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[PMID]: 23671731 [Au] Autor: Fajardo CA; Quiroga AJ; Coronado A; Labrador K; Acosta N; Delgado P; Jaramillo C; Bravo MM [Ad] Address: Carlos Alberto Fajardo, Andrés Javier Quiroga, Andrea Coronado, Karen Labrador, María Mercedes Bravo, Cancer and Infectious Agents Research Group, National Cancer Institute, Bogotá 110411, Colombia. [Ti] Title: CagA EPIYA polymorphisms in Colombian Helicobacter pylori strains and their influence on disease-associated cellular responses. [So] Source: World J Gastrointest Oncol;5(3):50-9, 2013 Mar 15. [Is] ISSN: 1948-5204 [Cp] Country of publication: China [La] Language: eng [Ab] Abstract: AIM: To investigate the influence of the CagA diversity in Helicobacter pylori (H. pylori) strains from Colombia on the host cell biology. METHODS: Eighty-four H. pylori-cagA positive strains with different Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs patterns, isolated from patients with gastritis (n = 17), atrophic gastritis (n = 17), duodenal ulcer (n = 16), intestinal metaplasia (n = 16) and gastric cancer (n = 18), were included. To determine the integrity of the cag pathogenicity island (cagPAI) we evaluated the presence of cagA, cagT, cagE, and cag10 genes by polymerase chain reaction. AGS gastric epithelial cells were infected with each strain and assayed for translocation and tyrosine phosphorylation of CagA by western blot, secretion of interleukin-8 (IL-8) by enzyme-linked immuno sorbent assay after taking supernatants from cocultures and cell elongation induction. For cell elongation quantification, coculture photographs were taken and the proportion of "hummingbird" cells (> 15 µm) was determined. RESULTS: Overall 72% (60/84) of the strains were found to harbor a functional cagPAI. Levels of phosphorylated CagA were significantly higher for isolates from duodenal ulcer than the ones in strains from gastritis, atrophic gastritis, intestinal metaplasia and gastric cancer (49.1% ± 23.1% vs 21.1% ± 19.5%, P < 0.02; 49.1% ± 23.1% vs 26.2% ± 14.8%, P < 0.045; 49.1% ± 23.1% vs 21.5% ± 19.5%, P < 0.043 and 49.1% ± 23.1% vs 29.5% ± 27.1%, P < 0.047 respectively). We observed variable IL-8 expression levels ranging from 0 to 810 pg/mL and from 8.8 to 1442 pg/mL at 6 h and 30 h post-infection, respectively. cagPAI-defective strains did not induce detectable levels of IL-8 at 6 h post-infection. At 30 h post-infection all strains induced IL-8 expression in AGS cells, although cagPAI-defective strains induced significantly lower levels of IL-8 than strains with a functional cagPAI (57.1 ± 56.6 pg/mL vs 513.6 ± 338.6 pg/mL, P < 0.0001). We did not observe differences in the extent of cell elongation induction between strains with a functional or a defective cagPAI in 6 h cocultures. At 24 h post infection strains with functional cagPAI showed high diversity in the extent of hummingbird phenotype induction ranging from 7% to 34%. cagPAI defective strains induced significantly lower levels of elongation than strains with functional cagPAI with one or more than one EPIYA-C motif (15.1% ± 5.2% vs 18.9% ± 4.7%, P < 0.03; and 15.1% ± 5.2% vs 20.0% ± 5.1%, P < 0.003 respectively). No differences were observed in cellular elongation induction or IL-8 expression among H. pylori strains bearing one and more than one EPIYA-C motifs, neither at 6 h nor at 24 h of coculture. There were no associations between the levels of induction of cell elongation or IL-8 expression and number of EPIYA motifs or pathology. CONCLUSION: The present work describes a lack of association between H. pylori CagA protein EPIYA motifs variations from Colombian isolates and disease-associated cellular responses. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [St] Status: In-Data-Review [do] DOI: 10.4251/wjgo.v5.i3.50

