bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Impact of Communal‐Mastery Versus Self‐Mastery on Emotional Outcomes During Stressful Conditions: A Prospective Study of Native American Women
Authors: Hobfoll Stevan E. , Jackson Anita , Hobfoll Ivonne , Pierce Charles A. , Young Sara 
Published: March 2003

AbstractPast research has examined the stress resiliency of individuals high in sense of personal‐mastery. However, it has been theorized that within more collectivist cultures, a sense of shared efficacy, which we call communal‐mastery, may be more central to people's resiliency in the face of challenging life circumstances. We compared the impact of sense of self‐mastery (i.e., “I am the key to my success”) to that of communal‐mastery (i.e., “I am successful by virtue of my social attachments”) in a prospective study among a group of rural 103 Native American women residing on Indian Reservations in Montana. We found that women high in communal‐mastery experienced less increase in depressive mood and anger, especially when faced with high stress circumstances, than women who were low in communal‐mastery. In addition, the beneficial impact of communal‐mastery was found to be more effective than self‐mastery for these women.
Mental Health and Welfare Transitions: Depression and Alcohol Abuse in AFDC Women
Authors: Dooley David , Prause JoAnn 
Published: March 2003

AbstractFrom a selection perspective, does prior dysfunction select women into welfare or serve as a barrier to leaving welfare? From a social causation perspective, does entering or exiting welfare lead to changes in well being? These questions were analyzed in panel data for over 3,600 women drawn from the National Longitudinal Survey of Youth for the period 1992–94. Welfare is associated with both depression and alcohol consumption cross‐sectionally. This link appears to derive in small part from selection into welfare by depression (in interaction with marital status), but depression and alcohol abuse did not operate as barriers to leaving welfare. Entering welfare was clearly associated with increased depression and alcohol consumption, but confidence in an apparent beneficial effect on alcohol symptoms of leaving welfare for employment was limited by small sample sizes. These findings are located in the context of the 1996‐welfare reform and the recent economic expansion. One implication is that community psychology should consider welfare entry as a risk factor similar to adverse employment changes such as job loss.
Sensing issues related to the clinical use of implantable loop recorders
Authors: Chrysostomakis S. I. , Klapsinos N. C. , Simantirakis E. N. , Marketou M. E. , Kambouraki D. C. , Vardas P. E. 
Published: March 2003

Abstract

Aims
The newer insertable loop recorder device (Reveal Plus 9526, Medtronic Inc, Minneapolis MN, U.S.A.) is equipped with auto-activation capabilities. In this study we investigated whether the new device encounters sensitivity problems in the form of oversensing or undersensing. We also tested whether body position changes influence the sensed electrogram's amplitude, therefore affecting the device's autosensing ability.

Methods and results
We enrolled 32 patients aged 58·1±11·7 years with a loop recorder implanted either in the left parasternal or in the heart's apex area, to investigate undiagnosed syncopal episodes after initial assessment.
During the follow-up period (5·7±2·7 months), that began 6 months after the device implantation, we analysed 284 auto-recorded episodes (103 undersensed and 181 correctly sensed). No oversensing episodes were recorded.
The recorded QRS amplitude in five different body positions: supine, left and right lateral, sitting and standing was measured. No statistically significant changes were observed in the different postures.
Even when patients were divided into subgroups according to implant site or the occurrence of undersensing episodes, no significant inter- or intra-group differences of the sensed electrogram were observed.

