bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of nortriptyline on cytosolic Ca2+ regulation and viability in PC3 human prostate cancer cells
Authors: Pan Chih‐Chuan , Shaw Chen‐Fu , Huang Jong‐Khing , Kuo Chun‐Chi , Kuo Daih‐Huang , Shieh Pochuen , Lu Ti , Chen Wei‐Chuan , Ho Chin‐Man , Jan Chung‐Ren 
Published: September 2010

AbstractThe effect of nortriptyline, a tricyclic antidepressant, on Ca2+ regulation and viability in human prostate cancer cells (PC3) is unclear. The present study examined whether nortriptyline altered basal [Ca2+]i levels in suspended PC3 cells using fura‐2 as a Ca2+‐sensitive fluorescent probe. Nortriptyline (50–500 µM) increased [Ca2+]i in a concentration‐dependent fashion. The Ca2+ signal was partially reduced by removing extracellular Ca2+, indicating that Ca2+ entry and release both contributed to the [Ca2+]i rise. Nortriptyline induced Mn2+ influx, leading to quench of fura‐2 fluorescence, suggesting Ca2+ influx. This Ca2+ influx was inhibited by activation of protein kinase C, but not by inhibition of L‐type Ca2+ channels. In Ca2+‐free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor, thapsigargin nearly abolished nortriptyline‐induced Ca2+ release. Conversely, pretreatment with nortriptyline greatly reduced the inhibitor‐induced [Ca2+]i rise, suggesting that nortriptyline released Ca2+ from the endoplasmic reticulum. Inhibition of phospholipase C did not change the nortriptyline‐induced [Ca2+]i rise. Nortriptyline at a concentration of 10 µM increased viability in a Ca2+‐independent manner. At 50 µM, nortriptyline killed 45% of cells. Nortriptyline at 10 µM did not induce apoptosis, but at 50 µM induced significant apoptosis measured by propidium iodide staining. Together, in PC3 cells, nortriptyline induced [Ca2+]i rises by causing the phospholipase C‐independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via the protein kinase C‐sensitive pathway. Nortriptyline also induced both cell proliferation and death in a concentration‐dependent manner. Apoptosis was involved in the cell death. Drug Dev Res 71:323–330, 2010. © 2010 Wiley‐Liss, Inc.
Glucose effectiveness and insulin sensitivity measurements derived from the non‐insulin‐assisted minimal model and the clamp techniques are concordant
Authors: Henriksen Jan Erik , Alford Frank , Ward Glenn , Thye‐Rønn Peter , Levin Klaus , Hother‐Nielsen Ole , Rantzau Christian , Boston Ray , Beck‐Nielsen Henning 
Published: September 2010

