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[PMID]: 25001638
[Au] Autor:Gilger BC; Mandal A; Shah S; Mitra AK
[Ti] Title:Episcleral, intrascleral, and suprachoroidal routes of ocular drug delivery - recent research advances and patents.
[So] Source:Recent Pat Drug Deliv Formul;8(2):81-91, 2014.
[Is] ISSN:2212-4039
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:Subconjunctival/episcleral, intrascleral, and suprachoroidal routes of drug delivery for treatment of posterior segment eye diseases have become more feasible and popular in the past few years. These routes have the advantage of bypassing the main barriers to topical drug penetration, the ocular surface epithelium, the conjunctivallymphatics, and in the case of deep intrascleral and suprachoroidial delivery, the sclera barrier. Many ocular drug delivery application devices, drug delivery methods, and therapeutics that have been developed for intravitreal use can also be used subconjunctivally, intrasclerally, and in the suprachoroidal space. Alternatively, site-specific devices, such microneedles, and therapeutics, such as hydrogel matrices, have been developed to enhance ocular drug delivery. This manuscript will review the recent research advances and patents on episcleral, intrascleral, and suprachoroidal routes of ocular drug delivery.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 248821 MEDLINE  
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[PMID]: 25000413
[Au] Autor:Gan H; McKenzie R; Hao Q; Idell S; Tang H
[Ad] Address:Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, Texas, United States of America....
[Ti] Title:Protein kinase d is increased and activated in lung epithelial cells and macrophages in idiopathic pulmonary fibrosis.
[So] Source:PLoS One;9(7):e101983, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive and usually fatal lung disease of unknown etiology for which no effective treatments currently exist. Hence, there is a profound need for the identification of novel drugable targets to develop more specific and efficacious therapeutic intervention in IPF. In this study, we performed immunohistochemical analyses to assess the cell type-specific expression and activation of protein kinase D (PKD) family kinases in normal and IPF lung tissue sections. We also analyzed PKD activation and function in human lung epithelial cells. We found that PKD family kinases (PKD1, PKD2 and PKD3) were increased and activated in the hyperplastic and regenerative alveolar epithelial cells lining remodeled fibrotic alveolar septa and/or fibroblast foci in IPF lungs compared with normal controls. We also found that PKD family kinases were increased and activated in alveolar macrophages, bronchiolar epithelium, and honeycomb cysts in IPF lungs. Interestingly, PKD1 was highly expressed and activated in the cilia of IPF bronchiolar epithelial cells, while PKD2 and PKD3 were expressed in the cell cytoplasm and nuclei. In contrast, PKD family kinases were not apparently increased and activated in IPF fibroblasts or myofibroblasts. We lastly found that PKD was predominantly activated by poly-L-arginine, lysophosphatidic acid and thrombin in human lung epithelial cells and that PKD promoted epithelial barrier dysfunction. These findings suggest that PKD may participate in the pathogenesis of IPF and may be a novel target for therapeutic intervention in this disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0101983

  3 / 248821 MEDLINE  
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[PMID]: 25000398
[Au] Autor:Nickerson KP; Homer CR; Kessler SP; Dixon LJ; Kabi A; Gordon IO; Johnson EE; de la Motte CA; McDonald C
[Ad] Address:Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America; Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio, United States of America....
[Ti] Title:The dietary polysaccharide maltodextrin promotes salmonella survival and mucosal colonization in mice.
[So] Source:PLoS One;9(7):e101789, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In the latter half of the 20th century, societal and technological changes led to a shift in the composition of the American diet to include a greater proportion of processed, pre-packaged foods high in fat and carbohydrates, and low in dietary fiber (a "Western diet"). Over the same time period, there have been parallel increases in Salmonella gastroenteritis cases and a broad range of chronic inflammatory diseases associated with intestinal dysbiosis. Several polysaccharide food additives are linked to bacterially-driven intestinal inflammation and may contribute to the pathogenic effects of a Western diet. Therefore, we examined the effect of a ubiquitous polysaccharide food additive, maltodextrin (MDX), on clearance of the enteric pathogen Salmonella using both in vitro and in vivo infection models. When examined in vitro, murine bone marrow-derived macrophages exposed to MDX had altered vesicular trafficking, suppressed NAPDH oxidase expression, and reduced recruitment of NADPH oxidase to Salmonella-containing vesicles, which resulted in persistence of Salmonella in enlarged Rab7+ late endosomal vesicles. In vivo, mice consuming MDX-supplemented water had a breakdown of the anti-microbial mucous layer separating gut bacteria from the intestinal epithelium surface. Additionally, oral infection of these mice with Salmonella resulted in increased cecal bacterial loads and enrichment of lamina propria cells harboring large Rab7+ vesicles. These findings indicate that consumption of processed foods containing the polysaccharide MDX contributes to suppression of intestinal anti-microbial defense mechanisms and may be an environmental priming factor for the development of chronic inflammatory disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0101789