Conclusion
Undoubtedly this device is the current gold standard for the diagnosis of unexplained syncope. In the population we studied though, the device faced undersensing problems. Consequently, the device should be equipped with more advanced software for QRS morphology recognition, to improve the diagnostic accuracy of the recorder.
Transplantation of Monocyte CC-Chemokine Receptor 2–Deficient Bone Marrow Into ApoE3–Leiden Mice Inhibits Atherogenesis
Authors: Guo Jian , Van Eck Miranda , Twisk Jaap , Maeda Nobuyo , Benson G. Martin , Groot Pieter H.E. , Van Berkel Theo J.C. 
Published: March 2003

Objective—To determine the role of leukocyte CC-chemokine receptor 2 (CCR2) in the early development of atherosclerosisMethods and Results—Bone marrow cells harvested from CCR2 (−/−) and CCR2 (+/+) mice were transplanted into ApoE3–Leiden mice, a mouse strain susceptible for diet-induced atherosclerosis. Eight weeks after bone marrow transplantation, the diet of regular chow was switched to a high-cholesterol diet (1% cholesterol, 15% fat, 0.5% cholate) for another 8 weeks to induce atherosclerosis. No significant differences in serum cholesterol and triglyceride levels were observed between the CCR2 (+/+) → ApoE3–Leiden and CCR2 (−/−) → ApoE3–Leiden mice. However, the mean cross-sectional aortic root lesion area of CCR2 (−/−) → ApoE3–Leiden mice was only 2.94±1.94×104μm2compared with 20.94±12.71×104μm2, for CCR2 (+/+) → ApoE3–Leiden mice. Thus, the absence of CCR2 on leukocytes induces an 86% reduction of aortic lesion area as compared with controls (n=10,P<0.01).Conclusion—These results provide direct evidence that CCR2 expressed by leukocytes plays a critical role in the initiation of early atherosclerosis and that pharmacological intervention in CCR2 function represents an attractive target to inhibit atherogenesis.
Novel protein RGPR‐p117: The gene expression in physiologic state and the binding activity to regucalcin gene promoter region in rat liver
Authors: Yamaguchi Masayoshi , Misawa Hiroyuki , Ma Zhong Jie 
Published: March 2003

AbstractThe binding activity of a novel regucalcin gene promoter region‐related protein (RGPR‐p117) to the TTGGC sequence of the rat regucalcin gene promoter region was investigated. The expression of RGPR‐p117 mRNA was seen in the liver tissues of male and female rats. The sexual difference of this expression was not found. Liver RGPR‐p117 mRNA expression was not changed with increasing age (1–50 weeks old), and its expression was not altered by fasting or refeeding. Nuclear factor I‐A1 (NF1‐A1) has been identified to be a transcription factor in stimulating the rat regucalcin gene promoter activity (Misawa and Yamaguchi [2002a] J Cell Biochem 84:795–802]. Recombinant nuclear factor I‐A1 (NF1‐A1) and RGPR‐p117 proteins were used gel mobility shift assay. RGPR‐p117 could not bind to TTGGC motif of the sequence between −525 and −504, which has been defined as a functional promoter element II‐b. NF1‐A1 was specifically bound to the II‐b oligonucleotide. Moreover, RGPR‐p117 was not bound to the II‐b oligonucleotide in the presence of NF1‐A1 or rat liver nuclear protein. The binding of NF1‐A1 to the II‐b oligonucleotide was not altered in the presence of RGPR‐p117. This study demonstrates that RGPR‐p117 mRNA, is expressed stably for physiologic change in rat liver, and that recombinant the protein does not directly bind to the TTGGC motif in rat regucalcin gene promoter. J. Cell. Biochem. 88: 1092–1100, 2003. © 2003 Wiley‐Liss, Inc.
Guidelines for Writing Letters to Patients
Authors: Baker Diane L. , Eash Timothy , Schuette Jane L. , Uhlmann Wendy R. 
Published: March 2003

