bluuebunny/crossref_metadata_2025_split huggingface dataset:
Paneth cell-derived interleukin-17A causes multiorgan dysfunction after hepatic ischemia and reperfusion injury
Authors: Park Sang Won , Kim Mihwa , Brown Kevin M. , D'Agati Vivette D. , Lee Thomas H. 
Published: February 2011

Abstract

Hepatic ischemia and reperfusion (IR) injury is a major clinical problem that leads to frequent extrahepatic complications including intestinal dysfunction and acute kidney injury (AKI). In this study we aimed to determine the mechanisms of hepatic IR-induced extrahepatic organ dysfunction. Mice subjected to 60 minutes of hepatic IR not only developed severe hepatic injury but also developed significant AKI and small intestinal injury. Hepatic IR induced small intestinal Paneth cell degranulation and increased interleukin-17A (IL-17A) levels in portal vein plasma and small intestine. We also detected increased levels of IL-17A messenger RNA (mRNA) and protein in Paneth cells after hepatic IR with laser capture dissection. IL-17A-neutralizing antibody treatment or genetic deletion of either IL-17A or IL-17A receptors significantly protected against hepatic IR-induced acute liver, kidney, and intestinal injury. Leukocyte IL-17A does not contribute to organ injury, as infusion of wildtype splenocytes failed to exacerbate liver and kidney injury in IL-17A-deficient mice after hepatic IR. Depletion of Paneth cell numbers by pharmacological (with dithizone) or genetic intervention (SOX9 flox/flox Villin cre+/− mice) significantly attenuated intestinal, hepatic, and renal injury following liver IR. Finally, depletion of Paneth cell numbers significantly decreased small intestinal IL-17A release and plasma IL-17A levels after liver IR.

Conclusion:

Taken together, the results show that Paneth cell-derived IL-17A plays a critical role in hepatic IR injury and extrahepatic organ dysfunction. Modulation of Paneth cell dysregulation may have therapeutic implications by reducing systemic complications arising from hepatic IR. (Hepatology 2011;)
Public health in Thailand: Emerging focus on non‐communicable diseases
Authors: Kaufman Nicholas D. , Chasombat Sanchai , Tanomsingh Saengchom , Rajataramya Benjaporn , Potempa Kathleen 
Published: February 2011

SUMMARYOver the past three decades, the public health landscape in Thailand has shifted remarkably. Currently chronic non‐communicable diseases represent the largest cause of mortality in the Thai population. In light of the current situation, this paper synthesizes what is known about the chronic non‐communicable disease situation in Thailand and analyzes current policy responses. Relevant contextual factors such as socio‐economic transitions, health systems development, and health workforce capacities are also considered. Primary data for this study were collected by a review of policy documents, government statements, and statistics reported by the Thailand Ministry of Public Health. Secondary data were obtained by a thorough review of the existing literature. The paper finds that while current policy responses to chronic non‐communicable diseases in the health sector have focused on improving prevention and control of risk factors, a stronger emphasis on chronic disease treatment and management may be needed in the future. The paper concludes with an exploration of the potential for developing and implementing realistic public health responses to the growing burden of chronic non‐communicable diseases in a Southeast Asian country context by utilizing existing capacities in research, policy, and health workforce development. Copyright © 2011 John Wiley & Sons, Ltd.
Fibroblast growth factor‐2 enhances NK sensitivity of hepatocellular carcinoma cells
Authors: Tsunematsu Hinako , Tatsumi Tomohide , Kohga Keisuke , Yamamoto Masashi , Aketa Hiroshi , Miyagi Takuya , Hosui Atsushi , Hiramatsu Naoki , Kanto Tatsuya , Hayashi Norio , Takehara Tetsuo 
Published: February 2011