AbstractBackgroundWe investigated the concordance between glucose effectiveness (SG) and insulin sensitivity (SI), derived from the unmodified dynamic non‐insulin‐assisted intravenous glucose tolerance test (IVGTT) implemented by SGMM and SIMM; simulation analysis and modelling/conversational interaction (SAAM/CONSAM) versus the eu/hyperglycaemic basal insulinaemic and the euglycaemic hyperinsulinaemic clamp (SGCLAMP and SICLAMP).MethodsTwenty‐seven of 30 normoglycaemic subjects completed a (1) euglycaemic hyperinsulinaemic clamp, (2) 6‐h eu/hyperglycaemic near‐normoinsulinaemic pancreatic clamp with hyperglycaemia present over the final 2 h of the clamp (Day 2 study), (3) identical clamp to (2) but with euglycaemia maintained over the entire 6 h (Day 3 study) and (4) IVGTT. SGCLAMP was calculated in two ways based on data from study (2) alone (Day 2 SGCLAMP210–240′) or from data from study day (2) and (3) (Day 2–3 SGCLAMP330–360′).ResultsSGMM was unrelated to the magnitude of endogenous insulin release (AIR). The single‐day (Day 2) and two‐day (Day 2 and 3) SGCLAMP protocols correlated (r = 0.72, p = 0.003), but SGCLAMP210–240′ was significantly (p = 0.001) higher than SGCLAMP330–360′. Employing the Day 2 and 3 SGCLAMP protocol, the whole body SGCLAMP330–360′ was similar to SGMM (1.80 ± 0.82 versus 1.73 ± 0.58 dL/min) and correlated (r = 0.45, p < 0.02). SGCLAMP210–240′ did not correlate with SGMM (r = 0.24). SIMM and SICLAMP were similar (0.093 ± 0.060 versus 0.087 ± 0.029 dL/min per mU/L) and correlated (r = 0.76, p < 0.001).ConclusionsThe time‐dependent increase in glucose disposal observed during a prolonged 6‐h clamp significantly influences the estimation of SGCLAMP, and significant concordance coefficients are observed between SGMM, and SGCLAMP330–360′, and SIMM and SICLAMP. Copyright © 2010 John Wiley & Sons, Ltd.
Characterization of immunoglobulin heavy chain knockout rats
Authors: Ménoret Séverine , Iscache Anne‐L. , Tesson Laurent , Rémy Séverine , Usal Claire , Osborn Michel J. , Cost Gregory J. , Brüggemann Marianne , Buelow Roland , Anegon Ignacio 
Published: September 2010

AbstractThe rat is a species frequently used in immunological studies but, until now, there were no models with introduced gene‐specific mutations. In a recent study, we described for the first time the generation of novel rat lines with targeted mutations using zinc‐finger nucleases. In this study, we compare immune development in two Ig heavy‐chain KO lines; one with truncated Cμ and a new line with removed JH segments. Rats homozygous for IgM mutation generate truncated Cμ mRNA with a de novo stop codon and no Cγ mRNA. JH‐deletion rats showed undetectable mRNA for all H‐chain transcripts. No serum IgM, IgG, IgA and IgE were detected in these rat lines. In both lines, lymphoid B‐cell numbers were reduced >95% versus WT animals. In rats homozygous for IgM mutation, no Ab‐mediated hyperacute allograft rejection was encountered. Similarities in B‐cell differentiation seen in Ig KO rats and ES cell‐derived Ig KO mice are discussed. These Ig and B‐cell‐deficient rats obtained using zinc‐finger nucleases‐technology should be useful as biomedical research models and a powerful platform for transgenic animals expressing a human Ab repertoire.
What are regulatory B cells?
Authors: Gray David , Gray Mohini 
Published: September 2010

AbstractB cells are now acknowledged to play multiple roles in the immune response, in addition to making antibodies. Their role in regulating T‐cell responses during inflammation has come into focus recently. Thus, IL‐10 production by B cells has been shown to be important in limiting auto‐reactive and pathogen‐driven immune pathology; however, the exact identity of the regulatory B cells remains elusive; do they belong to a committed subset or can all B cells regulate given the appropriate inducing stimuli? A study in this issue of the European Journal of Immunology provides insight into the IL‐10‐producing B cells in humans, suggesting that many B cells have the capacity to make IL‐10 when optimally stimulated via the BCR and TLR9. Despite producing significant amounts of inflammatory cytokines as well, these B cells suppress T‐cell proliferation. This Commentary places this study in the context of what we think we know about regulatory B cells and more importantly highlights the questions we still need to answer.
On the origin of cattle: How aurochs became cattle and colonized the world
Authors: Ajmone‐Marsan Paolo , Garcia José Fernando , Lenstra Johannes A. 
Published: September 2010

