELISA, RT‐PCR (VEGF‐A, HGF, and SDF‐1) and Western blot analysis (Akt1). The seeded scaffolds were transplanted onto damaged myocardium of Lewis rats 2 weeks after myocardial infarction. Six weeks later, their therapeutic potential in vivo was analyzed by measurement of infarction size and capillary density. Primary rat skeletal myoblasts seeded on PU scaffolds were efficiently transfected, achieving transfection rates of 20%. In vitro, we noted a significant increase in expression of VEGF‐A, HGF, SDF‐1, and Akt1 after transfection. In vivo, transplantation of growth factor‐producing myoblast‐seeded scaffolds resulted in enhanced angiogenesis (VEGF‐A, HGF, and Akt1) or a reduced infarction zone (SDF‐1 and Akt1) in the ischemically damaged myocardium. In summary, we constructed a growth factor‐producing myoblast‐seeded scaffold which combines the beneficial potential of stem cell transplantation with the promising effects of gene‐therapeutic approaches. Because this matrix also allows us to circumvent previous cell application drawbacks, it may represent a promising tool for tissue regeneration and the re‐establishment of cardiac function after myocardial infarction.
Association of UVRAG polymorphisms with susceptibility to non‐segmental vitiligo in a Korean sample
Authors: Jeong Taek‐Jo , Shin Min‐Kyung , Uhm Yoon‐Kyung , Kim Hak‐Jae , Chung Joo‐Ho , Lee Mu‐Hyoung 
Published: February 2010

Please cite this paper as: Association of UVRAG polymorphisms with susceptibility to non‐segmental vitiligo in a Korean sample. Experimental Dermatology 2010; 19: e323–e325.Abstract:  Autoimmune, self‐destructive, oxidative stress and genetic theories have been proposed for the pathogenesis of vitiligo. Autophagy is essential for cellular homeostasis and is implicated in many pathophysiological conditions such as cancer, response to oxidative stress and autoimmunity. The ultraviolet (UV) radiation resistance‐associated gene (UVRAG) activates the Beclin1‐PI(3)KC3 complex, promoting autophagy. To evaluate whether UVRAG polymorphisms are associated with non‐segmental vitiligo (NSV) patients in a Korean sample, we conducted a case–control association study of 225 NSV patients and 439 matched healthy controls. A total of five single nucleotide polymorphisms (SNPs) of UVRAG were selected for analysis. Among these, two SNPs (rs1458836, rs7933235) showed significant genotypic differences between the NSV patient group and the control group. These two SNPs were located within a strong linkage disequilibrium (LD) block. In addition, the haplotype of the UVRAG polymorphism was associated with NSV. This study suggests a possible association between UVRAG and NSV susceptibility.
Smoking but not homozygosity for CYP1A2 g‐163A allelic variant leads to earlier disease onset in patients with sporadic porphyria cutanea tarda
Authors: Fontanellas Antonio , Martínez‐Fresno María , Garrido‐Astray María Concepción , Perucho Teresa , Morán‐Jiménez María‐Josefa , García‐Bravo María , Méndez Manuel , Poblete‐Gutiérrez Pamela , Frank Jorge , Henriques‐Gil Nuno , De Salamanca Rafael Enríquez 
Published: February 2010

Please cite this paper as: Smoking but not homozygosity for CYP1A2 g‐163A allelic variant leads to earlier disease onset in patients with sporadic porphyria cutanea tarda. Experimental Dermatology 2010. Experimental Dermatology 2010; 19: e326–e328.Abstract:  Porphyria cutanea tarda (PCT) results from decreased activity of hepatic uroporphyrinogen decarboxylase (UROD). Both sporadic and familial forms are characterised by typical cutaneous lesions triggered by genetic/environmental factors. Studies in rodents showed that cytochrome P4501A2 (CYP1A2) plays a central role in the synthesis of a competitive inhibitor of hepatic UROD, but there is little evidence in humans. The impact of smoking and CYP1A2 g‐163C > A allelic variant upon first appearance of clinical signs was investigated in 102 patients (80 sporadic‐PCT) and 150 healthy donors from Spain. We found an increase in the frequency of CYP1A2 g‐163A allele in patients with PCT when compared with controls, although the more inducible A/A genotype had no effect on the onset age. In sporadic‐PCT, smoking leads to earlier onset of clinically overt disease in moderate‐to‐heavy smokers (≥10 cigarettes/day). In conclusion, this study provides evidence that smoking hastens the onset of cutaneous symptoms in sporadic‐PCT patients.
Marie Unna hereditary hypotrichosis caused by a novel mutation in the human hairless transcript
Authors: Ramot Yuval , Horev Liran , Smolovich Irena , Molho‐Pessach Vered , Zlotogorski Abraham 
Published: February 2010