AbstractPatient letters provide a permanent record of the genetic counseling that was provided and are unique in medical care; rarely do other health care providers send summaries written specifically to their patients and families. We surveyed genetic counseling training program directors and found that while the acquisition of patient letter‐writing skills was considered important, there were no specific guidelines made available to students. To develop letter‐writing guidelines, we evaluated patient letters, reviewed references on professional correspondence, surveyed the medical literature, and worked with a writing consultant. The guidelines we subsequently developed and present here include a format for writing patient letters, suggestions on presenting medical information in understandable terms, and wording considerations. These patient letter‐writing guidelines are intended to serve as a guide for teaching students this important skill and as a resource for practicing health care professionals.
Identification of two novel mutations inOCTN2from two Saudi patients with systemic carnitine deficiency
Authors: Rahbeeni Z. , Vaz F. M. , Al‐Hussein K. , Bucknall M. P. , Ruiter J. , Wanders R. J. , Rashed M. S. 
Published: March 2003

AbstractSystemic carnitine deficiency (CDSP) (McKusick 212140) is a rare autosomal recessive disease caused by defective plasma membrane uptake of carnitine. The disease is characterized by Reye syndrome, progressive cardiomyopathy, skeletal myopathy, hypoglycaemia and hyperammonaemia. CDSP is a treatable disease provided an early diagnosis is made and prompt treatment with L‐carnitine is initiated. The biochemical diagnosis of the disease is based on the findings of very low plasma and tissue carnitine concentrations. Recently, a human gene,SLC22A5, encoding a sodium‐dependent high‐affinity carnitine transporterOCTN2was cloned from human kidney and shown to be mutated in systemic carnitine deficiency. Here we report two unrelated Saudi CDSP patients who were detected by tandem mass spectrometric analysis (MS/MS) of blood spots. Studies in skin fibroblasts from the two patients showed a severely reduced carnitine uptake. Subsequent molecular studies led to the identification of two novel missense mutations in theOCTN2gene in the two patients.
Reversible fulminant lactic acidosis and liver failure in an infant with hepatic cytochrome‐c oxidase deficiency
Authors: Lev D. , Gilad E. , Leshinsky‐Silver E. , Houri S. , Levine A. , Saada A. , Lerman‐Sagie T. 
Published: March 2003

AbstractCytochrome‐c oxidase (COX) is the most common respiratory chain complex involved in liver failure, either as a single enzyme deficiency or as part of multiple enzyme deficiencies. We describe an infant who presented with fulminant lactic acidosis in the neonatal period. The lactic acidosis resolved spontaneously but liver and pancreatic insufficiency ensued. Isolated cytochrome‐c oxidase deficiency was found in liver but not in muscle and fibroblasts. mtDNA rearrangements or depletion were ruled out. By the age of one year, liver and pancreatic functions have normalized completely and neurodevelopment is normal.
The Structural Basis for the Susceptibility of Gangliosides to Enzymatic Degradation
Authors: Sonnino Sandro , Brocca Paola , Acquotti Domenico , Bernardi Anna , Raimondi Laura , Kiso Makoto , Ishida Hideharu , Li Su-Chen , Li Yu-Teh 
Published: March 2003

The conformational properties of GM2, GalNacβ-4(Neu5Acα-3) Galβ-4Glcβ-1Cer have been compared to those of 6′-GM2, in which the linkage between the GalNAc and Gal was altered from GalNacβ-4Galβ- to GalNacβ-6Galβ-, and to those of GD1a, Neu5Acα-3Galβ-3GalNAcβ-4(Neu5Acα-3)Galβ-4Glcβ-1Cer, and GalNAc-GD1a.
Our results revealed that unlike the compact and rigid oligosaccharide head group found in GM2, where the Neu5Ac and the GalNAc residues interact, the sugar chain of 6′-GM2 is in an open spatial arrangement, with the Neu5Ac no longer interacting with GalNAc, freely accessible to external interactions.
The structure of GD1a can be regarded as that of GM2 with an extension of the terminal Neu5Acα-3Galβ-disaccharide. The inner portion of GD1a is that of GM2 comprising the very rigid GalNAc-[Neu5Ac-]Gal trisaccharide. The terminal Neu5Ac-Gal linkage is flexible and fluctuates between two limiting conformations. In GalNAc-GD1a the outer sialic acid gains conformational rigidity due to the presence of the outer GalNAc in position 4 of galactose. This ganglioside has two ‘core’ GalNAc-[Neu5Ac-]Gal trisaccharide linked in tandem.
Increased Superoxide Production in Coronary Arteries in Hyperhomocysteinemia
Authors: Ungvari Zoltan , Csiszar Anna , Edwards John G. , Kaminski Pawel M. , Wolin Michael S. , Kaley Gabor , Koller Akos 
Published: March 2003