AbstractSince their domestication in the Neolithic, cattle have belonged to our cultural heritage. The reconstruction of their history is an active field of research1 that contributes to our understanding of human history. Archeological data are now supplemented by analyses of modern and ancient samples of cattle with DNA markers of maternal, paternal, or autosomal inheritance. The most recent genetic data suggest that maternal lineages of taurine cattle originated in the Fertile Crescent with a possible contribution of South‐European wild cattle populations, while zebu cattle originate from the Indus Valley. Subsequently, cattle accompanied human migrations, which led to the dispersal of domestic cattle of taurine, indicine, or mixed origin over Asia, Africa, Europe, and the New World. This has resulted in their adaptation to different environments and considerable variation in appearance and performance. More recently, rational management of breeding led to international movements of sires, which again changed the global patterns of genetic diversity.
Inhibition of inducible nitric oxide synthase reverses the loss of functional hyperemia in diabetic retinopathy
Authors: Mishra Anusha , Newman Eric A. 
Published: September 2010

AbstractNeuronal activity leads to arteriole dilation and increased blood flow in retinal vessels. This response, termed functional hyperemia, is diminished in the retinas of diabetic patients, possibly contributing to the development of diabetic retinopathy. The mechanism responsible for this loss is unknown. Here we show that light‐evoked arteriole dilation was reduced by 58% in a streptozotocin‐induced rat model of type 1 diabetes. Functional hyperemia is believed to be mediated by glial cells and we found that glial‐evoked vasodilation was reduced by 60% in diabetic animals. The diabetic retinas showed neither a decrease in the thickness of the retinal layers nor an increase in neuronal loss, although signs of early glial reactivity and an upregulation of inducible nitric oxide synthase (iNOS) were detected. Inhibition of iNOS restored both light‐ and glial‐evoked dilations to control levels. These findings suggest that high NO levels resulting from iNOS upregulation alters glial control of vessel diameter and may underlie the loss of functional hyperemia observed in diabetic retinopathy. Restoring functional hyperemia by iNOS inhibition may limit the progression of retinopathy in diabetic patients. © 2010 Wiley‐Liss, Inc.
Soil pore characteristics of evergreen and deciduous forests of the tropical monsoon region in Cambodia
Authors: Toriyama Jumpei , Ohta Seiichi , Araki Makoto , Kosugi Ken'ichirou , Nobuhiro Tatsuhiko , Kabeya Naoki , Shimizu Akira , Tamai Koji , Kanzaki Mamoru , Chann Sophal 
Published: September 2010

AbstractBoth evergreen and deciduous forests (Efs and Dfs) are widely distributed under similar climatic conditions in tropical monsoon regions. To clarify the hydraulic properties of the soil matrix in different forest types and their effects on soil water storage capacity, the soil pore characteristics (SPC) were investigated in Ef and Df stands in three provinces in Cambodia. Soils in the Ef group were characterized in common by large amounts of coarse pores with moderate pore size distribution and the absence of an extremely low Ks at shallow depths, compared to Df group soils. The mean available water capacity of the soil matrix (AWCsm) for all horizons of the Ef and Df group soils was 0·107 and 0·146 m3 m−3, respectively. The mean coarse pore volume of the soil matrix (CPVsm) in the Ef and Df groups was 0·231 and 0·115 m3 m−3, respectively. A water flow simulation using a lognormal distribution model for rain events in the early dry season indicated that variation in SPC resulted in a larger increase in available soil water in Ef soils than in Df soils. Further study on deeper soil layers in Ef and each soil type in Df is necessary for the deeper understanding of the environmental conditions and the hydrological modelling of each forest ecosystem. Copyright © 2010 John Wiley & Sons, Ltd.
Id3 modulates cellular localization of bHLH Ptf1‐p48 protein
Authors: Dufresne Marlène , Clerc Pascal , Dieng Madieng , Edir Anissa , Couvelard Anne , Delisle Marie‐Bernadette , Fourmy Daniel , Gigoux Véronique 
Published: September 2010

