tbuckley/cabot-search huggingface dataset:
Posttraumatic Stress Disorder and DementiaPosttraumatic Stress Disorder and Dementia
Authors: Roger K. Pitman
Journal: JAMA (2010)

Kristine Yaffe, MD; Eric Vittinghoff, PhD; Karla Lindquist, MS; Deborah Barnes, PhD; Kenneth E. Covinsky, MD, MPH; Thomas Neylan, MD; Molly Kluse, BA; Charles Marmar, MDContext: Posttraumatic stress disorder (PTSD) is highly prevalent among US veterans because of combat and may impair cognition.Objective: To determine whether PTSD is associated with the risk of developing dementia among older US veterans receiving treatment in Department of Veterans Affairs medical centers.Design: A stratified, retrospective cohort study conducted using the Department of Veterans Affairs National Patient Care Database.Setting: Department of Veterans Affairs medical centers in the United States.Participants: A total of 181 093 veterans 55 years or older without dementia from fiscal years 1997 through 2000 (53 155 veterans with and 127 938 veterans without PTSD).Main Outcome Measures: During the follow-up period between October 1, 2000, and December 31, 2007, 31 107 (17.2%) veterans were ascertained to have newly diagnosed dementia according to International Classification of Diseases, Ninth Revision, Clinical Modification codes.Results: The mean baseline age of the veterans was 68.8 years, and 174 806 (96.5%) were men. Veterans with PTSD had a 7-year cumulative incident dementia rate of 10.6%, whereas those without had a rate of 6.6% (P < .001). With age as the time scale, Cox proportional hazards models indicated that patients with PTSD were more than twice as likely to develop incident dementia compared with those without PTSD (hazard ratio, 2.31; 95% confidence interval, 2.24-2.39). After multivariable adjustment, patients with PTSD were still more likely to develop dementia (hazard ratio, 1.77; 95% confidence interval, 1.70-1.85). Results were similar when we excluded those with a history of head injury, substance abuse, or clinical depression.Conclusions: In a predominately male veteran cohort, those diagnosed as having PTSD were at a nearly 2-fold higher risk of developing dementia compared with those without PTSD. Mechanisms linking these important disorders need to be identified with the hope of finding ways to reduce the increased risk of dementia associated with PTSD.
Lactose intolerance associated with adjuvant 5-fluorouracil-based chemotherapy for colorectal cancer
Authors: Pia Österlund, Tarja Ruotsalainen, Katri Peuhkuri, Riitta Korpela, Anneli Ollus, Minna Ikonen, Heikki Joensuu, Inkeri Elomaa
Journal: Clinical Gastroenterology and Hepatology (2004)
Oxford Textbook of Clinical Nephrology
Authors: George Dunea
Journal: JAMA (1992)

It is the common fate of accumulating human knowledge that periodically large tracts of it become enshrined in beautifully bound volumes engraved with golden letters, to be neatly arranged on shelves by generally shortsighted librarians. Such volumes have adorned the massive halls of famous libraries at least since the time of the great library of Alexandria and certainly since the Middle Ages, giving rise to the nagging question of how so many people could have written so much when so little was known. In nephrology, however, much has been learned since the early days after World War II, when dialysis, transplantation, and renal biopsy began to transform a once sleepy academic pursuit into a dynamic subspecialty that has affected and saved the lives of thousands. All this knowledge Professor Cameron and his collaborators have now assembled into three excellent volumes written by some 210 collaborators from all over the world,
Instability of dinucleotide repeats in Hodgkin's disease
Authors: Z. Mark, A. Toren, N. Amariglio, G. Schiby, F. Brok-Simoni, G. Rechavi
Journal: American Journal of Hematology (1998)

Tumorigenesis has been shown to proceed through a series of genetic alterations involving protooncogenes and tumor suppressor genes. However, the investigation of genomic instability of microsatellites has disclosed a new mechanism for human carcinogenesis, which is involved not only in hereditary nonpolyposis colon cancer (HNPCC) but in a number of other malignancies as well. To determine whether microsatellite instability is involved in Hodgkin's disease, we screened 16 such tumors using 7 microsatellite marker loci on 6 chromosome arms 4, 5, 9p, 9q, 11, 14, and 17. Using the polymerase chain reaction method, DNA samples from the tumors and from normal peripheral blood leukocytes from each patient were compared for the allelic pattern produced at each locus. Five cases of genomic instability were identified, suggesting that this mechanism is relevant to the pathogenesis of HD.
Effects of different mechanical ventilation strategies on the mucociliary system
Authors: Vivien S. Piccin, Christiane Calciolari, Kelly Yoshizaki, Susimeire Gomes, Cláudia Albertini-Yagi, Marisa Dolhnikoff, Mariângela Macchione, Elia G. Caldini, Paulo H. N. Saldiva, Elnara M. Negri
Journal: Intensive Care Medicine (2010)
Localized dermographism at the site of a fixed drug eruption
Authors: R. Pellicano, F. Camassa, M. Lomuto
Journal: British Journal of Dermatology (1995)

