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[PMID]: 25963063
[Au] Autor:Linardi RL; Megee SO; Mainardi SR; Senoo M; Galantino-Homer HL
[Ad] Address:Department of Clinical Studies, New Bolton Center, 382 West Street Road, Kennett Square, PA, 19348, USA....
[Ti] Title:Expression and localization of epithelial stem cell and differentiation markers in equine skin, eye and hoof.
[So] Source:Vet Dermatol;26(4):213-e47, 2015 Aug.
[Is] ISSN:1365-3164
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The limited characterization of equine skin, eye and hoof epithelial stem cell (ESC) and differentiation markers impedes the investigation of the physiology and pathophysiology of these tissues. HYPOTHESIS/OBJECTIVES: To characterize ESC and differentiation marker expression in epithelial tissues of the equine eye, haired skin and hoof capsule. METHODS: Indirect immunofluorescence microscopy and immunoblotting were used to detect expression and tissue localization of keratin (K) isoforms K3, K10, K14 and K124, the transcription factor p63 (a marker of ESCs) and phosphorylated p63 [pp63; a marker of ESC transition to transit-amplifying (TA) cell] in epithelial tissues of the foot (haired skin, hoof coronet and hoof lamellae) and the eye (limbus and cornea). RESULTS: Expression of K14 was restricted to the basal layer of epidermal lamellae and to basal and adjacent suprabasal layers of the haired skin, coronet and corneal limbus. Coronary and lamellar epidermis was negative for both K3 and K10, which were expressed in the cornea/limbus epithelium and haired skin epidermis, respectively. Variable expression of p63 with relatively low to high levels of phosphorylation was detected in individual basal and suprabasal cells of all epithelial tissues examined. CONCLUSIONS: To the best of the author's knowledge, this is the first report of the characterization of tissue-specific keratin marker expression and the localization of putative epithelial progenitor cell populations, including ESCs (high p63 expression with low pp63 levels) and TA cells (high expression of both p63 and pp63), in the horse. These results will aid further investigation of epidermal and corneal epithelial biology and regenerative therapies in horses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/vde.12214

  2 / 257800 MEDLINE  
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[PMID]: 26010981
[Au] Autor:Tynyakov J; Bentov S; Abehsera S; Khalaila I; Manor R; Katzir Abilevich L; Weil S; Aflalo ED; Sagi A
[Ad] Address:Department of Life Sciences, Ben-Gurion University, Beer-Sheva, Israel; National Institute for Biotechnology in the Negev, Ben-Gurion University, Beer-Sheva, Israel....
[Ti] Title:A novel chitin binding crayfish molar tooth protein with elasticity properties.
[So] Source:PLoS One;10(5):e0127871, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The molar tooth of the crayfish Cherax quadricarinatus is part of the mandible, and is covered by a layer of apatite (calcium phosphate). This tooth sheds and is regenerated during each molting cycle together with the rest of the exoskeleton. We discovered that molar calcification occurs at the pre-molt stage, unlike calcification of the rest of the new exoskeleton. We further identified a novel molar protein from C. quadricarinatus and cloned its transcript from the molar-forming epithelium. We termed this protein Cq-M13. The temporal level of transcription of Cq-M13 in an NGS library of molar-forming epithelium at different molt stages coincides with the assembly and mineralization pattern of the molar tooth. The predicted protein was found to be related to the pro-resilin family of cuticular proteins. Functionally, in vivo silencing of the transcript caused molt cycle delay and a recombinant version of the protein was found to bind chitin and exhibited elastic properties.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150617
[Lr] Last revision date:150617
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0127871

