bluuebunny/crossref_metadata_2025_split huggingface dataset:
The IL1A (−889) gene polymorphism is associated with chronic periodontal disease in a sample of Brazilian individuals
Authors: Moreira P. R. , Costa J. E. , Gomez R. S. , Gollob K. J. , Dutra W. O. 
Published: November 2006

Background and Objective:  It has been proposed that genotypes reflective of polymorphisms in cytokine genes can predispose individuals to disease by enhancing inflammatory processes. The C/T polymorphism at position −889 of the IL1A gene influences interleukin‐1α expression, with the T allele inducing higher expression. The aim of this study was to evaluate the association of the IL1A (−889) gene polymorphism in Brazilian individuals with different clinical forms of periodontitis and severity of disease.Material and Methods:  DNA was obtained from oral swabs of 163 Brazilian individuals and was amplified using the polymerase chain reaction (PCR). Products were submitted to digestion and were analyzed by electrophoresis to distinguish the C and T alleles.Results:  A significant difference in the genotype distribution was observed when comparing the chronic periodontitis group with the control group, evaluating only nonsmokers (chi‐squared analysis = 9.91; p = 0.007), as well as when smokers were included (chi‐squared analysis = 6.36; p = 0.04). Moreover, we observed a higher incidence of the T allele in the chronic periodontitis group (37.8%) when compared with the control group (18.4%) in nonsmokers (p = 0.006, odds ratio = 2.69, confidence interval = 1.27–5.68) and also when smokers were included (p = 0.03, odds ratio = 1.87, confidence interval = 0.98–3.56). No statistical difference was observed when the aggressive periodontitis group was compared with the control group. With regard to severity of disease, no statistical difference was observed.Conclusion:  These data show an association of the IL1A (−889) polymorphism with chronic periodontitis in Brazilian individuals.
Risk factors for new episodes of sick leave due to neck or back pain in a working population. A prospective study with an 18-month and a three-year follow-up
Authors: Bergström Gunnar , Bodin Lennart , Bertilsson Helena , Jensen Irene B 
Published: November 2006

Objectives:To identify risk factors for new episodes of sick leave due to neck or back pain.Methods:This prospective study comprised an industrial population of 2187 employees who were followed up at 18 months and 3 years after a comprehensive baseline measurement. The potential risk factors comprised physical and psychosocial work factors, health-related and pain-related characteristics and lifestyle and demographic factors. The response rate at both follow-ups was close to 73%.Results:At the 18-month follow-up, 151 participants reported at least one episode of sick-listing due to neck or back pain during the previous year. Risk factors assessed at baseline for sick leave due to neck or back pain at the follow-up were blue-collar work, back pain one or several times during the previous year, 1–99 days of cumulative sickness absence during the previous year (all causes except neck or back pain), uncertainty of one’s own working ability in 2 years’ time and the experience of few positive challenges at work. After 3 years, 127 participants reported at least one episode of sick leave due to back or neck pain during the year previous to follow-up. The risk factors for this pain-related sick leave were blue-collar work, several earlier episodes of neck pain, no everyday physical activities during leisure time (cleaning, gardening and so on), lower physical functioning and, for blue-collar workers separately, repetitive work procedures.Conclusion:The most consistent risk factors for new episodes of sick leave due to neck or back pain found during both the follow-ups were blue-collar work and several earlier episodes of neck or back pain assessed at baseline. Preventive efforts to decrease sick leave due to neck or back pain may include measures to increase the occurrence of positive challenges at work and to minimise repetitive work procedures. An evidence-based secondary prevention of neck and back pain including advice to stay active is also warranted.
Occupational asthma: an assessment of diagnostic agreement between physicians
Authors: Fishwick David , Bradshaw Lisa , Henson Mandy , Stenton Chris , Hendrick David , Burge Sherwood , Niven Rob , Warburton Chris , Rogers Trevor , Rawbone Roger , Cullinan Paul , Barber Chris , Pickering Tony , Williams Nerys , Ayres Jon , Curran Andrew D 
Published: November 2006