Journal Article Localized dermographism at the site of a fixed drug eruption Get access R. Pellicano, R. Pellicano Department of Dermatology, IRCCS ‘Casa Sollievo della Sofferenza', Viale Cappuccini, 71013 San Giovanni Rotondo, Italy Search for other works by this author on: Oxford Academic Google Scholar F. Camassa, F. Camassa Department of Dermatology, IRCCS ‘Casa Sollievo della Sofferenza', Viale Cappuccini, 71013 San Giovanni Rotondo, Italy Search for other works by this author on: Oxford Academic Google Scholar M. Lomuto M. Lomuto Department of Dermatology, IRCCS ‘Casa Sollievo della Sofferenza', Viale Cappuccini, 71013 San Giovanni Rotondo, Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 132, Issue 1, 1 January 1995, Pages 156–158, https://doi.org/10.1111/j.1365-2133.1995.tb08648.x Published: 01 January 1995
The role of capillarization in hepatic failure: Studies in carbon tetrachloride-induced cirrhosis
Authors: Antonio Martinez-Hernandez, Jose Martinez
Journal: Hepatology (1991)

During the cirrhotic process, the hepatic microvascular phenotype is transformed from sinusoids (discontinuous capillaries) into continuous capillaries. This transformation has been termed capillarization. Many hepatic functions depend on the rapid, bidirectional exchange of macromolecules between plasma and hepatocytes. To determine whether capillarization contributes to hepatic failure in cirrhosis, we decided to study the plasma clearance ( 125 I) and hepatocyte uptake (electron microscopy) of three tracers in normal and cirrhotic rats. The tracers chosen were a hemeundecapeptide with peroxidatic activity (fluidphase pinocytosis), asialofetuin (receptor-mediated endocytosis of a medium size protein) and ferritin (receptor-mediated endocytosis of a large size protein). The results demonstrate a decreased hepatocyte uptake of hemeundecapeptide; a significant delay in plasma clearance of asialofetuin; and a minor delay in plasma clearance of ferritin, but a striking trapping of ferritin in the cirrhotic capillary basement membrane. The delayed plasma clearance in cirrhosis cannot be ascribed to a decreased number of surface receptors because, in isolated hepatocytes, the number of molecules bound per cell was equivalent in normal and cirrhotic livers. These findings support the concept of capillarization with the formation of continuous diffusion and filtration barriers between plasma and hepatocytes, representing a significant hindrance to the bidirectional macromolecular exchange normally taking place between these two compartments. Furthermore, at least in the case of ferritin, the capiliary basement membrane of cirrhotic livers seems to be the major filtration barrier. This hindrance to hepatocyte uptake, and presumably also to secretion, may be the cause (or at least a major determinant) of the hepatic failure characteristic of cirrhosis. (Hepatology 1991;14: 864-874).
The changing face of ectopic pregnancy
Authors: L. Mascarenhas, J. Williamson, S. Smith
Journal: BMJ (1997)

Physician assisted suicide, euthanasia, or withdrawal of treatmentDistinguishing between them clarifies moral, legal, and practical positions T he Supreme Court of the United States has returned the vexing question of physician assisted suicide to state governments.In unanimous rulings last month, Chief Justice Rehnquist, writing for the court, held that there is no fundamental right to assistance in committing suicide 1 and that, legally, distinguishing between refusing life saving medical treatment and requesting assistance in suicide "comports with fundamental legal principles of causation and intent." 2 By its rulings, the Supreme Court invalidated the decisions of two of the American Courts of Appeal.In March 1996 the appeals court for the Ninth Circuit had lifted a ban by Washington state on physician assisted suicide in Compassion in Dying v Washington. 3 That court, which has jurisdiction in 13 western states, including Hawaii, had concluded that "a competent adult ... has a strong liberty interest in choosing a dignified and humane death"-including not just refusal of treatment but also "hastening one's own death."However, the Supreme Court held that the interest in question, which Chief Justice Rehnquist characterised as the "right to commit suicide with another's assistance," is not one of the "fundamental rights and liberties ... 'deeply rooted in this Nation's history and tradition'."
Overexpression of calcineurin in mouse causes sudden cardiac death associated with decreased density of K+ channels
Authors: D Dong
Journal: Cardiovascular Research (2003)