  3 / 257800 MEDLINE  
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[PMID]: 26010977
[Au] Autor:Faron M; Fletcher JR; Rasmussen JA; Apicella MA; Jones BD
[Ad] Address:Graduate Program in Genetics, University of Iowa, Iowa City, Iowa, United States of America....
[Ti] Title:Interactions of Francisella tularensis with Alveolar Type II Epithelial Cells and the Murine Respiratory Epithelium.
[So] Source:PLoS One;10(5):e0127458, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Francisella tularensis is classified as a Tier 1 select agent by the CDC due to its low infectious dose and the possibility that the organism can be used as a bioweapon. The low dose of infection suggests that Francisella is unusually efficient at evading host defenses. Although ~50 cfu are necessary to cause human respiratory infection, the early interactions of virulent Francisella with the lung environment are not well understood. To provide additional insights into these interactions during early Francisella infection of mice, we performed TEM analysis on mouse lungs infected with F. tularensis strains Schu S4, LVS and the O-antigen mutant Schu S4 waaY::TrgTn. For all three strains, the majority of the bacteria that we could detect were observed within alveolar type II epithelial cells at 16 hours post infection. Although there were no detectable differences in the amount of bacteria within an infected cell between the three strains, there was a significant increase in the amount of cellular debris observed in the air spaces of the lungs in the Schu S4 waaY::TrgTn mutant compared to either the Schu S4 or LVS strain. We also studied the interactions of Francisella strains with human AT-II cells in vitro by characterizing the ability of these three strains to invade and replicate within these cells. Gentamicin assay and confocal microscopy both confirmed that F. tularensis Schu S4 replicated robustly within these cells while F. tularensis LVS displayed significantly lower levels of growth over 24 hours, although the strain was able to enter these cells at about the same level as Schu S4 (1 organism per cell), as determined by confocal imaging. The Schu S4 waaY::TrgTn mutant that we have previously described as attenuated for growth in macrophages and mouse virulence displayed interesting properties as well. This mutant induced significant airway inflammation (cell debris) and had an attenuated growth phenotype in the human AT-II cells. These data extend our understanding of early Francisella infection by demonstrating that Francisella enter significant numbers of AT-II cells within the lung and that the capsule and LPS of wild type Schu S4 helps prevent murine lung damage during infection. Furthermore, our data identified that human AT-II cells allow growth of Schu S4, but these same cells supported poor growth of the attenuated LVS strain in vitro. Collectively, these data further our understanding of the role of AT-II cells in Francisella infections.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1505
[Cu] Class update date: 150617
[Lr] Last revision date:150617
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0127458

  4 / 257800 MEDLINE  
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[PMID]: 25992581
[Au] Autor:Squires JE; Shivakumar P; Mourya R; Bessho K; Walters S; Bezerra JA
[Ad] Address:Department of Pediatrics of the University of Cincinnati College of Medicine, the Division of Gastroenterology, Hepatology and Nutrition and the Pediatric Liver Care Center of Cincinnati Children's Hospital Medical Center; Cincinnati, Ohio, United States of America....
[Ti] Title:Natural killer cells promote long-term hepatobiliary inflammation in a low-dose rotavirus model of experimental biliary atresia.
[So] Source:PLoS One;10(5):e0127191, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Biliary atresia is a rapidly progressive obstructive cholangiopathy of infants. Mechanistic studies in the mouse model of Rhesus rotavirus (RRV)-induced biliary atresia have linked the importance of effector lymphocytes to the pathogenesis of extrahepatic bile duct (EHBD) injury and obstruction in experimental biliary atresia; however, studies of the progressive liver injury have been limited by early death of newborn mice. Here, we aimed to determine 1) if a lower inoculum of RRV induces obstruction of EHBDs while allowing for ongoing liver inflammation, and 2) if NK cells regulate intrahepatic injury. The administration of 0.25 x 10(6) fluorescence forming units of RRV induced an obstructive extrahepatic cholangiopathy, but allowed for restoration of the duct epithelium, increased survival, and the development of a progressive intrahepatic inflammatory injury with molecular and cellular signatures equivalent to the traditional infectious model. Investigating the mechanisms of liver injury, we found that NK cell depletion at the onset of jaundice decreased liver inflammation, suppressed the expression of fibrosis and inflammation/immunity genes, lowered plasma ALT and bilirubin and improved survival. CONCLUSIONS: Lower inoculation of RRV-induced progressive liver injury and fibrosis via NK cells. These findings point to the potential use of NK cell-depleting strategies to block progression of liver disease in biliary atresia.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1505
[Cu] Class update date: 150530
[Lr] Last revision date:150530
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0127191