  4 / 248821 MEDLINE  
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[PMID]: 25000203
[Au] Autor:Fiore AP; Osaki LH; Gama P
[Ad] Address:Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, SP Brazil.
[Ti] Title:Transforming Growth Factor ß1 Increases p27 Levels via Synthesis and Degradation Mechanisms in the Hyperproliferative Gastric Epithelium in Rats.
[So] Source:PLoS One;9(7):e101965, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Throughout postnatal development, the gastric epithelium expresses Transforming Growth Factor beta1 (TGFß1), but it is also exposed to luminal peptides that are part of milk. During suckling period, fasting promotes the withdrawal of milk-born molecules while it stimulates gastric epithelial cell proliferation. Such response can be reversed by exogenous TGFß1, as it directly affects cell cycle through the regulation of p27 levels. We used fasting condition to induce the hyperproliferation of gastric epithelial cells in 14-day-old Wistar rats, and evaluated the effects of TGFß1 gavage on p27 expression, phosphorylation at threonine 187 (phospho-p27Thr187) and degradation. p27 protein level was reduced during fasting when compared to suckling counterparts, while phospho-p27Thr187/p27 ratio was increased. TGFß1 gavage reversed this response, which was confirmed through immunostaining. By using a neutralizing antibody against TGFß1, we found that it restored the p27 and phosphorylation levels detected during fasting, indicating the specific role of the growth factor. We noted that neither fasting nor TGFß1 changed p27 expression, but after cycloheximide administration, we observed that protein synthesis was influenced by TGFß1. Next, we evaluated the capacity of the gastric mucosa to degrade p27 and we recorded a higher concentration of the remaining protein in pups treated with TGFß1, suggesting augmented stability under this condition. Thus, we showed for the first time that luminal TGFß1 increased p27 levels in the rat gastric mucosa by up- regulating translation and reducing protein degradation. We concluded that such mechanisms might be used by rapidly proliferating cells to respond to milk-born TGFß1 and food restriction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0101965

  5 / 248821 MEDLINE  
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[PMID]: 24952647
[Au] Autor:Palczewska G; Dong Z; Golczak M; Hunter JJ; Williams DR; Alexander NS; Palczewski K
[Ad] Address:Polgenix, Cleveland, Ohio, USA....
[Ti] Title:Noninvasive two-photon microscopy imaging of mouse retina and retinal pigment epithelium through the pupil of the eye.
[So] Source:Nat Med;20(7):785-9, 2014 Jul.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Two-photon excitation microscopy can image retinal molecular processes in vivo. Intrinsically fluorescent retinyl esters in subcellular structures called retinosomes are an integral part of the visual chromophore regeneration pathway. Fluorescent condensation products of all-trans-retinal accumulate in the eye with age and are also associated with age-related macular degeneration (AMD). Here, we report repetitive, dynamic imaging of these compounds in live mice through the pupil of the eye. By leveraging advanced adaptive optics, we developed a data acquisition algorithm that permitted the identification of retinosomes and condensation products in the retinal pigment epithelium by their characteristic localization, spectral properties and absence in genetically modified or drug-treated mice. This imaging approach has the potential to detect early molecular changes in retinoid metabolism that trigger light- and AMD-induced retinal defects and to assess the effectiveness of treatments for these conditions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/nm.3590