AbstractPtf1‐p48 is a pancreas‐specific bHLH transcriptional protein, which, in the normal adult pancreas, shows a restricted expression in acinar cells where it is predominantly localized in the nucleus and activates the transcription of exocrine‐specific genes. Ptf1‐p48 partners with two proteins to form the PTF1 active complex: a bHLH E‐protein and suppressor of hairless RBP‐J. Cytoplasmic mislocalization of Ptf1‐p48 has been reported in pancreatic pathologies, suggesting its contribution in the early steps of pancreatic carcinogenesis. The aim of the our work was to elucidate the mechanisms regulating Ptf1‐p48 subcellular localization. We hypothesized a role of Id proteins acting in a dominant‐negative fashion by heterodimerizing with bHLH proteins. We reproduced Ptf1‐p48 cytoplasmic mislocalization in acinar AR4‐2J cells and demonstrated that a proliferative signal elicited by gastrin leads to increases in Id3 protein expression and levels of Id3/E47 and Id3/Ptf1‐p48 interactions, and a decrease in the level of E47/Ptf1‐p48 interaction. By contrast, Id3 silencing reversed the cytoplasmic mislocalization of Ptf1‐p48 induced by gastrin. As E47 is responsible for the nuclear import of the PTF1 complex, disruption of this complex via Id3 interactions with both E47 and Ptf1‐p48 appears to induce cytoplasmic mislocalization of Ptf1‐p48. We then found that Ptf1‐p48 is either absent or mislocalized in the cytoplasm and Id3 is overexpressed in human and murine pancreatic preneoplastic lesions. Our data provide novel insight into the regulation of Ptf1‐p48 function and provide evidence that Ptf1‐p48 cytoplasmic mislocalization and Id3 overexpression are early events in pancreatic cancer progression.
Identification of p10 as a neurotoxic product generated from the proteolytic cleavage of the neuronal Cdk5 activator
Authors: Chew Jenny , Chen Minghui Jessica , Lee Alan Yiu‐Wah , Peng Zhao Feng , Chong Kevin Wai Yin , He Lisheng , Bay Boon Huat , Ng Jian Ming Jeremy , Qi Robert Z. , Cheung Nam Sang 
Published: September 2010

AbstractThe involvement of cyclin‐dependent kinase‐5 (Cdk5) and p25, the proteolytic fragment of activator p35, has long been implicated in the development of neuron‐fibrillary tangles (NFTs), a hallmark of Alzheimer's disease (AD). Findings in this area over the past decade have been highly controversial and inconclusive. Here we report unprecedented detection of endogenous p10, the smaller proteolytic fragment of the Cdk5 activator p35 in treated primary cortical neurons that underwent significant apoptosis, triggered by proteasome inhibitors MG132 and lactacystin, and protein kinase inhibitor staurosporine (STS). p10 appeared exclusively in the detergent‐resistant fraction made up of nuclear matrix, membrane‐bound organelles, insoluble membrane proteins, and cytoskeletal components. Intriguingly, transient overexpression of p10 in neural cells induced apoptotic morphologies, suggesting that p10 may play an important role in mediating neuronal cell death in neurodegenerative diseases. We demonstrated for the first time that p10‐mediated apoptosis occurred via a caspases‐independent pathway. Furthermore, as p10 may contain the myristoylation signal for p35 which is responsible for binding p35 to several intracellular components and the membrane, all in all these novel results present that the accumulation of p10 to the detergent‐insoluble fraction may be a crucial pathological event to triggering neuronal cell death. J. Cell. Biochem. 111: 1359–1366, 2010. © 2010 Wiley‐Liss, Inc.
Berberine induces autophagic cell death and mitochondrial apoptosis in liver cancer cells: The cellular mechanism
Authors: Wang Ning , Feng Yibin , Zhu Meifen , Tsang Chi‐Man , Man Kwan , Tong Yao , Tsao Sai‐Wah 
Published: September 2010