AbstractThe roles of fibroblast growth factor‐2 (FGF‐2) in the hepatocellular carcinoma (HCC) development are still controversial. In this study, we investigated the expression of FGF‐2 in chronic hepatitis (CH) type C patients with or without HCC and the immunoregulation of FGF‐2 in NK sensitivity of HCC cells. The FGF‐2 expressions were detected in the liver tissues of patients, but not in normal liver. The serum FGF‐2 levels of the patients with CH, liver cirrhosis (LC) or HCC were significantly higher than those of healthy volunteers. The serum FGF‐2 levels of patients decreased with the progression of chronic liver disease. HCC occurrence of LC patients with high levels of serum FGF‐2 was significantly lower than that with low levels of serum FGF‐2. Proinflammatory cytokines, such as IL‐1β and IL‐6, induced FGF‐2 expressions in HCC cells and normal hepatocytes. FGF‐2 stimulation resulted in increasing the expression of the membrane‐bound major histocompatibility complex class I‐related chain A (MICA), an NK activating molecule, and decreasing that of human leukocyte antigen (HLA) class I, an NK inhibitory molecule, on HCC cells. This did not occur with normal hepatocytes. Adding anti‐FGF receptor‐2 neutralizing antibody resulted in inhibiting the change of MICA and HLA class I expressions on FGF‐2 stimulated HCC cells. FGF‐2 stimulation on HCC cells resulted in increasing NK sensitivity against HCC cells. These findings indicate that FGF‐2 produced by HCC cells or normal hepatocytes of chronic liver disease may play critical roles in eliminating HCC cells by innate immunity.
A reduction of recipient regulatory T cells by cyclophosphamide contributes to an anti‐tumor effect of nonmyeloablative allogeneic stem cell transplantation in mice
Authors: Takeuchi Ario , Eto Masatoshi , Yamada Hisakata , Tatsugami Katsunori , Naito Seiji , Yoshikai Yasunobu 
Published: February 2011

AbstractWe have recently established a unique model system of nonmyeloablative allogeneic stem cell transplantation (SCT) for treatment of murine solid tumors, based on cyclophosphamide‐induced tolerance. An injection of allogeneic donor spleen cells and bone marrow cells (BMC) followed by cyclophosphamide treatment induced a stable mixed chimerism with long lasting tolerance to the allografts. A donor lymphocyte infusion (DLI) in the cyclophosphamide‐induced tolerant mice exerted strong anti‐tumor effects on an MBT‐2 murine bladder tumor, MBT‐2 via their graft versus tumor (GVT) activity. In the present study, we determined whether a cyclophosphamide‐induced reduction of naturally occurring regulatory T cells (Tregs) was associated with the anti‐tumor activity in our nonmyeloablative SCT system. The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3‐ T cells. An adoptive transfer of CD4+ CD25+ T cells from naïve C3H/He x AKR/J F1 mice into recipient mice 1 day after DLI significantly suppressed the expansion and IFN‐γ production of host‐reactive donor CD4+T cells and hampered the MBT‐2 anti‐tumor activity when compared with the transfer of CD4+ CD25‐ T cells. These results indicated that cyclophosphamide‐induced reduction of recipient Tregs is associated with retardation of tumor progression via the expansion of host‐reactive donor T cells and IFN‐γ production after DLI in our nonmyeloablative SCT system.
Controlling the Molecular Assembly of Polyoxometalates from the Nano to the Micron Scale: Molecules to Materials
Authors: Hutin Marie , Long De‐Liang , Cronin Leroy 
Published: February 2011

AbstractPolyoxometalates (POMs) represent a class of metal‐oxide units based upon oxides of Mo, W, V, and Nb. Such cluster building blocks can also be subsequently self‐organized in complex 1D, 2D, and 3D frameworks leading to functional materials with diverse properties that span size ranges from 1 to 7 nm in terms of the size of the largest molecular units/clusters. However, since the cluster building blocks have great structural flexibility, the design of architectures is non‐trivial due to the sensitive dependence on reaction parameters such as pH, cation type, temperature, templating and linking units, ionic strength, redox agents. Therefore, the ability to control the aggregation or linking of the building blocks to give pre‐defined structure‐types as well as engineering the physical properties — for example, optical, electronic, catalytic activity/reactivity — is a tremendous challenge. In this review we survey our work from the control/design point of view and show how it is becoming possible to control the assembly of POM‐based architectures. We also describe the polyoxometalate‐based molecules‐to‐material transformations that can be seen as an osmotically driven crystal morphogenesis producing tubular architectures. This can be described as a new type of emergent phenomenon.
MicroRNA‐16 targets zyxin and promotes cell motility in human laryngeal carcinoma cell line HEp‐2
Authors: Wu Haidong , Liu Tao , Wang Renjie , Tian Shuang , Liu Min , Li Xin , Tang Hua 
Published: February 2011

AbstractMicroRNAs are small noncoding RNAs that negatively regulate target mRNAs at the posttranscription level. Here, we show that miR‐16 is upregulated in human laryngeal carcinoma tissues. Inhibition of miR‐16 in HEp‐2 laryngeal cancer cell line could suppress cell migration and enhance cell–cell adhesion. Subsequently, zyxin, whose expression is negatively regulated by miR‐16, is confirmed to be a direct target gene of miR‐16. Furthermore, overexpression of zyxin could also restrain cell movement and enhance cell–cell adhesion. The study of miR‐16 and its target zyxin will shed light on diagnosis and therapy of laryngeal cancer. © 2011 IUBMB IUBMB Life, 63(2): 101–108, 2011
Signaling to the ribosome in cancer—It is more than just mTORC1
Authors: Hannan Katherine M. , Sanij Elaine , Hein Nadine , Hannan Ross D. , Pearson Richard B. 
Published: February 2011