  6 / 248821 MEDLINE  
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[PMID]: 25000866
[Au] Autor:O'Brart DP
[Ad] Address:Keratoconus Research Institute, Department of Ophthalmology, St. Thomas' Hospital, London SE1 7EH, United Kingdom. Electronic address: davidobrart@aol.com.
[Ti] Title:Corneal collagen cross-linking: A review.
[So] Source:J Optom;7(3):113-24, 2014 Jul-Sep.
[Is] ISSN:1989-1342
[Cp] Country of publication:Spain
[La] Language:eng
[Ab] Abstract:The aim was to review the published literature on corneal collagen cross-linking. The emphasis was on the seminal publications, systemic reviews, meta-analyses and randomized controlled trials. Where such an evidence did not exist, selective large series cohort studies, case controlled studies and case series with follow-up preferably greater than 12 months were included. Riboflavin/Ultraviolet A (UVA) corneal collagen cross-linking appears to be the first treatment modality to halt the progression of keratoconus and other corneal ectatic disorders with improvement in visual, keratometric and topographic parameters documented by most investigators. Its precise mechanism of action at a molecular level is as yet not fully determined. Follow-up is limited to 4-6 years at present but suggests continued stability and improvement in corneal shape with time. Most published data are with epithelium-off techniques. Epithelium-on studies suggest some efficacy but less than with the epithelium-off procedures and long-term data are not currently available. The use of Riboflavin/UVA CXL for the management of infectious and non-infectious keratitis appears very promising. Its use in the management of bullous keratopathy is equivocal. Investigation of other methodologies for CXL are under investigation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 248821 MEDLINE  
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[PMID]: 25001447
[Au] Autor:Naidu SR; Hegde RJ; Devrukhkar VN; Patel AR
[Ad] Address:Department of Paediatric and Preventive Dentistry, Bharati Vidyapeeth Dental College and Hospital, Navi Mumbai, Maharashtra, India.
[Ti] Title:Conservative management of unicystic ameloblastoma in a young child: A case report.
[So] Source:J Indian Soc Pedod Prev Dent;32(3):251-4, 2014 Jul-Sep.
[Is] ISSN:1998-3905
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Unicystic ameloblastoma is a rare, benign, locally invasive odontogenic neoplasm of young age that shows clinical, radiographical or gross features of an odontogenic cyst, but it histologically shows typical ameloblastomatous epithelium lining part of the cyst cavity, with or without luminal and/or mural tumor growth. A case of asymptomatic unicystic ameloblastoma in an 11- year-old-female, who was treated by surgical enucleation followed by Carnoy's solution application for 5 minutes, is presented. The present case report describes the clinical and radiological behaviors, its importance and complexity of a differential diagnosis and treatment protocol of lesions in the mandibular molar-ramus area considering the special problems in children.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:D
[St] Status:In-Data-Review
[do] DOI:10.4103/0970-4388.135842