Objective—In coronary arteries, hyperhomocysteinemia (HHcy, a known risk factor for coronary heart disease) impairs flow-induced dilations, which can be reversed by superoxide dismutase (SOD). To evidence increased O2.−generation and elucidate its source, we characterized changes in activity (lucigenin chemiluminescence, hydroethidine staining) and expression of arterial pro- and antioxidant systems (Western blotting, immunohistochemistry, cDNA microarray, reverse-transcription polymerase chain reaction) in the coronary arteries of rats by using methionine diet-induced HHcy.Methods and Results—The increased generation of O2.−by HHcy coronary arteries was inhibited by SOD, diphenyleneiodonium, apocynin, and apocynin plus amino guanidine but was unaffected by allopurinol and rotenone. Also, diphenyleneiodonium-sensitive NADPH-driven O2.−generation was increased in HHcy vessels. In HHcy arteries expression of the smooth muscle-confined NAD(P)H oxidase subunit nox1 and that of iNOS was increased. Expression of p67phox, p22phox, and p47phoxsubunits and that of endothelial nitric oxide synthase, Cu,Zn-SOD, Mn-SOD, extracellular SOD (mRNA), and xanthine oxidase was unchanged. Microarray analysis showed increased expression of tumor necrosis factor (TNF)-α (confirmed by reverse-transcription polymerase chain reaction, Western blotting, and immunohistochemistry) that was localized in smooth muscle. In vitro incubation (18 hours) of HHcy arteries with anti-TNF-α antibody decreased O2.−production, whereas incubation of control vessels with TNF-α increased O2.−generation and nox1 expression.Conclusions—In coronary arteries, HHcy increases TNF-α expression, which enhances oxidative stress through upregulating a nox1-based NAD(P)H oxidase and inducible nitric oxide synthase. Thus, TNF-α induces a proinflammatory vascular phenotype in HHcy that potentially contributes to the development of coronary atherosclerosis.
Regulation of hematopoietic‐specific G‐protein Gα15 and Gα16 by protein kinase C
Authors: Gu Jennifer L. , Lu Wei , Xia Chunzhi , Wu Xiushan , Liu Mingyao 
Published: March 2003

AbstractHeterotrimeric G proteins mediate cell growth and differentiation by coupling cell surface receptors to intracellular effector enzymes. The G‐protein α subunit, Gα16, and its murine homologue Gα15, are expressed specifically in hematopoietic cells and their expression is highly regulated during differentiation of normal and leukemic cells. In this study, we examined the phosphorylation of Gα15/Gα16 and its role in receptor and effector coupling. We observed a PMA‐stimulated intact cell phosphorylation of Gα15 in COS7 cells transfected with Gα15 and protein kinase Cα (PKCα), and phosphorylation of endogenous Gα16 in HL60 cells. We also showed that peptides derived from the two G‐proteins were phosphorylated in vitro using purified brain PKC. Furthermore, we identified the putative phosphorylation site and showed that mutation or deletion of this PKC phosphorylation site inhibited phospholipase C (PLC) activation. The behavior of double mutants with the constitutively active G‐protein mutation (QL‐mutant) and mutation in the putative phosphorylation site suggests that the phosphorylation site of Gα15/16 is essential for receptor‐coupled activation of PLC, but not for direct interaction of the G‐protein with PLC‐β. J. Cell. Biochem. 88: 1101–1111, 2003. © 2003 Wiley‐Liss, Inc.
Vascular smooth muscle cells efficiently activate a new proteinase cascade involving plasminogen and fibronectin
Authors: Houard Xavier , Monnot Catherine , Dive Vincent , Corvol Pierre , Pagano Maurice 
Published: March 2003