AbstractIt is becoming increasingly clear that dysregulation of protein synthesis contributes to a range of diseases characterized by tissue overgrowth. These include arterial stenosis, cardiac hypertrophy, hamartomas, and cancer. The central hub for the regulation of protein synthesis is the ribosome, where the key signaling pathways downstream of RAS, MYC, and phosphatidylinositol‐3‐kinase (PI3K) converge to confer exquisite, coordinated control of ribosome synthesis and function. Such cooperation ensures strict regulation of protein synthesis rates and cell growth. This review will focus on the role the PI3K/AKT/mammalian target of rapamycin complex 1 (mTORC1) pathway plays in regulating ribosome function during both health and disease, its interaction with the other key growth regulatory pathways activated by RAS and MYC, and the therapeutic potential for targeting this network. © 2011 IUBMB IUBMB Life, 63(2): 79–85, 2011
Gsα activity is reduced in erythrocyte membranes of patients with psedohypoparathyroidism due to epigenetic alterations at the GNAS locus
Authors: Zazo Celia , Thiele Susanne , Martín Cesar , Fernandez-Rebollo Eduardo , Martinez-Indart Lorea , Werner Ralf , Garin Intza , Group Spanish PHP , Hiort Olaf , Perez de Nanclares Guiomar 
Published: February 2011

Abstract
In pseudohypoparathyroidism (PHP), PTH resistance results from impairment of signal transduction of G protein–coupled receptors caused by a deficiency of the Gsα-cAMP signaling cascade due to diminished Gsα activity in maternally imprinted tissues. In PHP-Ia, inactivating mutations of the GNAS gene lead to haploinsufficiency in some tissues with biallelic expression, so in addition to PHP, Albright's hereditary osteodystrophy (AHO) is also present. In PHP-Ib, caused by methylation defects at the GNAS locus, diminished Gsα activity was thought to be limited to maternally imprinted tissues, such as the renal proximal tubule and the thyroid, leading to a lack of AHO. Recently, we demonstrated methylation defects in patients with AHO signs, indicating a connection between epigenetic changes and AHO. Our objective was to determine Gsα activity in erythrocyte membranes in patients with epigenetic defects at the GNAS locus compared to normal controls and patients with inactivating GNAS mutations. Gsα activity and expression, mutation of the GNAS locus, and methylation status were studied in patients with PHP and mild signs of AHO (PHP-Ia: 12; PHP-Ib: 17, of which 8 had some features of AHO). Then, we statistically compared the Gsα activity of the different PHP subtypes. Patients with methylation defects at the GNAS locus show a significant decrease in erythrocyte Gsα activity compared to normal controls (PHP-Ib versus controls, p &lt; .001). This was significantly lower in patients with AHO signs (PHP-Ib + mild-AHO versus PHP-Ib, p &lt; .05). Our research shows that PHP-Ia and PHP-Ib classification is not only overlapped genetically, as reported, but also in terms of Gsα activity. Reduced expression of GNAS due to methylation defects could downregulate Gsα activity in other tissues beyond those described and could also be causative of AHO. © 2011 American Society for Bone and Mineral Research
Bone biopsy findings and correlation with clinical, radiological, and biochemical parameters in children with fractures
Authors: Mäyränpää Mervi K , Tamminen Inari S , Kröger Heikki , Mäkitie Outi 
Published: February 2011