AbstractExtensive studies have revealed that berberine, a small molecule derived fromCoptidis rhizoma(Huanglian in Chinese) and many other plants, has strong anti‐tumor properties. To better understand berberine‐induced cell death and its underlying mechanisms in cancer, we examined autophagy and apoptosis in the human hepatic carcinoma cell lines HepG2 and MHCC97‐L. The results of this study indicate that berberine can induce both autophagy and apoptosis in hepatocellular carcinoma cells. Berberine‐induced cell death in human hepatic carcinoma cells was diminished in the presence of the cell death inhibitor 3‐methyladenine, or following interference with the essential autophagy gene Atg5. Mechanistic studies showed that berberine may activate mitochondrial apoptosis in HepG2 and MHCC97‐L cells by increasing Bax expression, the formation of permeable transition pores, cytochrome C release to cytosol, and subsequent activation of the caspases 3 and 9 execution pathway. Berberine may also induce autophagic cell death in HepG2 and MHCC97‐L cells through activation of Beclin‐1 and inhibition of the mTOR‐signaling pathway by suppressing the activity of Akt and up‐regulating P38 MAPK signaling. This is the first study to describe the role of Beclin‐1 activation and mTOR inhibition in berberine‐induced autophagic cell death. These results further demonstrate the potential of berberine as a therapeutic agent in the emerging list of cancer therapies with novel mechanisms. J. Cell. Biochem. 111: 1426–1436, 2010. © 2010 Wiley‐Liss, Inc.
Morphological and molecular pathology of CCL4‐induced hepatic fibrosis in connexin43‐deficient mice
Authors: Cogliati Bruno , Da silva Tereza Cristina , Aloia Thiago Pinheiro Arrais , Chaible Lucas Martins , Real‐Lima Mirela Aline , Sanches Daniel Soares , Matsuzaki Patrícia , Hernandez‐Blazquez Francisco Javier , Dagli Maria Lúcia Zaidan 
Published: September 2010

AbstractGap junction channels, formed by connexins (Cx), are involved in the maintenance of tissue homeostasis, cell growth, differentiation, and development. Several studies have shown that Cx43 is involved in the control of wound healing in dermal tissue. However, it remains unknown whether Cx43 plays a role in the control of liver fibrogenesis. Our study investigated the roles of Cx43 heterologous deletion on carbon tetrachloride (CCl4)‐induced hepatic fibrosis in mice. We administered CCl4 to both Cx43‐deficient (Cx43+/−) and wild‐type mice and examined hepatocellular injury and collagen deposition by histological and ultrastructural analyses. Serum biochemical analysis was performed to quantify liver injury. Hepatocyte proliferation was analyzed immunohistochemically. Protein and messenger RNA (mRNA) expression of liver connexins were evaluated using immunohistochemistry as well as immunoblotting analysis and quantitative real‐time PCR. We demonstrated that Cx43+/− mice developed excessive liver fibrosis compared with wild‐type mice after CCl4‐induced chronic hepatic injury, with thick and irregular collagen fibers. Histopathological evaluation showed that Cx43+/− mice present less necroinflammatory lesions in liver parenchyma and consequent reduction of serum aminotransferase activity. Hepatocyte cell proliferation was reduced in Cx43+/− mice. There was no difference in Cx32 and Cx26 protein or mRNA expression in fibrotic mice. Protein expression of Cx43 increased in CCl4‐treated mice, although with aberrant protein location on cytoplasm of perisinusoidal cells. Our results demonstrate that Cx43 plays an important role in the control and regulation of hepatic fibrogenesis. Microsc. Res. Tech., 2011. © 2010 Wiley‐Liss, Inc.
Hip screw migration testing: First results for hip screws and helical blades utilizing a new oscillating test method
Authors: Born Christopher T. , Karich Bernhard , Bauer Christoph , von Oldenburg Geert , Augat Peter 
Published: September 2010