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[PMID]: 23462254 [Au] Autor: Dabrowska M [Ad] Address: Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur Street, 02-093 Warsaw, Poland. Electronic address: mada@nencki.gov.pl. [Ti] Title: Inflammatory phenotype of the nurse cell harboring Trichinella spp. [So] Source: Vet Parasitol;194(2-4):150-4, 2013 May 20. [Is] ISSN: 1873-2550 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: The nurse cell (NC), formed from muscle cells upon infection with the parasitic nematode Trichinella spp. constitutes a confined habitat for muscle larvae of encapsulating species. Signaling pathway-directed analysis of microarray data allowed identification of the stage of NC cell cycle arrest as being of G1-like type, accompanied by cellular senescence. In accord with the specificity of senescent cellular systems, up-regulation of pro-inflammatory molecules was also found within the NC preparations. Potential immune-related activities associated with NCs as inferred from the aforementioned analysis, are reviewed herein. Transcriptional data suggest that the NC which harbors the larvae may exhibit the following immune-related functions: (i) production of complement components, (ii) antigen presentation and phagocytosis, (iii) pro-inflammatory cytokine secretion, (iv) oxidative stress generation and (v) eicosanoid synthesis. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

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[PMID]: 23111618 [Au] Autor: Hasegawa S; Harada K; Morokoshi Y; Tsukamoto S; Furukawa T; Saga T [Ad] Address: Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba, 263-8555, Japan, shase@nirs.go.jp. [Ti] Title: Growth retardation and hair loss in transgenic mice overexpressing human H-ferritin gene. [So] Source: Transgenic Res;22(3):651-8, 2013 Jun. [Is] ISSN: 1573-9368 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: H-ferritin (HF) is a core subunit of the iron storage protein ferritin, and plays a central role in the regulation of cellular iron homeostasis. Recent studies revealed that ferritin and HF are involved in a wide variety of iron-independent functions, including regulating biological processes during physiological and pathological conditions, and can be overexpressed in some human diseases. To investigate the in vivo function of HF, we generated transgenic (tg) mice overexpressing the human HF gene (hHF-tg). We established two independent hHF-tg mouse lines. Although both lines of hHF-tg mice were viable, they showed reduced body size compared to wild-type (WT) mice at 4-12 weeks of age. Serum iron concentration and blood parameters of hHF-tg mice such as hemoglobin and red blood cell counts were comparable to those of WT mice. At 3-5 weeks of age, hHF-tg mice exhibited temporary loss of coat hair on the trunk, but not on the head or face. Histological analyses revealed that although initial hair development was normal, hHF-tg mice had epidermal hyperplasia with hyperkeratosis, dilated hair follicles, bended hair shafts and keratinous debris during the hairless period. In conclusion, we showed that hHF-tg mice exhibited mild growth retardation and temporary hairless phenotype. Our findings highlight the physiological roles of HF and demonstrate that hHF-tg mice are useful for understanding the in vivo functions of HF. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1007/s11248-012-9669-0

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[PMID]: 23666564 [Au] Autor: Yamamoto Y; Takahashi Y; Imai K; Miyakawa K; Nishimura S; Kasai R; Ikeda H; Takayama R; Mogami Y; Yamaguchi T; Terada K; Matsuda K; Inoue Y; Kagawa Y [Ad] Address: *Department of Clinical Research, National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Ulushiyama, Aoi-ku; and †Department of Clinical Pharmaceutics, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Yada, Suruga-ku, Shizuoka-shi, Shizuoka, Japan. [Ti] Title: Influence of CYP2C19 Polymorphism and Concomitant Antiepileptic Drugs on Serum Clobazam and N-Desmethyl Clobazam Concentrations in Patients With Epilepsy. [So] Source: Ther Drug Monit;35(3):305-12, 2013 Jun. [Is] ISSN: 1536-3694 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: OBJECTIVE: : The aims of this study were to identify the factors influencing the metabolism of clobazam (CLB) and its active metabolite [N-desmethyl clobazam (NCLB)] and to evaluate the NCLB concentration as an indicator for CYP2C19 polymorphism in epileptic patients. METHODS: : A total of 302 serum samples from 238 Japanese patients were evaluated. The ratios of the serum CLB and NCLB concentrations to the CLB dose (CD ratios) were calculated and compared with CYP2C19 phenotypes. RESULTS: : The mean CD ratio of NCLB in extensive metabolizers (EM: *1/*1), intermediate metabolizers (IM: *1/*2 or *1/*3), and poor metabolizers (PM: *2/*2, *3/*3, or *2/*3) was 3.1, 4.9, and 21.6 (µg/mL)/(mg/kg), respectively. In the EM and IM groups, the concomitant use of hepatic enzyme inducers (phenytoin and carbamazepine) reduced the CD ratio of CLB and increased that of NCLB. In the PM group, these inducers also decreased the CD ratio for CLB but did not elevate the CD ratio for NCLB. Using multiple regression analysis, body weight showed a positive correlation with an increased CD ratio for NCLB. The concomitant use of zonisamide and stiripentol also elevated the CD ratio for NCLB in the EM and IM groups, but that of the PM group was almost unchanged. When the cut-off value of the CD ratio for NCLB was set as 10.0 (µg/mL)/(mg/kg) for predicting the CYP2C19 PM status, the sensitivity and specificity were 94.4% and 95.7%, respectively. CONCLUSIONS: : The interaction between NCLB and other antiepileptic drugs showed marked differences among CYP2C19 phenotypes. Measurement of the serum NCLB concentration is clinically useful for identifying the PM phenotype. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1097/FTD.0b013e318283b49a