  5 / 257800 MEDLINE  
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[PMID]: 25903670
[Au] Autor:Sahin C; Sarikaya S; Basak K; Cetinel CA; Narter F; Eryildirim B; Saglam E; Sarica K
[Ad] Address:Department of Urology, Dr. Lutfi Kirdar Kartal Research and Training Hospital, Istanbul, Turkey, cahitsahin129@gmail.com.
[Ti] Title:Limitation of apoptotic changes and crystal deposition by Tutukon following hyperoxaluria-induced tubular cell injury in rat model.
[So] Source:Urolithiasis;43(4):313-22, 2015 Aug.
[Is] ISSN:2194-7236
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:This study aimed at evaluating the protective effects of a herbal medication (Tutukon) on the hyperoxaluria induced apoptotic changes and crystal deposition in renal tubular epithelium in rat model. 60 male wistar rats were divided into three different groups (each group n: 20). In Group I severe hyperoxaluria was induced by ethylene glycol (EG) (0.75 %) administration for 28 days. In Group II, in addition to hyperoxaluria induction, animals were treated with Tutukon for 28 days. Group III animals constituted the controls without any specific medication and/or intervention. While the presence and degree of crystal deposition in the tubular lumen were examined histopathologically under light microscopy, tubular apoptotic changes were evaluated using immunohistochemical staining for cysteine-aspartic acid protease-3 (Caspase-3) and tumor necrosis factor alpha (TNF-α) positivity on days 14 and 28, respectively. Evaluation of apoptotic changes by Caspase-3 positivity showed that while the majority of animals undergoing EG only showed evident apoptotic changes (n: 9), Tutukon application demonstrated a significant limitation with limited or no apoptosis (n: 7) in these animals. Similar data were noted for TNF alpha expression; while apoptotic changes were evident in 8 (80 %) in Group I animals, limited changes were noted in Tutukon Group (n: 2). Regarding crystal deposition despite evident changes in Group I (9 animals), like apoptotic alterations, it was again significantly limited in animals receiving Tutukon (4 animals). Renal tubular crystal deposition and apoptotic changes induced by hyperoxaluria play a role in the pathogenesis of urolithiasis and the limitation of these changes might be instituted by Tutukon as a result of its antioxidant and antiinflammatory effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00240-015-0777-1

  6 / 257800 MEDLINE  
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[PMID]: 25612669
[Au] Autor:Corfe BM; Harden CJ; Bull M; Garaiova I
[Ad] Address:Molecular Gastroenterology Research Group,Academic Unit of Surgical Oncology,Department of Oncology,University of Sheffield,Beech Hill Road,Sheffield S10 2RX,UK....
[Ti] Title:The multifactorial interplay of diet, the microbiome and appetite control: current knowledge and future challenges.
[So] Source:Proc Nutr Soc;74(3):235-44, 2015 Aug.
[Is] ISSN:1475-2719
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The recent availability of high-throughput nucleic acid sequencing technologies has rapidly advanced approaches to analysing the role of the gut microbiome in governance of human health, including gut health, and also metabolic, cardiovascular and mental health, inter alia. Recent scientific studies suggest that energy intake (EI) perturbations at the population level cannot account for the current obesity epidemic, and significant work is investigating the potential role of the microbiome, and in particular its metabolic products, notably SCFA, predominantly acetate, propionate and butyrate, the last of which is an energy source for the epithelium of the large intestine. The energy yield from dietary residues may be a significant factor influencing energy balance. This review posits that the contribution towards EI is governed by EI diet composition (not just fibre), the composition of the microbiome and by the levels of physical activity. Furthermore, we hypothesise that these factors do not exist in a steady state, but rather are dynamic, with both short- and medium-term effects on appetite regulation. We suggest that the existing modelling strategies for bacterial dynamics, specifically for growth in chemostat culture, are of utility in understanding the dynamic interplay of diet, activity and microbiomic organisation. Such approaches may be informative in optimising the application of dietary and microbial therapy to promote health.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1017/S0029665114001670