Please cite this paper as: Marie Unna hereditary hypotrichosis caused by a novel mutation in the human hairless transcript. Experimental Dermatology 2010; 19: e320–e322.Abstract:  Recently the causes for various forms of hypotrichosis and atrichia have been identified, increasing our understanding of the pathways involved in hair cycling and morphogenesis. Loss‐of‐function mutations of an inhibitory upstream ORF in the human hairless transcript were found as the cause for autosomal dominant Marie Unna hereditary hypotrichosis. At present, only two studies identified several pathogenic mutations. We ascertained a Jewish Ashkenazi family with hypotrichosis simplex of the Marie Unna type in a mother and her two children. Sequencing of the upstream ORF U2HR in the 5′ UTR of the hairless gene resulted in the identification of a novel heterozygous missense mutation c.74C > T resulting in the amino acid change p.P25L. Functional assays confirmed that this mutation led to increased translation of the main HR ORF. This finding extends the mutations’ spectrum of U2HR, and emphasizes its major role in hair growth.
HSP70 inducers from Chinese herbs and their effect on melanin production
Authors: Yamashita Yasuhiro , Hoshino Tatsuya , Matsuda Minoru , Kobayashi Chisa , Tominaga Aya , Nakamura Yasuhiko , Nakashima Koumei , Yokomizo Kazumi , Ikeda Tsuyoshi , Mineda Kazutaka , Maji Daisuke , Niwano Yoshimi , Mizushima Tohru 
Published: February 2010

Please cite this paper as: HSP70 inducers from Chinese herbs and their effect on melanin production. Experimental Dermatology 2010; 19: e340–e342.Abstract:  Skin hyperpigmentation disorders as a result of abnormal melanin production induced by ultraviolet (UV) irradiation are both a clinical and a cosmetic problem. This melanin production is mediated by tyrosinase whose expression is positively regulated by microphthalmia‐associated transcription factor (MITF). We recently found that expression of heat shock protein 70 (HSP70) inhibits melanin production. In this study, we searched for HSP70 inducers from Chinese herbs and selected an ethanol extract of Eupatorium lindleyanum (E. lindleyanum). Not only melanin production but also the activity and expression of tyrosinase were significantly suppressed in cells treated with E. lindleyanum extract as well as in HSP70‐overexpressing cells. The expression of MITF was clearly suppressed in cells treated with E. lindleyanum extract but not in HSP70‐overexpressing cells. These results suggest that E. lindleyanum extract suppresses the expression of tyrosinase and melanin production through both HSP70‐dependent and HSP70‐independent mechanisms.
Increased levels of serum IL‐31 in chronic spontaneous urticaria*
Authors: Raap Ulrike , Wieczorek Dorothea , Gehring Manuela , Pauls Inga , Ständer Sonja , Kapp Alexander , Wedi Bettina 
Published: February 2010

Please cite this paper as: Increased levels of serum IL‐31 in chronic spontaneous urticaria. Experimental Dermatology 2010; 19: 464–466.Abstract:  IL‐31 represents a novel cytokine involved in pruritic skin diseases including atopic dermatitis (AD). We, therefore, aimed at investigating IL‐31 levels in chronic spontaneous urticaria (CU). We included 46 patients with CU, 26 non‐atopic skin healthy subjects as negative and 28 patients with AD as positive controls. IL‐31 serum levels were analysed using commercial ELISA kit. IL‐31 serum levels were higher in patients with CU compared to healthy controls (P < 0.001), but lower compared to patients with AD (P < 0.001). There was no difference in IL‐31 serum levels in autologous serum skin test positive or negative CU patients and patients with infectious trigger factors including helicobacter pylori infection. IL‐31 serum levels may play a role in the pathophysiology of CU. This is supported by the finding that not all patients with CU respond to antihistamine treatment but to the treatment with immunosuppressive drugs.
Novel ELISA systems for antibodies to desmoglein 1 and 3: correlation of disease activity with serum autoantibody levels in individual pemphigus patients
Authors: Schmidt Enno , Dähnrich Cornelia , Rosemann Anke , Probst Christian , Komorowski Lars , Saschenbrecker Sandra , Schlumberger Wolfgang , Stöcker Winfried , Hashimoto Takashi , Bröcker Eva‐Bettina , Recke Andreas , Rose Christian , Zillikens Detlef 
Published: February 2010