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[PMID]: 23668869 [Au] Autor: Ko JM; Sohn YB; Jeong SY; Kim HJ; Messiaen LM [Ad] Address: Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea. Electronic address: jmko@snu.ac.kr. [Ti] Title: Mutation Spectrum of NF1 and Clinical Characteristics in 78 Korean Patients With Neurofibromatosis Type 1. [So] Source: Pediatr Neurol;48(6):447-53, 2013 Jun. [Is] ISSN: 1873-5150 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Neurofibromatosis type 1 (NF1) is one of the most common autosomal dominant disorders in humans. NF1 is caused by mutations of the NF1 gene. Mutation detection is complex owing to the large size of the NF1 gene, the presence of pseudogenes, and the great variety of mutations. Also, few probable genotype-phenotype correlations have been found in NF1. In this study 78 Korean patients from 60 families were screened for NF1 mutations. Mutation analysis of the entire coding region and flanking splice sites was carried out and included the use of a combination of reverse transcription polymerase chain reaction, multiplex ligation probe amplification, or fluorescence in situ hybridization. Mutation spectrum and genotype-phenotype relationship were assessed. Fifty-two distinct NF1 mutations were identified in 60 families. The mutations included 30 single base substitutions (12 missense and 18 nonsense), 11 missplicing mutations, seven small insertion or deletions, and four gross deletions. Sixteen (30.8%) mutations were novel; c.1A>G, c.2033_2034insC, c.2540T>C, c.4537C>T, c.5546G>A, c.6792C>A, and c.6792C>G were recurrently identified. The mutations were evenly distributed across exon 1 through intron 47 of NF1, and no mutational hot spots were found. A genotype-phenotype analysis suggests that there is no clear relationship between specific mutations and clinical features. This analysis revealed a wide spectrum of NF1 mutations in Korean patients. As technologies advance in molecular genetics, the mutation detection rate will increase. Considering that 30.8% of detected mutations were novel, exhaustive mutation analysis of NF1 may be an important tool in early diagnosis and genetic counseling. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

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[PMID]: 23671706 [Au] Autor: Riera M; Burguera D; Garcia-Fernàndez J; Gonzàlez-Duarte R [Ad] Address: Departament de Genètica, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain ; Institut de Biomedicina (IBUB), Universitat de Barcelona, Barcelona, Spain ; CIBERER, Instituto de Salud Carlos III, Barcelona, Spain. [Ti] Title: CERKL Knockdown Causes Retinal Degeneration in Zebrafish. [So] Source: PLoS One;8(5):e64048, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: The human CERKL gene is responsible for common and severe forms of retinal dystrophies. Despite intense in vitro studies at the molecular and cellular level and in vivo analyses of the retina of murine knockout models, CERKL function remains unknown. In this study, we aimed to approach the developmental and functional features of cerkl in Danio rerio within an Evo-Devo framework. We show that gene expression increases from early developmental stages until the formation of the retina in the optic cup. Unlike the high mRNA-CERKL isoform multiplicity shown in mammals, the moderate transcriptional complexity in fish facilitates phenotypic studies derived from gene silencing. Moreover, of relevance to pathogenicity, teleost CERKL shares the two main human protein isoforms. Morpholino injection has been used to generate a cerkl knockdown zebrafish model. The morphant phenotype results in abnormal eye development with lamination defects, failure to develop photoreceptor outer segments, increased apoptosis of retinal cells and small eyes. Our data support that zebrafish Cerkl does not interfere with proliferation and neural differentiation during early developmental stages but is relevant for survival and protection of the retinal tissue. Overall, we propose that this zebrafish model is a powerful tool to unveil CERKL contribution to human retinal degeneration. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0064048