Objectives:To investigate the levels of agreement between expert respiratory physicians when making a diagnosis of occupational asthma.Methods:19 cases of possible occupational asthma were identified as part of a larger national observational cohort. A case summary for each case was then circulated to 12 physicians, asking for a percentage likelihood, from the supplied information, that this case represented occupational asthma. The resulting probabilities were then compared between physicians using Spearman’s rank correlation and Cohen’s κ coefficients.Results:Agreement between the 12 physicians for all 19 cases was generally good as assessed by Spearman’s rank correlation. For all 66 physician–physician interactions, 45 were found to correlate significantly at the 5% level. The agreement assessed by κ analysis was more variable, with a median κ value of 0.26, (range –0.2 to +0.76), although 7 of the physicians agreed significantly (p<0.05) with ⩾5 of their colleagues. Only in one case did the responses for probability of occupational asthma all exceed the “on balance” 50% threshold, although 12 of the 19 cases had an interquartile range of probabilities not including 50%, implying “on balance” agreement. The median probability values for each physician (all assessing the identical 19 cases) varied from 20% to 70%. Factors associated with a high probability rating were the presence of a positive serial peak expiratory flow Occupation Asthma SYStem (OASYS)-2 chart, and both the presence of bronchial hyper-reactivity and significant change in reactivity between periods of work and rest.Conclusions:Despite the importance of the diagnosis of occupational asthma and reasonable physician agreement, certain variations in diagnostic assessment were seen between UK expert centres when assessing paper cases of possible occupational asthma. Although this may in part reflect the absence of a normal clinical consultation, a more unified national approach to these patients is required.
Hypertensive Intracerebral Hemorrhage in Young People
Authors: Ruiz-Sandoval José L. , Romero-Vargas Samuel , Chiquete Erwin , Padilla-Martínez Juan J. , Villarreal-Careaga Jorge , Cantú Carlos , Arauz Antonio , Barinagarrementería Fernando 
Published: November 2006

Background and Purpose—Hypertensive intracerebral hemorrhage (ICH) in young people has been the object of only succinct analyses. Therefore, it is unclear whether extrapolation of the information obtained from older patients is also valid for the young. Here we describe young persons with hypertensive ICH and compare them with their older counterparts to determine whether age-related clinical differences exist.Methods—From 1988 to 2004, we studied 35 consecutive young patients with ICH (60% men; mean age, 33 years; range, 15 to 40 years) for whom the etiology of the brain hemorrhage was hypertension. For clinical comparisons, sex-matched persons with hypertensive ICH, aged >40 years, were randomly selected by a factor of 3:1 (n=105).Results—Essential hypertension was present in 26 (74%) young patients and secondary hypertension in 9 (26%), with renovascular hypertension being the most common cause (n=5, 55%). Compared with older patients, the young had higher blood pressures, smaller hemorrhage volumes, lower rates of ventricular extensions (for all,P<0.05), and different distribution pattern of ICHs (P=0.05), without cerebellar and lobar locations. Thirty-day mortality was markedly lower in the young than in older persons (P=0.001), nevertheless at the expense of more incapacitating disabilities.Conclusions—Young people presenting with hypertensive ICH differ in clinical characteristics and have a different prognosis when compared with their older counterparts. These findings suggest underlying age-related differences in disease pathogenesis.
Increased mitochondrial mass characterizes the survival defect of HIV-specific CD8+ T cells
Authors: Petrovas Constantinos , Mueller Yvonne M. , Dimitriou Ioannis D. , Altork Susan R. , Banerjee Anupam , Sklar Peter , Mounzer Karam C. , Altman John D. , Katsikis Peter D. 
Published: November 2006

AbstractWhat governs the increased apoptosis sensitivity of HIV-specific CD8+ T cells is poorly understood. Here, we examined the involvement of mitochondria in this apoptosis. Remarkably higher mitochondrial mass (MM) was found in HIV-specific compared with CMV-specific CD8+ T cells from HIV+ patients and this could not be attributed to their different differentiation status. MMHigh phenotype characterized those CD8+ T cells from HIV+ patients that are sensitive to spontaneous and CD95/Fas-induced apoptosis. CD38 expression did not correlate with high MM, whereas Bcl-2 levels were significantly reduced in both CD38+ and CD38− HIV-specific CD8+ T cells. Although CD38+ HIV-specific CD8+ T cells were more susceptible to apoptosis, CD38 expression does not explain on its own the selective apoptosis sensitivity of HIV-specific CD8+ T cells, as CD38− HIV-specific CD8+ T cells were more apoptotic than CD38+ CMV-specific ones. Proapoptotic HIV-specific CD8+ T cells were CD38+Bcl-2LowMMHigh. Copolarization of mitochondria with CD95/Fas capping, very early in CD95/Fas-induced apoptosis of HIV-specific CD8+ T cells, suggests that mitochondria act as an amplification step for this apoptosis. Thus, an extensive mitochondrial network contributes to apoptosis sensitivity of CD8+ T cells and, when this occurs together with reduced levels of Bcl-2 and chronic activation, determines the proapoptotic state of HIV-specific CD8+ T cells.
SDX-308, a nonsteroidal anti-inflammatory agent, inhibits NF-κB activity, resulting in strong inhibition of osteoclast formation/activity and multiple myeloma cell growth
Authors: Feng Rentian , Anderson Gülsüm , Xiao Guozhi , Elliott Gary , Leoni Lorenzo , Mapara Markus Y. , Roodman G. David , Lentzsch Suzanne 
Published: November 2006