Background: Overexpression of calcineurin in transgenic (TG) mice results in cardiac hypertrophy and unexpected deaths. Methods and results: None of the TG survived beyond 24 weeks (n=38) whereas all of the wildtype (WT, n=47) survived. Prolongation of repolarization preceded the development of sustained pleomorphic ventricular tachycardia and high degree atrioventricular block, which occurred during spontaneous sudden deaths. Since depolarization-activated K+ channels contribute dominantly to repolarization in mice, we hypothesized that the TG would decrease these K+ currents and that the in vivo administration of cyclosporin A (CsA), a calcineurin inhibitor, would reduce this effect. CsA reversed cardiac hypertrophy: capacitance measurements of WT left ventricular myocytes (127±7 pF; n=45) and CsA-treated TG (129±14 pF; n=17) were significantly lower than in placebo-treated TG (220±11 pF; n=41; P<0.001 by ANOVA). Independent of whether the data fit a bi- or a tri-exponential model, the density of Itof was significantly reduced in TG versus WT and CsA reversed this effect. While Itos and IKslow were also reduced in TG, CsA does not reverse this change because long-term in vivo CsA treatment of WT also reduces Itos and IKslow. To assess whether the decreased 'repolarization reserve' contributed to arrhythmogenesis, the residual IKr was blocked by dofetilide precipitating pleomorphic ventricular tachycardias. Conclusion: Since the downregulation of Itof was observed with overexpression of calcineurin and was also reversed by the calcineurin inhibitor CsA, we conclude that downregulation of Itof is a consequence of calcineurin overexpression.
IGF-I and TGF-beta 1 incorporated in a poly(d,l-lactide) implant coating maintain their activity over long-term storage—cell culture studies on primary human osteoblast-like cells
Authors: B. Wildemann, M. Lübberstedt, N.P. Haas, M. Raschke, G. Schmidmaier
Journal: Biomaterials (2003)
Erratum: CORRIGENDUM: Experimental autoimmune encephalomyelitis repressed by microglial paralysis
Authors: F L Heppner, M Greter, D Marino, J Falsig, G Raivich, N Hövelmeyer, A Waisman, T Rülicke, M Prinz, J Priller, B Becher, A Aguzzi
Journal: Nature Medicine (2005)
Contractile dysfunction and ATP depletion after transient calcium overload in perfused ferret hearts.
Authors: M Kitakaze, H F Weisman, E Marban
Journal: Circulation (1988)

Although a number of lines of evidence hint that an elevation of intracellular calcium leads to myocardial injury, the cellular consequences of transient Ca overload remain unclear. To determine the contractile, histologic, and metabolic sequelae of transient Ca overload, we measured developed pressure (DP) in isovolumetric Langendorff-perfused ferret hearts at 37 degrees C before and 20 min after three 5 min periods of perfusion with a 10 mM [Ca]o, 1 mM [Mg]o solution (high-Ca group, n = 8) without ischemia, and in control hearts (n = 5) exposed transiently to the same total divalent cation concentration without a change in [Ca]o (9 mM [Mg]o, 2mM [Ca]o). DP, measured at various [Ca]o (0.5 to 5 mM), was depressed in the high-Ca group relative to control (p less than .001). Representative hearts from the control group were histologically normal, whereas hearts from the high-Ca group exhibited rare foci of predominantly "reversible" injury (mitochondrial swelling, glycogen deposition, and clumping of nuclear chromatin). Maximal Ca++-activated pressure (MCAP), measured from tetani after exposure to ryanodine, was also decreased in the high-Ca group (230 +/- 4 vs 262 +/- 6 mm Hg, p less than .001). Cao sensitivity, determined by normalization of the DP-[Ca]o relationship to the corresponding MCAP, was shifted to higher [Ca]o in the high-Ca group. Phosphorus nuclear magnetic resonance spectra were obtained in four high-Ca hearts. [ATP] declined by 30% to 40% after exposure to high [Ca]o, but inorganic phosphate, phosphocreatine, and pH remained unchanged. These results indicate that transient exposure to high [Ca]o without ischemia leaves behind distinctive contractile, metabolic, and histologic sequelae. The possible implications for the pathogenesis of postischemic contractile dysfunction are discussed.
Abstract 2124: Analysis of FAM111A, a newly identified AR regulated gene, in prostate cancer
Authors: Maria Mudryj, Stephen J. Libertini, Alan P. Lombard, Salma Saddiqui, Paramita M. Ghosh
Journal: Cancer Research (2014)