Please cite this paper as: Novel ELISA systems for antibodies to desmoglein 1 and 3: correlation of disease activity with serum autoantibody levels in individual pemphigus patients. Experimental Dermatology 2010; 19: 458–463.Abstract:  Pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are intraepidermal blistering skin diseases. PV is characterised by autoantibodies directed against desmoglein (Dsg) 3 and in patients with the mucocutaneous variant also against Dsg 1, whereas in PF, only Dsg 1 is targeted. Here, ectodomains of Dsg 3 and Dsg 1 were recombinantly expressed in a human cell line (HEK293) and applied as authentic solid phases in ELISA test systems. Autoantibodies against Dsg 3 and/or Dsg 1 could be detected in 71 (100%) of 71 PV sera and against Dsg 1 in 48 (96%) of 50 PF sera. Control sera showed reactivity with Dsg 3 and Dsg 1 in 0.2% and 0.7%, respectively, of 401 healthy blood donors and in 2.1% of 48 randomly selected patients with bullous pemphigoid. No reactivity with Dsg 1 and 3 was detected in 21 patients with linear IgA disease. For both pemphigus variants, a statistically significant correlation between clinical severity and autoantibody levels was observed as demonstrated for 10 PV and 5 PF patients. In conclusion, the use of the ectodomains of Dsg 3 and 1 as target antigens expressed in a human cell line resulted in sensitive and specific ELISA systems for both diagnosis and monitoring of PV and PF.
Vitamin C attenuates ERK signalling to inhibit the regulation of collagen production by LL‐37 in human dermal fibroblasts
Authors: Park Hyun Jeong , Ock Sun Myeong , Kim Hee Jung , Park Hong Jin , Lee Young Bok , Choi Jung Min , Cho Chul Soo , Lee Jun Young , Cho Baik Kee , Cho Dae Ho 
Published: February 2010

Please cite this paper as: Vitamin C attenuates ERK signalling to inhibit the regulation of collagen production by LL‐37 in human dermal fibroblasts. Experimental Dermatology 2010; 19: e258–e264.Abstract:  Vitamin C is used as an anti‐ageing agent because of its collagen enhancing effects. The precise cellular signalling mechanism of vitamin C is not well known. Here, we investigate the profibrotic mechanism of vitamin C against LL‐37. Antimicrobial peptide LL‐37 decreases collagen expression at mRNA and protein levels in human dermal fibroblasts (HDFs). The ability of LL‐37 to inhibit collagen expression is dependent on phosphorylation of extracellular signal‐regulated kinase (ERK). HDFs and human keloid fibroblasts were treated with vitamin C followed by 2 h of LL‐37 treatment. Collagen mRNA expression and total soluble collagen production inhibited by LL‐37 was enhanced by treatment with 0.5 mm vitamin C. Vitamin C also decreased intracellular reactive oxygen intermediates (ROI) levels that were increased by LL‐37. Furthermore, the phosphorylation of ERK was analysed by Western blot following treatment with vitamin C and LL‐37. Vitamin C turned off phosphorylation of ERK that was induced by LL‐37. Ets‐1 transcriptional factor, which is involved in the regulation of collagen expression by LL‐37, was also inhibited by vitamin C. This study shows that vitamin C enhances collagen production by inhibiting the ERK pathway induced by LL‐37.
REVIEW ARTICLE: Interleukin‐10: A Multi‐Faceted Agent of Pregnancy
Authors: Thaxton Jessica E. , Sharma Surendra 
Published: February 2010

Citation Thaxton JE, Sharma S. Interleukin‐10: a multi‐faceted agent of pregnancy. Am J Reprod Immunol 2010It is widely accepted that pregnancy constitutes a unique developmental event. Unprecedented intrauterine actions of angiogenesis, immunity, and neuroendocrine regulation are juxtaposed to mechanisms of senescence that enable fetal growth and protection. The suppressive and regulatory factors that facilitate healthy pregnancy are under investigation. In non‐pregnant systems of infection and inflammation, the cytokine interleukin‐10 (IL‐10) has been widely investigated because of its potential as a key immunosuppressant in response to a multitude of inflammatory events. In the context of pregnancy, IL‐10 levels increase markedly in women during early pregnancy and remain elevated well into the third trimester immediately prior to onset of labor. The role of IL‐10 during pregnancy as a suppressor of active maternal immunity to allow acceptance of the fetal allograft has been a point of study. Moreover, secretion of IL‐10 by a diverse set of maternal and fetal cells has proven to aid in the orchestration of normal processes of pregnancy. Interestingly, some of the more profound findings regarding the actions of IL‐10 during pregnancy have manifested from research that focuses on aberrant pregnancy outcomes as a result of inflammation, hormonal imbalances, or gene–environment interactions. This review focuses on the role of IL‐10 as a facilitator of successful pregnancy both as an immune suppressive agent and a mediator of cross talk between the placenta and the decidua. Importantly, we discuss investigations on adverse pregnancy conditions to further elucidate the multifarious role of IL‐10 at the maternal–fetal interface.