AbstractMultiple myeloma is characterized by increased osteoclast activity that results in bone destruction and lytic lesions. With the prolonged overall patient survival achieved by new treatment modalities, additional drugs are required to inhibit bone destruction. We focused on a novel and more potent structural analog of the nonsteroidal anti-inflammatory drug etodolac, known as SDX-308, and its effects on osteoclastogenesis and multiple myeloma cells. SDX-101 is another structural analog of etodolac that is already used in clinical trials for the treatment of B-cell chronic lymphocytic leukemia (B-CLL). Compared with SDX-101, a 10-fold lower concentration of SDX-308 induced potent (60%-80%) inhibition of osteoclast formation, and a 10- to 100-fold lower concentration inhibited multiple myeloma cell proliferation. Bone resorption was completely inhibited by SDX-308, as determined in dentin-based bone resorption assays. SDX-308 decreased constitutive and RANKL-stimulated NF-κB activation and osteoclast formation in an osteoclast cellular model, RAW 264.7. SDX-308 effectively suppressed TNF-α–induced IKK-γ and IκB-α phosphorylation and degradation and subsequent NF-κB activation in human multiple myeloma cells. These results indicate that SDX-308 effectively inhibits multiple myeloma cell proliferation and osteoclast activity, potentially by controlling NF-κB activation signaling. We propose that SDX-308 is a promising therapeutic candidate to inhibit multiple myeloma growth and osteoclast activity and that it should receive attention for further study.
Alcoholic pancreatitis: mechanisms of viral infections as cofactors in the development of acute and chronic pancreatitis and fibrosis
Authors: Jerrells Thomas R , Vidlak Debbie , Strachota Jennifer M 
Published: November 2006

AbstractAcute and chronic pancreatitis is associated with alcohol abuse, but symptomatic pancreatitis develops in only a small proportion of persons (10–20%) who abuse alcohol. This apparent paradox has led to the notion that additional cofactors are involved in the development of alcoholic pancreatitis. Potential cofactors, such as diet and smoking, have been suggested, but there are no compelling epidemiologic data to support this idea. A number of viruses and some bacteria have been shown to infect the pancreas and produce pancreatitis. One important mediator of pancreatitis in persons with a compromised immune system is a viral infection. The increased susceptibility of immunocompromised persons to viral pancreatitis led to the hypothesis, described in this paper, that the well-known immunosuppression associated with alcohol abuse would result in a more severe viral pancreatitis in mice, which are provided ethanol, than in control animals. To test this hypothesis, C57BL/6 mice were infected with a virulent strain of coxsackievirus B3, which preferentially induces pancreatitis, or with a strain that is naturally avirulent. The study findings presented in this paper show that ethanol consumption alone does not produce pancreas damage but results in a more severe and prolonged pancreatitis after infection with a virulent virus and interestingly, after infection with the avirulent strain of virus. This was associated with an increased number of viruses in the pancreas and spleen, which correlated with decreased humoral immune responses to the virus.
Insulin Represses Phosphoenolpyruvate Carboxykinase Gene Transcription by Causing the Rapid Disruption of an Active Transcription Complex: A Potential Epigenetic Effect
Authors: Hall Robert K. , Wang Xiaohui L. , George Leena , Koch Stephen R. , Granner Daryl K. 
Published: November 2006