Abstract Prostate carcinoma (PCa) is the most commonly diagnosed cancer in men in the United States. Most PCas are dependent on the androgen receptor (AR) for growth and survival, and this dependency is exploited as androgen deprivation is the major therapeutic intervention. However, PCa inevitably progress to become castration resistant, yet remain reliant on the activity of the AR. Further understanding the mechanisms that mediate castration resistance and the pathways downstream of the AR will enhance our ability to treat this stage of the disease. RNA-seq studies of two castrate resistant cell lines following AR ablation identified a number of transcripts that were AR regulated. The studies identified FAM111A as an AR regulated gene. While little is known about FAM111A, a previous study has shown that the FAM111A gene harbors a PCa susceptibility SNP and that the FAM111A protein interacts with SV40 T-Ag. Our studies indicate that AR represses FAM111A in cell culture and xenograft models of CaP. Additionally, the expression of the only known FAM111A paralogue, FAM111B, was reciprocally regulated in cell lines and in the xenograft. FAM111A is expressed in all cultured prostate derived cell lines we looked at, and we found that there are two FAM111A isoforms. Furthermore, a siRNA mediated ablation of FAM111A modified apoptotic responses to chemotherapeutic stimuli. An immunohistochemical analysis of a prostate tumor tissue array was used to assess the expression of FAM111A. FAM111A is expressed in the cytoplasmic and nuclear compartments and expression in the cytoplasmic compartment in non-tumor prostate tissue is higher than in adjacent tumor cells. In conclusions, FAM111a is an AR regulated gene, has been associated with PCa in a GWAS study, interacts with the SV40 T-antigen and is expressed at lower levels in tumor cells. This suggests that FAM111A may be have a role in prostate tumorigenesis. Citation Format: Maria Mudryj, Stephen J. Libertini, Alan P. Lombard, Salma Saddiqui, Paramita M. Ghosh. Analysis of FAM111A, a newly identified AR regulated gene, in prostate cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2124. doi:10.1158/1538-7445.AM2014-2124
High illness loads (physical and social) do not always force high levels of mass religiosity
Authors: Gregory S. Paul
Journal: Behavioral and Brain Sciences (2012)

Abstract The hypothesis that high levels of religiosity are partly caused by high disease loads is in accord with studies showing that societal dysfunction promotes mass supernaturalism. However, some cultures suffering from high rates of disease and other socioeconomic dysfunction exhibit low levels of popular religiosity. At this point, it appears that religion is hard pressed to thrive in healthy societies, but poor conditions do not always make religion popular, either.
Death and serious injury in child motorcyclists.
Authors: S A Henderson, H K Graham, J Piggot
Journal: BMJ (1987)

Death and serious injury in child motorcyclistsThe increasing number of children aged under 16 years who have been injured while riding motorcycles has been called an epidemic.I We report on 10 children admitted to hospital with serious injuries as a result of riding motorcycles and on another child who died before admission-the first death, to our knowledge, of a child motorcyclist reported in the United Kingdom.
Abstract 3201: Parthenolide ameliorates experimental colitis associated colon cancer by inhibition of NF-kB signaling
Authors: Se Lim Kim, Sang-Wook Kim, Seong Hun Kim, In Hee Kim, Seung Ok Lee, Soo Teik Lee, Dae Ghon Kim
Journal: Cancer Research (2014)

Abstract Parthenolide (PT), a NF-kB inhibitor, has recently been demonstrated as a promising anticancer agent that promotes apoptosis of cancer cells. We previously showed that PT suppresses tumor growth in a xenograft model of colorectal cancer cells by regulation of Bcl-2 family. Unfortunately, little is known about its role in the process of tumor development in colitis associated colon cancer (CAC). Therefore, this study was designed to investigate the effects of PT on an experimental murine CAC model. Experimental CAC was induced by azoxymethane (AOM) and dextran sulfate sodium (DSS). Mice were divided into 3 groups: AOM+DSS, AOM+DSS+2mg/kg PT and AOM+DSS+4mg/kg PT. We demonstrated that administration of PT significantly reduced the severity of AOM/DSS-induced CAC as assessed by histological analysis, and resulted in downregulation of phospho-NF-κB p65 expression by the blockade of phosphorylation and subsequent degradation of IκB-a. Administration of PT ameliorated the carcinogenesis through the downregulation of antiapoptotic protein Bcl-2 and Bcl-xL mediated by inhibition of NF-kB activation. Moreover, apoptosis and caspase-3 expression also increased markedly in PT administration group. These findings demonstrate that PT downregulates NF-kB resulting in initiation of apoptosis and eventual suppression of CAC development, suggesting that PT exerts beneficial effects in experimental CAC and could therefore be a potential chemopreventive and therapeutic agent of CAC. Citation Format: Se Lim Kim, Sang-Wook Kim, Seong Hun Kim, In Hee Kim, Seung Ok Lee, Soo Teik Lee, Dae Ghon Kim. Parthenolide ameliorates experimental colitis associated colon cancer by inhibition of NF-kB signaling. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3201. doi:10.1158/1538-7445.AM2014-3201
Chief medical officers: the need for public health at the heart of government
Authors: G. Scally
Journal: BMJ (2013)