AbstractThe plasminogen/plasmin system is involved in vascular wall remodeling after injury, through extracellular matrix (ECM) degradation and proteinase activation. Vascular smooth muscle cells (VSMCs) synthesize various components of the plasminogen/plasmin system. We investigated the conversion of plasminogen into plasmin in primary cultured rat VSMCs. VSMCs efficiently converted exogenous plasminogen into plasmin in a time‐ and dose‐dependent manner. We measured plasmin activity by monitoring the hydrolysis of Tosyl‐G‐P‐R‐Mca, a fluorogenic substrate of plasmin. Cell‐mediated plasmin activation was associated with the degradation of ECM, as revealed by fibronectin proteolysis. Plasmin also activated a proteinase able to hydrolyze Mca‐P‐L‐G‐L‐Dpa‐A‐R‐NH2, a fluorogenic substrate of matrix metalloproteinases (MMPs). However, this proteinase was not inhibited by an MMP inhibitor. Furthermore, this proteinase displayed similar biochemical and pharmacological properties to fibronectin‐proteinase, a recently identified zinc‐dependent metalloproteinase located in the gelatin‐binding domain of fibronectin. These results show that VSMCs convert exogenous plasminogen into plasmin in their pericellular environment. By hydrolyzing matrix protein plasmin activates a latent metalloproteinase that differs from MMP, fibronectin‐proteinase. This metalloproteinase may participate to vascular wall remodeling, in concert with other proteinases. J. Cell. Biochem. 88: 1188–1201, 2003. © 2003 Wiley‐Liss, Inc.
Ref‐1 protein enhances the IL‐2‐stimulated telomerase activity
Authors: Xu Weijing , Yan Mingda , Sun Lanying , Zheng Zhongcheng , Liu Xinyuan 
Published: March 2003

AbstractTelomerase is an important ribonucleoprotein enzyme involved in cellular proliferation and senescence. Activation of telomerase has been detected in a vast majority of human cancer cells. In this article, we demonstrated that Interleukin‐2 (IL‐2) which is the pivotal cytokine in the immune system could stimulate the activity of telomerase in the cultured BA/F3β cells. It was also found that the level of IL‐2‐induced telomerase activity was decreased by the treatment with chemical oxidant in vitro. Since IL‐2 stimulation produces a oxidative shift of the intracellular environment, the activation and maintenance of telomerase in this oxidative circumstance requires particular protection. Here we proved the redox factor‐1 (Ref‐1) protein was involved in this process. The addition of GST–Ref‐1 protein increased the level of IL‐2‐induced telomerase activity in the TRAP assay, while elimination of the endogenous Ref‐1 protein by immunodepletion decreased it. Consistent with these in vitro results, IL‐2‐induced telomerase activity could be enhanced by transient overexpression of Ref‐1 protein in BA/F3β cells. Taken together, these findings proved that Ref‐1 protein benefits the activation of telomerase activity in the oxidative microenvironment of the BA/F3β cells stimulated by IL‐2. J. Cell. Biochem. 88: 1120–1128, 2003. © 2003 Wiley‐Liss, Inc.
TE2 and TE1 sub‐elements of the testis‐specific histone H1t promoter are functionally different
Authors: Wilkerson Donald C. , Wolfe Steven A. , Grimes Sidney R. 
Published: March 2003