  8 / 248821 MEDLINE  
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[PMID]: 24704289
[Au] Autor:Romano C; Chiaro A; Lucarelli S; Santarelli C; Cucchiara S; Guadagnini T; Miele E; Di Nardo G
[Ad] Address:Department of Pediatrics, Paediatric Endoscopy Unit, University of Messina, Italy....
[Ti] Title:Mucosal cytokine profiles in paediatric eosinophilic oesophagitis: A case-control study.
[So] Source:Dig Liver Dis;46(7):590-5, 2014 Jul.
[Is] ISSN:1878-3562
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Eosinophilic oesophagitis is an inflammatory condition characterized by a dense eosinophilic infiltrate. The migration of eosinophils into the oesophagus is influenced by cytokines such as IL-5, IL-13 and eotaxin-3. The aim of this study was to evaluate changes in the cytokine expression profiles (IL-5, IL-13 and eotaxin-3/CCL26) in children after topical steroid treatment. METHODS: a prospective case-control study was performed in 23 paediatric patients (age 5-16 years) with a histological diagnosis of eosinophilic oesophagitis. Histological evaluation and cytokine levels assay (IL-5, IL-13 and eotaxin-3/CCL26) in the proximal and distal oesophagus were performed before, and after 8 weeks of topical budesonide. Data were compared with a matched healthy control group. RESULTS: quantitative expression levels of IL-5, IL-13 and eotaxin-3 were significantly higher in the eosinophilic oesophagitis group both compared to healthy subjects (p<0.0001). A significant reduction of the eosinophil infiltrate as well as of IL-5, IL-13 and eotaxin-3 mucosal profiles was observed after steroid treatment both at the proximal and distal oesophagus (p<0.0001). CONCLUSIONS: IL-5, IL-13 and eotaxin-3/CCL26 are significantly over-expressed in the oesophageal epithelium of children with eosinophilic oesophagitis. Topical steroid treatment (inhaled and swallowed budesonide) can induce clinical response with partial mucosal remission.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 248821 MEDLINE  
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[PMID]: 23369183
[Au] Autor:Tarulli GA; De Silva D; Ho V; Kunasegaran K; Ghosh K; Tan BC; Bulavin DV; Pietersen AM
[Ti] Title:Hormone-sensing cells require Wip1 for paracrine stimulation in normal and premalignant mammary epithelium.
[So] Source:Breast Cancer Res;15(1):R10, 2013.
[Is] ISSN:1465-542X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The molecular circuitry of different cell types dictates their normal function as well as their response to oncogene activation. For instance, mice lacking the Wip1 phosphatase (also known as PPM1D; protein phosphatase magnesium-dependent 1D) have a delay in HER2/neu (human epidermal growth factor 2), but not Wnt1-induced mammary tumor formation. This suggests a cell type-specific reliance on Wip1 for tumorigenesis, because alveolar progenitor cells are the likely target for transformation in the MMTV(mouse mammary tumor virus)-neu but not MMTV-wnt1 breast cancer model. METHODS: In this study, we used the Wip1-knockout mouse to identify the cell types that are dependent on Wip1 expression and therefore may be involved in the early stages of HER2/neu-induced tumorigenesis. RESULTS: We found that alveolar development during pregnancy was reduced in Wip1-knockout mice; however, this was not attributable to changes in alveolar cells themselves. Unexpectedly, Wip1 allows steroid hormone-receptor-positive cells but not alveolar progenitors to activate STAT5 (signal transducer and activator of transcription 5) in the virgin state. In the absence of Wip1, hormone-receptor-positive cells have significantly reduced transcription of RANKL (receptor activator of nuclear factor kappa-B ligand) and IGF2 (insulin-like growth factor 2), paracrine stimulators of alveolar development. In the MMTV-neu model, HER2/neu activates STAT5 in alveolar progenitor cells independent of Wip1, but HER2/neu does not override the defect in STAT5 activation in Wip1-deficient hormone-sensing cells, and paracrine stimulation remains attenuated. Moreover, ERK (extracellular signal-regulated kinase) activation by HER2/neu in hormone-sensing cells is also Wip1 dependent. CONCLUSIONS: We identified Wip1 as a potentiator of prolactin and HER2/neu signaling strictly in the molecular context of hormone-sensing cells. Furthermore, our findings highlight that hormone-sensing cells convert not only estrogen and progesterone but also prolactin signals into paracrine instructions for mammary gland development. The instructive role of hormone-sensing cells in premalignant development suggests targeting Wip1 or prolactin signaling as an orthogonal strategy for inhibiting breast cancer development or relapse.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/bcr3381

  10 / 248821 MEDLINE  
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[PMID]: 24970044
[Au] Autor:Jimenez FR; Lewis JB; Belgique ST; Wood TT; Reynolds PR
[Ti] Title:Developmental lung expression and transcriptional regulation of Claudin-6 by TTF-1, Gata-6, and FoxA2.
[So] Source:Respir Res;15(1):70, 2014.
[Is] ISSN:1465-993X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Claudins are transmembrane proteins expressed in tight junctions that prevent paracellular transport of extracellular fluid and a variety of other substances. However, the expression profile of Claudin-6 (Cldn6) in the developing lung has not been characterized. METHODS AND RESULTS: Cldn6 expression was determined during important periods of lung organogenesis by microarray analysis, qPCR and immunofluorescence. Expression patterns were confirmed to peak at E12.5 and diminish as lung development progressed. Immunofluorescence revealed that Cldn6 was detected in cells that also express TTF-1 and FoxA2, two critical transcriptional regulators of pulmonary branching morphogenesis. Cldn6 was also observed in cells that express Sox2 and Sox9, factors that influence cell differentiation in the proximal and distal lung, respectively. In order to assess transcriptional control of Cldn6, 0.5, 1.0, and 2.0-kb of the proximal murine Cldn6 promoter was ligated into a luciferase reporter and co-transfected with expression vectors for TTF-1 or two of its important transcriptional co-regulators, FoxA2 and Gata-6. In almost every instance, TTF-1, FoxA2, and Gata-6 activated gene transcription in cell lines characteristic of proximal airway epithelium (Beas2B) and distal alveolar epithelium (A-549). CONCLUSIONS: These data revealed for the first time that Cldn6 might be an important tight junctional component expressed by pulmonary epithelium during lung organogenesis. Furthermore, Cldn6-mediated aspects of cell differentiation may describe mechanisms of lung perturbation coincident with impaired cell junctions and abnormal membrane permeability.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1407
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/1465-9921-15-70


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