  7 / 257800 MEDLINE  
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[PMID]: 25497601
[Au] Autor:Chambers ES; Morrison DJ; Frost G
[Ad] Address:Faculty of Medicine,Nutrition and Dietetic Research Group,Section of Investigative Medicine,Hammersmith Campus,Imperial College London,UK.
[Ti] Title:Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?
[So] Source:Proc Nutr Soc;74(3):328-36, 2015 Aug.
[Is] ISSN:1475-2719
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2- or FFAR3-deficient animal models suggest that SCFA-mediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1017/S0029665114001657

  8 / 257800 MEDLINE  
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[PMID]: 26033267
[Au] Autor:Yang SH; Kang CK; Hu YC; Yen LC; Tsai SC; Hsieh YL; Lee TH
[Ad] Address:Department of Life Sciences, National Chung Hsing University, 250, Kuo-Kuang Road, Taichung, 402, Taiwan.
[Ti] Title:Comparisons of two types of teleostean pseudobranchs, silver moony (Monodactylus argenteus) and tilapia (Oreochromis mossambicus), with salinity-dependent morphology and ion transporter expression.
[So] Source:J Comp Physiol B;185(6):677-93, 2015 Aug.
[Is] ISSN:1432-136X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:There are essentially four different morphological types of pseudobranchs in teleosts, including lamellae-free, lamellae semi-free, covered, and embedded types. In the euryhaline silver moony (Monodactylus argenteus), the pseudobranch belongs to the lamellae semi-free type, which is characterized by one row of filaments on the opercular membrane and fusion on the buccal edge. The pseudobranchial epithelium of the moony contains two types of Na(+), K(+)-ATPase (NKA)-rich cells: chloride cells (CCs) and pseudobranch-type cells (PSCs). Our results revealed increased expression of NKA, the Na(+), K(+), 2Cl(-) cotransporter (NKCC), and the cystic fibrosis transmembrane conductance regulator (CFTR) for Cl(-) secretion and CCs profiles in the pseudobranchs of seawater (SW)-acclimated silver moonies, which indicates the potential role of pseudobranchs containing CCs in hypo-osmoregulation. In contrast, the pseudobranch of the Mozambique tilapia (Oreochromis mossambicus) belongs to the embedded type, which is covered by the connective tissues and only contains PSCs but not CCs. No sign of NKCC and CFTR-immunoreactivity (IR) was found in the pseudobranchs of SW and freshwater (FW) tilapia. However, higher NKA protein expression and larger sizes of NKA-IR PSCs were found in the pseudobranchs of FW-acclimated tilapia. Moreover, in the FW-acclimated moony, NKA-IR PSCs also exhibited higher numbers and larger sizes than in the SW individuals. Taken together, similar responses in low-salinity environments in different types of pseudobranchs indicated that the salinity-dependent morphologies of PSCs might be involved in critical functions for FW teleosts.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00360-015-0913-9