Abstract
In children the diagnosis of osteoporosis is based on fracture history and DXA-derived BMD. Bone biopsy is an invasive but accurate method for studying bone characteristics. In this study we evaluated bone biopsy findings and their correlation with noninvasive measures of bone health. Transiliac bone biopsy was performed on 24 consecutive children (17 boys, median age 12 years, range 6 to 16 years) evaluated for suspected primary osteoporosis. Biopsy findings were compared with normative data and correlated with clinical, radiological, biochemical, and densitometric findings. The patients had sustained altogether 64 nonvertebral fractures (median 2.5) from low- or moderate-energy traumas, and 14 patients (58%) had vertebral fractures. The median lumbar spine BMD Z-score was −1.2 (range −3.1 to +1.0). Hypovitaminosis D was present in 58%. Histomorphometry showed low bone volume in 7 patients and normal bone volume in 17. Bone turnover was high in 7, low in 7, and normal in 10 patients. Histomorphometric findings correlated poorly with fracture history, serum bone turnover markers, and DXA findings. Vitamin D deficiency and low lumbar BMD were associated with high bone turnover in the biopsy. These findings underscore the difficulties in diagnosing pediatric osteoporosis. Bone histomorphometry gives additional information and may be useful when considering bisphosphonate treatment in children with suspected primary osteoporosis. © 2011 American Society for Bone and Mineral Research
Effects of miR-335-5p in modulating osteogenic differentiation by specifically downregulating Wnt antagonist DKK1
Authors: Zhang Jin , Tu Qisheng , Bonewald Lynda F , He Xi , Stein Gary , Lian Jane , Chen Jake 
Published: February 2011

Abstract
Dickkopf-related protein 1 (DKK1) is essential to maintain skeletal homeostasis as an inhibitor of Wnt signaling and osteogenic differentiation. The purpose of this study was to investigate the molecular mechanisms underlying the developmental stage–specific regulation of the DKK1 protein level. We performed a series of studies including luciferase reporter assays, micro-RNA microarray, site-specific mutations, and gain- and loss-of-function analyses. We found that the DKK1 protein level was regulated via DKK1 3' UTR by miRNA control, which was restricted to osteoblast-lineage cells. As a result of decreased DKK1 protein level by miR-335-5p, Wnt signaling was enhanced, as indicated by elevated GSK-3β phosphorylation and increased β-catenin transcriptional activity. The effects of miR-335-5p were reversed by anti-miR-335-5p treatment, which downregulated endogenous miR-335-5p. In vivo studies showed high expression levels of miR-335-5p in osteoblasts and hypertrophic chondrocytes of mouse embryos, indicating a pivotal role of miR-335-5p in regulating bone development. In conclusion, miR-335-5p activates Wnt signaling and promotes osteogenic differentiation by downregulating DKK1. This cell- and development-specific regulation is essential and mandatory for the initiation and progression of osteogenic differentiation. miR-335-5p proves to be a potential and useful targeting molecule for promoting bone formation and regeneration. © 2011 American Society for Bone and Mineral Research
Periodontal disease and bisphosphonates induce osteonecrosis of the jaws in the rat
Authors: Aghaloo Tara L , Kang Ben , Sung Eric C , Shoff Michael , Ronconi Matthew , Gotcher Jack E , Bezouglaia Olga , Dry Sarah M , Tetradis Sotirios 
Published: February 2011

Abstract
Bisphosphonates (BPs) are medications used commonly to treat primary and metastatic bone cancer, as well as osteoporosis. Although BPs improve bone mineral density, reduce fracture risk, and reduce hypercalcemia of malignancy, some patients develop BP-related osteonecrosis of the jaws (BRONJ). This devastating complication is defined as clinically exposed bone in the maxillofacial region for more than 8 weeks. Despite an increasing number of BRONJ cases since first reported, the disease pathophysiology remains largely unknown. Since published studies suggest a significant role for dental disease in the pathophysiology of BRONJ, we developed a BRONJ animal model where aggressive periodontal disease is induced by ligature placement around the crown of the right maxillary first molar in the presence of vehicle (veh) or zoledronic acid (ZA), a potent BP. Ligature placement induced significant alveolar bone loss, which was attenuated by ZA treatment. Osteonecrosis was observed associated with ligature-induced periodontitis in the ZA-treated group. This was seen as sequestration and extensive periosteal alveolar bone formation on micro–computed tomography (µCT) in the ligated site of BP-treated animals. Histologic examination confirmed these findings, seen as necrotic bone with diffuse loss of osteocytes and empty lacunae, rimming of the necrotic bone by squamous epithelium and inflammation, and exposure to the oral cavity. Importantly, the rat lesions were strikingly similar to those of BRONJ patients. Our data suggest that dental disease and potent BP therapy are sufficient for BRONJ development in the rat. © 2011 American Society for Bone and Mineral Research
Enhanced chondrocyte proliferation and mesenchymal stromal cells chondrogenesis in coculture pellets mediate improved cartilage formation
Authors: Acharya Chitrangada , Adesida Adetola , Zajac Paul , Mumme Marcus , Riesle Jens , Martin Ivan , Barbero Andrea 
Published: February 2011