As the global economic crisis continues to have detrimental effects on health and health services around the world, there has never been a greater need for powerful advocates for public health at the heart of government. The need for an articulate and authoritative voice that can tell elected politicians the potential health consequences of their actions and inactions has been recognised in many democracies since the pinnacle of the sanitary revolution of the 19th century.

Many countries around the world have such a post designated in their governmental structures to provide expert advice on current and potential hazards to public health. There is, however, enormous variation in how this national role is positioned. In the countries of the European Union it ranges from a top level office occupied by a public health physician to a post at a lower level of government, or even separate from it, and occupied by an administrator rather than a physician.1

Perhaps the two most prominent posts globally are the surgeon general of the United States and the chief medical officer (CMO) of England, which incorporates the role of chief medical adviser to the UK government. These two posts show the advantages and hazards …
The influence of hypertension on management and outcome of acute coronary syndrome
Authors: Silia K. Majahalme, Dean E. Smith, Jeanna V. Cooper, Eva M. Kline-Rogers, Yassar Almanaseer, Eyad Akhras, Rajendra H. Mehta, Kim A. Eagle, John D. Bisognano
Journal: Journal of the American College of Cardiology (2002)
Antisense Oligonucleotide Directed to Human Apolipoprotein B-100 Reduces Lipoprotein(a) Levels and Oxidized Phospholipids on Human Apolipoprotein B-100 Particles in Lipoprotein(a) Transgenic Mice
Authors: Esther Merki, Mark J. Graham, Adam E. Mullick, Elizabeth R. Miller, Rosanne M. Crooke, Robert E. Pitas, Joseph L. Witztum, Sotirios Tsimikas
Journal: Circulation (2008)

Lipoprotein (a) [Lp(a)] is a genetic cardiovascular risk factor that preferentially binds oxidized phospholipids (OxPL) in plasma. There is a lack of therapeutic agents that reduce plasma Lp(a) levels.Transgenic mice overexpressing human apolipoprotein B-100 (h-apoB-100 [h-apoB mice]) or h-apoB-100 plus human apo(a) to generate genuine Lp(a) particles [Lp(a) mice] were treated with the antisense oligonucleotide mipomersen directed to h-apoB-100 mRNA or control antisense oligonucleotide for 11 weeks by intraperitoneal injection. Mice were then followed up for an additional 10 weeks off therapy. Lp(a) levels [apo(a) bound to apoB-100] and apo(a) levels ["free" apo(a) plus apo(a) bound to apoB-100] were measured by chemiluminescent enzyme-linked immunoassay and commercial assays, respectively. The content of OxPL on h-apoB-100 particles (OxPL/h-apoB) was measured by capturing h-apoB-100 in microtiter wells and detecting OxPL by antibody E06. As expected, mipomersen significantly reduced plasma h-apoB-100 levels in both groups of mice. In Lp(a) mice, mipomersen significantly reduced Lp(a) levels by approximately 75% compared with baseline (P<0.0001) but had no effect on apo(a) levels or hepatic apo(a) mRNA expression. OxPL/h-apoB levels were much higher at baseline in Lp(a) mice compared with h-ApoB mice (P<0.0001) but decreased in a time-dependent fashion with mipomersen. There was no effect of the control antisense oligonucleotide on lipoprotein levels or oxidative parameters.Mipomersen significantly reduced Lp(a) and OxPL/apoB levels in Lp(a) mice. The present study demonstrates that h-apoB-100 is a limiting factor in Lp(a) particle synthesis in this Lp(a) transgenic model. If applicable to humans, mipomersen may represent a novel therapeutic approach to reducing Lp(a) levels and their associated OxPL.