  9 / 257800 MEDLINE  
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[PMID]: 25786037
[Au] Autor:Chandra V; Choi YB; Hwang HL; Lee JH; Park SY; Kim HK; Poojan S; Koh JS; Kim HS; Hong KM
[Ad] Address:Research Institute, National Cancer Center, Ilsandong-gu, Goyang, Korea....
[Ti] Title:Immunohistochemical localization of LLC1 in human tissues and its limited expression in non-small cell lung cancer.
[So] Source:Histol Histopathol;30(9):1111-20, 2015 Sep.
[Is] ISSN:1699-5848
[Cp] Country of publication:Spain
[La] Language:eng
[Ab] Abstract:We have shown both LLC1 expression in the lung epithelium by in situ hybridization and its inactivation in lung cancer by epigenetic modification. However, LLC1 protein's cellular localization or its role in normal lung or cancer tissues has not yet been evaluated. In the present study, a monoclonal antibody against recombinant LLC1 was produced, and immunohistochemical staining was performed on arrays including various human tissues, normal lung and non-small cell lung cancer (NSCLC) tissues for LLC1 localization. The immunohistochemical results showed LLC1 expression in the cilia of normal-airway epithelial cells and in the cytoplasm of type II pneumocytes in bronchiectatic patients, but no expression in most of the NSCLC tissues, which is consistent with our previous report positing LLC1 as a tumor suppressor. However, LLC1 over-expression in NSCLC cell lines NCI-H1299 and NCI-H23 did not show any change in proliferation or migration, which does not indicate any LLC1 tumor-suppressor role. As for the other human tissues, LLC1 was localized in renal tubular cells, pancreatic acinar cells, and epithelial cells of the stomach, duodenum, and gallbladder. In summary, our findings suggest that LLC1 is not a tumor suppressor, and that it is localized in the cilia of the normal lung epithelium but is absent in most NSCLC cases, probably due to the loss of cilia during lung carcinogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.14670/HH-11-608

  10 / 257800 MEDLINE  
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[PMID]: 25901598
[Au] Autor:Li N; Mruk DD; Wong CK; Han D; Lee WM; Cheng CY
[Ad] Address:Center for Biomedical Research (N.L., D.D.M., C.Y.C.), Population Council, New York, New York 10065; Department of Biology (C.K.C.W.), Hong Kong Baptist University, Hong Kong, China; Department of Cell Biology (D.H.), Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking U...
[Ti] Title:Formin 1 Regulates Ectoplasmic Specialization in the Rat Testis Through Its Actin Nucleation and Bundling Activity.
[So] Source:Endocrinology;156(8):2969-83, 2015 Aug.
[Is] ISSN:1945-7170
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:During spermatogenesis, developing spermatids and preleptotene spermatocytes are transported across the adluminal compartment and the blood-testis barrier (BTB), respectively, so that spermatids line up near the luminal edge to prepare for spermiation, whereas preleptotene spermatocytes enter the adluminal compartment to differentiate into late spermatocytes to prepare for meiosis I/II. These cellular events involve actin microfilament reorganization at the testis-specific, actin-rich Sertoli-spermatid and Sertoli-Sertoli cell junction called apical and basal ectoplasmic specialization (ES). Formin 1, an actin nucleation protein known to promote actin microfilament elongation and bundling, was expressed at the apical ES but limited to stage VII of the epithelial cycle, whereas its expression at the basal ES/BTB stretched from stage III to stage VI, diminished in stage VII, and was undetectable in stage VIII tubules. Using an in vitro model of studying Sertoli cell BTB function by RNA interference and biochemical assays to monitor actin bundling and polymerization activity, a knockdown of formin 1 in Sertoli cells by approximately 70% impeded the tight junction-permeability function. This disruptive effect on the tight junction barrier was mediated by a loss of actin microfilament bundling and actin polymerization capability mediated by changes in the localization of branched actin-inducing protein Arp3 (actin-related protein 3), and actin bundling proteins Eps8 (epidermal growth factor receptor pathway substrate 8) and palladin, thereby disrupting cell adhesion. Formin 1 knockdown in vivo was found to impede spermatid adhesion, transport, and polarity, causing defects in spermiation in which elongated spermatids remained embedded into the epithelium in stage IX tubules, mediated by changes in the spatiotemporal expression of Arp3, Eps8, and palladin. In summary, formin 1 is a regulator of ES dynamics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.1210/en.2015-1161


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