AbstractIn this study, we aimed at investigating the interactions between primary chondrocytes and mesenchymal stem/stromal cells (MSC) accounting for improved chondrogenesis in coculture systems. Expanded MSC from human bone marrow (BM‐MSC) or adipose tissue (AT‐MSC) were cultured in pellets alone (monoculture) or with primary human chondrocytes from articular (AC) or nasal (NC) cartilage (coculture). In order to determine the reached cell number and phenotype, selected pellets were generated by combining: (i) human BM‐MSC with bovine AC, (ii) BM‐MSC from HLA‐A2+ with AC from HLA‐A2− donors, or (iii) human green fluorescent protein transduced BM‐MSC with AC. Human BM‐MSC and AC were also cultured separately in transwells. Resulting tissues and/or isolated cells were assessed immunohistologically, biochemically, cytofluorimetrically, and by RT‐PCR. Coculture of NC or AC (25%) with BM‐MSC or AT‐MSC (75%) in pellets resulted in up to 1.6‐fold higher glycosaminoglycan content than what would be expected based on the relative percentages of the different cell types. This effect was not observed in the transwell model. BM‐MSC decreased in number (about fivefold) over time and, if cocultured with chondrocytes, increased type II collagen and decreased type X collagen expression. Instead, AC increased in number (4.2‐fold) if cocultured with BM‐MSC and maintained a differentiated phenotype. Chondro‐induction in MSC–chondrocyte coculture is a robust process mediated by two concomitant effects: MSC‐induced chondrocyte proliferation and chondrocyte‐enhanced MSC chondrogenesis. The identified interactions between progenitor and mature cell populations may lead to the efficient use of freshly harvested chondrocytes for ex vivo cartilage engineering or in situ cartilage repair. J. Cell. Physiol. 227: 88–97, 2012. © 2011 Wiley Periodicals, Inc.
Hindered settling of organic pigment dispersions in hydrocarbon liquids
Authors: McKay Robert B. 
Published: February 2011

AbstractA modified Steinour hindered settling method has been developed for the study of dispersed organic pigment species containing a large proportion of associated immobile liquid. These species are termed flow units with effective volumes and densities different from those of the pigment itself. The effective volume and density are calculated from the final sediment volume fraction after correction (if practicable) by an appropriate packing factor. The mean flow unit diameter (or a size parameter) can then be estimated. The present method has been satisfactorily tested using formalin‐fixed yeast cells as model flow units which can be sized readily by optical microscopy. Data for organic pigment dispersions compare well with their appearance under the optical microscope. Various uses of simplified versions of the present technique in studies of dispersibility and dispersion stability of organic pigments are described and exemplified using mainly copper phthalocyanine pigments in hydrocarbon solvents.
Studies on β‐alkoxypropionitriles as solvents for extractive distillation
Authors: Kuchhal Rakesh K. , Mallik Kanai L. 
Published: February 2011

AbstractFive solvents of the β‐alkoxypropionitrile series have been studied by gas‐chromatography in order to examine their potential usefulness as solvents for extractive distillation. Four isomers of C4‐olefin and a diene were used as solutes for the determination of activity coefficients at infinite dilution at 30°C. Relative volatilities were calculated for these solvents and compared with those for other commercial solvents used currently. Relative volatilities of seven C4‐hydrocarbons in two solvents were also studied and compared with the existing literature data for β‐methoxypropionitrile containing 5% antisolvent. The present g.c. studies show that besides the well‐studied β‐methoxypropionitrile, the second member of the series, β‐ethoxypropionitrile, also has the potential for use as a selective solvent.
Studies on cyanine dyes: II. Preparation of ferrocene cyanines
Authors: Osman Abdel Megied , Hassan Khairy M. , Khalil Zarif H. , Turin Vlademir D. 
Published: February 2011

AbstractThe condensation of ferrocene aldehyde with quaternary salts of 2‐methyl heterocyclic compounds, in the presence of piperidine as a catalyst, afforded ferrocenyl cyanines. Interaction of ferrocene aldehyde with the non‐quaternised heterocyclic compounds, in the presence of pyridine and sodium ethoxide as a condensing agent, afforded styryl ferrocenes.
A rapid attenuated total reflectance infrared method for tolylene diisocyanate isomer ratio determination
Authors: Corbett J. K. 
Published: February 2011

AbstractAn attenuated total reflectance (ATR) infrared method is described for the determination of the 2,4‐/2,6‐isomer ratio in tolylene diisocyanate. The absorption band intensity ratio at 1076 cm−1 (2,4‐isomer) and 780 cm−1 (2,6‐isomer) is measured.