AbstractDespite continued improvement in the methods and devices used to treat intertrochanteric fractures, there remains an unacceptable amount of failures. The cut‐out rate for hip screws has been recorded up to 8.3%. To evaluate the migration of different implants under physiological loads, a multiplanar biomechanical test method for hip screws was developed, the first to incorporate a simulation of the human gait cycle by an oscillating flexion/extension movement of the test device. The new method was used to compare different hip screw and blade designs with respect to their directional migration resistance. The test method generated failure modes that were consistent with those observed clinically. Under cyclic loading, the hip screws migrated predominantly in a cephalad direction. In contrast, the helical blades exhibited a distinct migration in their axial direction. The Gamma3 hip screw design showed a significantly higher migration resistance compared with other screw and helical blade designs. The results demonstrate the ability of hip screws to significantly reduce axial migration and prevent cut‐out under simulated walking loads. Further, the new multiplanar test method creates a physiological environment that can be used to optimize designs for intertrochanteric fracture fixation. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:760–766, 2011
Block method of human temporal bone removal: A technical modification to permit rapid removal
Authors: Walvekar Rohan R. , Harless Lucas D. , Loehn Bridget C. , William Swartz  
Published: September 2010

AbstractObjectives/Hypothesis:To describe a technical modification to the block method (BM) of harvesting human cadaveric temporal bones for otolaryngology resident education and training.Study Design:Human cadaveric study.Methods:Human cadavers previously dissected by medical students in a professional health science program were identified as potential candidate specimens for temporal bone removal. Cadaveric heads were prepared for temporal bone harvesting by excising the calvarium and brain via standard techniques. A reciprocating saw was used to make four bone cuts to harvest two temporal bone specimens.Results:Temporal bone specimens could be harvested using only four bone cuts to release both temporal bones from one human cadaver as opposed to four bone cuts for a single temporal bone per the traditional BM. All temporal bones were inspected and found to have all the anatomical landmarks necessary for resident education and training intact.Conclusions:The modified BM for temporal bone removal is a rapid, efficient, and reproducible method of harvesting two complete and intact temporal bones per cadaver with fewer bone cuts as compared to the traditional BM. Laryngoscope, 2010
Effect of eradication of Helicobacter pylori in children with chronic immune thrombocytopenia: A prospective, controlled, multicenter study
Authors: Russo Giovanna , Miraglia Vito , Branciforte Francesca , Matarese Sofia Maria Rosaria , Zecca Marco , Bisogno Gianni , Parodi Emilia , Amendola Giovanni , Giordano Paola , Jankovic Momcilo , Corti Annalisa , Nardi Margherita , Farruggia Piero , Battisti Laura , Baronci Carlo , Palazzi Giovanni , Tucci Fabio , Ceppi Stefania , Nobili Bruno , Ramenghi Ugo , De Mattia Domenico , Notarangelo Lucia ,   the AIEOP‐ITP Study Group
Published: September 2010

AbstractBackgroundThe eradication of Helicobacter pylori has been associated with remission of immune thrombocytopenia (ITP) in approximately half of eradicated patients. Data on children are limited to small case series.ProcedureChildren from 16 centers in Italy, who were less than 18 years of age and diagnosed with chronic ITP (cITP), were screened for H. pylori infection. Positive patients underwent standard triple therapy with amoxicillin, clarithromycin, and omeprazole. The eradication response was defined as follows: complete response, platelet (PLT) count ≥150 × 109/L; partial response, PLT count of at least 50 × 109/L; no response, PLT count <50 × 109/L.ResultsOf 244 screened patients, 50 (20%) had H. pylori infection, 37 of which received eradication therapy and completed follow‐up. Eradication was successful in 33/37 patients (89%). PLT recovery was demonstrated in 13/33 patients after eradication (39%), whereas spontaneous remission was observed in 17/166 (10%) H. pylori‐negative patients (P < 0.005). Responders more often required second line eradication (9/13), whereas a second cycle was required in 3/20 non‐responders (P < 0.005).ConclusionsAmong the large cohort of patients, those who underwent successful H. pylori eradication showed a significantly higher PLT response. Therefore, it may be appropriate to look for H. pylori and eventually eradicate it in children with cITP. Pediatr Blood Cancer 2011;56:273–278. © 2010 Wiley‐Liss, Inc.