AbstractThe testis‐specific linker histone H1t gene is transcribed exclusively in pachytene primary spermatocytes. Tissue specific expression of the gene is mediated in part by transcriptional factors that bind elements located within the proximal and distal promoter. A 40 bp promoter element, designated H1t/TE, that is located within the proximal promoter between the CCAAT‐box and AC‐box, is known to be essential for H1t gene transcription in transgenic animals. In the present study, we show by SDS–PAGE analysis of UV crosslinked protein and DNA and by electrophoretic mobility shift assays (EMSA) of testis nuclear proteins separated on a non‐denaturing glycerol gradient that the TE1 sub‐element is bound by a protein complex. Mutation of TE1 leads to a drop in H1t promoter activity in germinal GC‐2spd cells as well as in nongerminal Leydig, NIH3T3, and C127I cell lines. Although TE1 and TE2 sub‐elements have similar sequences, mutation of the TE2 sub‐element causes an increase in promoter activity in C127I and Leydig cells. The rat TE1 but not TE2 contains a CpG dinucleotide and this cytosine is methylated in liver but not in primary spermatocytes. Methylation of the cytosine at this site almost eliminates nuclear protein binding. Thus, there are significant functional differences in the TE2 and TE1 sub‐elements of the H1t promoter with TE1 serving as a transcriptional activator binding site and TE2 serving as a repressor binding site in some cell lines. J. Cell. Biochem. 88: 1177–1187, 2003. © 2003 Wiley‐Liss, Inc.
Characterization of PTH/PTHrP receptor in rat duodenum: Effects of ageing
Authors: Gentili Claudia , Morelli Susana , de Boland Ana Russo 
Published: March 2003

AbstractIn rat enterocytes, signaling through the paratyroid hormone (PTH)/PTH‐related peptide receptor type 1(PTHR1) includes stimulation of adenylyl cyclase, increases of intracellular calcium, activation of phospholipase C, and the MAP kinase pathway, mechanisms that suffer alterations with ageing. The purpose of this study was to evaluate whether an alteration at the level of the PTH receptor (PTHR1) is the basis for impaired PTH signaling in aged rat enterocytes. Western Blot analysis with a specific monoclonal anti‐PTHR1 antibody revealed that a 85 kDa PTH binding component, the size expected for the mature PTH/PTHrP receptor, localizes in the basolateral (BLM) and brush border (BBM) membranes of the enterocyte, being the protein expression about 7‐fold higher in the BLM. Two other bands of 105 kDa (corresponding to highly glycosylated, incompletely processed receptor form) and 65 kDa (proteolytic fragment) were also seen. BLM PTHR1 protein expression significantly decreases with ageing, while no substantial decrease was observed in the BBM from old rats. PTHR1 immunoreactivity was also present in the nucleus where PTHR1 protein levels were similar in enterocytes from young and aged rats. Immunohistochemical analysis of rat duodenal sections showed localization of PTHR1 in epithelial cells all along the villus with intense staining of BBM, BLM, and cytoplasm. The nuclei of these cells were reactive to the PTHR1 antiserum, but not all cells showed the same nuclear staining. The receptor was also detected in the mucosae lamina propria cells, but was absent in globets cells from epithelia. In aged rats, PTHR1 immunoreactivity was diffused in both membranes and cytoplasm and again, PTH receptor expression was lower than in young animals, while the cell nuclei showed a similar staining pattern than in young rats. Ligand binding to PTHR1 was performed in purified BLM. rPTH(1‐34) displaced [I125]PTH(1‐34) binding to PTHR1 in a concentration‐dependent fashion. In both, aged (24 months) and young (3 months) rats, binding of [I125]PTH was characterized by a single class of high‐affinity binding sites. The affinity of the receptor for PTH was not affected by age. The maximum number of specific PTHR1 binding sites was decreased by 30% in old animals. The results of this study suggest that age‐related declines in PTH regulation of signal transduction pathways in rat enterocytes may be due, in part, to the loss of hormone receptors. J. Cell. Biochem. 88: 1157–1167, 2003. © 2003 Wiley‐Liss, Inc.