AbstractInsulin represses gluconeogenesis, in part, by inhibiting the transcription of genes that encode rate-determining enzymes, such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase). Glucocorticoids stimulate expression of the PEPCK gene but the repressive action of insulin is dominant. Here, we show that treatment of H4IIE hepatoma cells with the synthetic glucocorticoid, dexamethasone (dex), induces the accumulation of glucocorticoid receptor, as well as many transcription factors, coregulators, and RNA polymerase II, on the PEPCK gene promoter. The addition of insulin to dex-treated cells causes the rapid dissociation of glucocorticoid receptor, polymerase II, and several key transcriptional regulators from the PEPCK gene promoter. These changes are temporally related to the reduced rate of PEPCK gene transcription. A similar disruption of the G-6-Pase gene transcription complex was observed. Additionally, insulin causes the rapid demethylation of arginine-17 on histone H3 of both genes. This rapid, insulin-induced, histone demethylation is temporally related to the disruption of the PEPCK and G-6-Pase gene transcription complex, and may be causally related to the mechanism by which insulin represses transcription of these genes.
A Scaleable and Defined System for Generating Neural Stem Cells from Human Embryonic Stem Cells
Authors: Joannides Alexis J. , Fiore-Hériché Christelle , Battersby Alysia A. , Athauda-Arachchi Pandula , Bouhon Isabelle A. , Williams Lydia , Westmore Kristine , Kemp Paul J. , Compston Alastair , Allen Nicholas D. , Chandran Siddharthan 
Published: November 2006

Abstract
The ability to differentiate human ESCs (hESCs) to defined lineages in a totally controlled manner is fundamental to developing cell-based therapies and studying human developmental mechanisms. We report a novel, scaleable, and widely applicable system for deriving and propagating neural stem cells from hESCs without the use of animal products, proprietary formulations, or genetic manipulation. This system provides a definitive platform for studying human neural development and has potential therapeutic implications.
Hypolipidemic effect of a pro-drug containing nicotinic acid in rats
Authors: Filip Cristiana , Albu Elena , Gheorghita Nastasia , Ghitler Nicolae , Mocanu Georgeta , Nechifor Mihai 
Published: November 2006

Abstract
We studied the release of nicotinic acid from a macromolecular pro-drug containing niacin bound to a polymeric support of dextran. Using a modified High-performance Liquid Chromatography (HPLC) method to provide an improved separation between nicotinic acid and its metabolites, we compared the plasma levels of nicotinic acid 24 h after administration of the pro-drug or a similar dose of unbound nicotinic acid to rats. Nicotinic acid exerts a number of pharmacological activities among which is the hypolipidemic effect. To determine the hypolipidemic effect of the pro-drug, we measured the triglyceride levels and examined the correlation with the plasma levels of nicotinic acid.Starting 6 h after administration of the pro-drug, the plasma levels of nicotinic acid were high enough to cause a decrease in the triglyceride level. These results suggest that nicotinic acid was gradually released from the polymeric support, leading to the sustained presence of the active substance and, therefore, a reduction in the level of triglycerides.
Methodological issues regarding confounding and exposure misclassification in epidemiological studies of occupational exposures
Authors: Blair Aaron , Stewart Patricia , Lubin Jay H. , Forastiere Francesco 
Published: November 2006

AbstractBackgroundConfounding and exposure misclassification are issues that concern epidemiologists because of their potential to bias results of studies and complicate interpretations. In occupational epidemiology both are routinely raised to argue that an observed result is either a false positive or a false negative finding. Although it is important to consider the potential for limitations of epidemiologic investigations, judgment regarding their importance should be based on their actual likelihood of occurrence.MethodsThis paper is based on our experience in epidemiologic analyses and a brief review of the literature regarding confounding and exposure misclassification.ResultsExamples of substantial confounding are rare in occupational epidemiology. In fact, even for studies of occupational exposures and lung cancer, tobacco‐adjusted relative risks rarely differ appreciably from the unadjusted estimates. This is surprising because it seems the perfect situation for confounding to occur. Yet, despite the lack of evidence that confounding is a common problem, nearly every epidemiologic paper includes a lengthy discussion on uncontrolled or residual confounding. On the other hand, exposure misclassification probably occurs in all studies. The only question is, how much? The direction and magnitude of nondifferential exposure misclassification (the type most likely to occur in cohort studies) on estimates of relative risks can be largely predicted given knowledge on the degree of misclassification, that is, relatively small amounts of misclassification can bias relative risks substantially towards the null. The literature, however, is full of discussions implying that misclassification of exposure is an explanation for a positive finding.ConclusionsThese comments are not to suggest that all potential limitations for epidemiologic studies should not be considered and evaluated. We do believe, however, that the likelihood of occurrence and the direction and magnitude of the effect should be more carefully and realistically considered when making judgments about study design or data interpretation. Am. J. Ind. Med. 50: 199–207, 2007. © 2006 Wiley‐Liss, Inc.
Identification and characterization of Kentucky self‐employed occupational injury fatalities using multiple sources, 1995–2004
Authors: Bunn Terry , Costich Julia , Slavova Svetla 
Published: November 2006