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[PMID]: 23671668 [Au] Autor: Snodgrass SM; Cihil KM; Cornuet PK; Myerburg MM; Swiatecka-Urban A [Ad] Address: Division of Pediatric Pulmonology, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. [Ti] Title: Tgf-ß1 Inhibits Cftr Biogenesis and Prevents Functional Rescue of ΔF508-Cftr in Primary Differentiated Human Bronchial Epithelial Cells. [So] Source: PLoS One;8(5):e63167, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: CFTR is an integral transmembrane glycoprotein and a cAMP-activated Cl(-) channel. Mutations in the CFTR gene lead to Cystic Fibrosis (CF)-an autosomal recessive disease with majority of the morbidity and mortality resulting from airway infection, inflammation, and fibrosis. The most common disease-associated mutation in the CFTR gene-deletion of Phe508 (ΔF508) leads to a biosynthetic processing defect of CFTR. Correction of the defect and delivery of ΔF508-CFTR to the cell surface has been highly anticipated as a disease modifying therapy. Compared to promising results in cultured cell this approach was much less effective in CF patients in an early clinical trial. Although the cause of failure to rescue ΔF508-CFTR in the clinical trial has not been determined, presence of factor(s) that interfere with the rescue in vivo could be considered. The cytokine TGF-ß1 is frequently elevated in CF patients. TGF-ß1 has pleiotropic effects in different disease models and genetic backgrounds and little is known about TGF-ß1 effects on CFTR in human airway epithelial cells. Moreover, there are no published studies examining TGF-ß1 effects on the functional rescue of ΔF508-CFTR. Here we found that TGF-ß1 inhibits CFTR biogenesis by reducing mRNA levels and protein abundance in primary differentiated human bronchial epithelial (HBE) cells from non-CF individuals. TGF-ß1 inhibits CFTR biogenesis without compromising the epithelial phenotype or integrity of HBE cells. TGF-ß1 also inhibits biogenesis and impairs the functional rescue of ΔF508-CFTR in HBE cells from patients homozygous for the ΔF508 mutation. Our data indicate that activation of TGF-ß1 signaling may inhibit CFTR function in non-CF individuals and may interfere with therapies directed at correcting the processing defect of ΔF508-CFTR in CF patients. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0063167

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[PMID]: 23671605 [Au] Autor: Horácek I; Knitlová M; Wagner J; Kordos L; Nadachowski A [Ad] Address: Department of Zoology, Charles University, Praha, Czech Republic. [Ti] Title: Late cenozoic history of the genus micromys (mammalia, rodentia) in central europe. [So] Source: PLoS One;8(5):e62498, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Molecular phylogeography suggests that Micromys minutus, the sole extant species of the genus, colonized its extensive range quite recently, during the Late Pleistocene-Holocene period. Rich Pliocene and Pleistocene fossil records both from Europe and China suggest rather continuous and gradual in situ phenotype rearrangements from the Pliocene to the Recent periods. To elucidate the discrepancy we reexamined a considerable part of the European fossil record of the genus (14 sites from MN15 to Q3, 0.4-4.2 Ma, including the type series of M. preaminutus from MN15 Csarnóta 2), analyzed them with the aid of detailed morphometric comparisons, and concluded that: (a) The European Pliocene form, M. praeminutus, differs significantly from the extant species; (b) it exhibits a broad phenotypic variation covering the presumptive diagnostic characters of MN16 M. caesaris; (c) despite having smaller dimensions, the Early and Middle Pleistocene forms (MN17-Q3, 2.6-0.4 Ma) seem to be closer to M. praeminutus than to the extant species; (d) the extinction of M. praeminutus during Q3 and the re-occupation of its niche by the recent expansion of M. minutus from E-European - C Asiatic sources (suggested by phylogeographic hypotheses) cannot be excluded. Discussing interpretations of the phylogenetic past of the genus we emphasize the distinct history of the West Palearctic clade (Late Miocene-Early Pleistocene) terminating with M. praeminutus and the East Asiatic clade (chalceus, tedfordi, minutus), and the possible identity of the Western clade with the Late Miocene genus Parapodemus. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0062498

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[PMID]: 23671609 [Au] Autor: Dean A; Mungall W; McKinnell C; Sharpe RM [Ad] Address: MRC Centre for Reproductive Health, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, Scotland, United Kingdom. [Ti] Title: Prostaglandins, masculinization and its disorders: effects of fetal exposure of the rat to the cyclooxygenase inhibitor- indomethacin. [So] Source: PLoS One;8(5):e62556, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Recent studies have established that masculinization of the male reproductive tract is programmed by androgens in a critical fetal 'masculinization programming window' (MPW). What is peculiar to androgen action during this period is, however, unknown. Studies from 20 years ago in mice implicated prostaglandin (PG)-mediation of androgen-induced masculinization, but this has never been followed up. We therefore investigated if PGs might mediate androgen effects in the MPW by exposing pregnant rats to indomethacin (which blocks PG production by inhibiting cyclooxygenase activity) during this period and then examining if androgen production or action (masculinization) was affected. Pregnant rats were treated with indomethacin (0.8 mg/kg/day; e15.5-e18.5) to encompass the MPW. Indomethacin exposure decreased fetal bodyweight (e21.5), testis weight (e21.5) and testicular PGE2 (e17.5, e21.5), but had no effect on intratesticular testosterone (ITT; e17.5) or anogenital index (AGI; e21.5). Postnatally, AGI, testis weight and blood testosterone were unaffected by indomethacin exposure and no cryptorchidism or hypospadias occurred. Penis length was normal in indomethacin-exposed animals at Pnd25 but was reduced by 26% (p<0.001) in adulthood, an effect that is unexplained. Our results demonstrate that indomethacin can effectively decrease intra-testicular PGE2 level. However, the resulting male phenotype does not support a role for PGs in mediating androgen-induced masculinization during the MPW in rats. The contrast with previous mouse studies is unexplained but may reflect a species difference. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0062556

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[PMID]: 23671414 [Au] Autor: Wang Y; Vik JO; Omholt SW; Gjuvsland AB [Ad] Address: Centre for Integrative Genetics (CIGENE), Department of Animal and Aquacultural Sciences, Norwegian University of Life Sciences, Ås, Norway. [Ti] Title: Effect of Regulatory Architecture on Broad versus Narrow Sense Heritability. [So] Source: PLoS Comput Biol;9(5):e1003053, 2013 May. [Is] ISSN: 1553-7358 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Additive genetic variance (VA ) and total genetic variance (VG ) are core concepts in biomedical, evolutionary and production-biology genetics. What determines the large variation in reported VA /VG ratios from line-cross experiments is not well understood. Here we report how the VA /VG ratio, and thus the ratio between narrow and broad sense heritability (h(2) /H(2) ), varies as a function of the regulatory architecture underlying genotype-to-phenotype (GP) maps. We studied five dynamic models (of the cAMP pathway, the glycolysis, the circadian rhythms, the cell cycle, and heart cell dynamics). We assumed genetic variation to be reflected in model parameters and extracted phenotypes summarizing the system dynamics. Even when imposing purely linear genotype to parameter maps and no environmental variation, we observed quite low VA /VG ratios. In particular, systems with positive feedback and cyclic dynamics gave more non-monotone genotype-phenotype maps and much lower VA /VG ratios than those without. The results show that some regulatory architectures consistently maintain a transparent genotype-to-phenotype relationship, whereas other architectures generate more subtle patterns. Our approach can be used to elucidate these relationships across a whole range of biological systems in a systematic fashion. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pcbi.1003053

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