AbstractBackgroundIdentification and characterization of occupational injury fatalities in self‐employed workers typically relies on a single data source and thus may miss some cases.MethodsKentucky self‐employed worker injury fatalities were identified using Fatality Assessment and Control Evaluation (FACE) program data (1995–2004) and compared to non self‐employed worker data. Occupations and industries listed on death certificates were compared to those in which the decedent was actually engaged.ResultsOf 1,281 Kentucky worker injury deaths, 28% were self‐employed. Death certificates failed to identify 31% of these deaths as work‐related; industry and occupation were incorrectly identified in 27% and 16%, respectively. Fifty‐seven percent of the deaths were in agriculture, primarily tractor‐related. For Kentucky, the self‐employed crude death rate was higher (27.6/100,000) than the non self‐employed worker (5.4/100,000) rate or the US (11.5/100,000) self‐employed rate.ConclusionsMultiple information sources improve identification of self‐employed status in work‐related injury fatalities. Effective prevention requires accurate surveillance and examination of contributing factors. Self‐employed worker injuries in high‐risk industries should be more fully examined for development of effective injury prevention programs. Am. J. Ind. Med. 2006. © 2006 Wiley‐Liss, Inc.
Synthesis of poly(amide‐ester)s by microwave methods
Authors: Borriello Anna , Nicolais Luigi , Fang Xiaomei , Huang Samuel J. , Scola Daniel A. 
Published: November 2006

AbstractThe polycondensation of sebacic acids and ω‐amino alcohols by microwave irradiation was studied. The results were compared to those obtained from conventional melt polycondensation of poly(amide‐ester)s. It was found that the reaction proceeded at a much higher rate upon microwave irradiation. A high yield of thermally stable poly(amide‐ester)s was obtained. The microwave‐synthesized compounds were fully characterized by FTIR and 1H‐NMR spectroscopy, gel permeation chromatography, and a solubility test. The thermal properties of the poly(amide‐ester)s also were investigated. The results showed that the chemical‐physical properties of the polymers were in good agreement with those of polymers obtained by conventional synthesis. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 103: 1952–1958, 2007
Thermal and crystalline properties of water‐borne polyurethanes based on IPDI, DMPA, and PEBA/HNA
Authors: Zhang Shubiao , Jiang Huiming , Xu Yingmei , Zhang Donghui 
Published: November 2006

AbstractA series of water‐borne polyurethanes (WPUs) with different soft segments, various COOH contents, and various hard segment contents were prepared through a prepolymerization process. Thermal and crystalline properties of their films were studied by the measurement of differential scanning calorimetry (DSC), X‐ray diffraction (XRD), and thermogravimetry (TG), respectively. Two Tg areas in DSC of WPUs with polyethylene‐butylene adipate glycol (PEBA) as the soft segment were found; an endothermic peak at ∼ 33°C was also found with polyhexane neopentyl adipate glycol (HNA) as the soft segment. The DSC of WPUs with the mixture of PEBA/HNA as soft segment was investigated to show similarity to those from HNA, but with a relatively smaller endothermic peak at ∼ 34°C. Three sharp diffraction peaks at 2θ = 20.50°, 21.72°, and 24.54° in XRD of water‐borne PUs from HNA were found to indicate the crystallization of soft segments, which was disrupted by the addition of polyacrylate (PA), as evidenced by the amorphous shoulder at ∼ 2θ = 20°. TG analysis and differential thermogravimetric (DTG) analysis were measured to indicate that the films lost weight in two stages, and the decomposition temperatures of the films depended on the COOH content. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 103: 1936–1941, 2007