tbuckley/cabot-search huggingface dataset:
Health Care for Prisoners
Authors: B. Jaye Anno
Journal: JAMA (1993)

The article by Keller et al<sup>1</sup>addressing diabetic ketoacidosis among recently arrested prisoners raises some disturbing issues. The authors found that 70% of the prisoners brought to a single hospital in New York City during a 30-month period with this life-threatening condition had not received their insulin during the period immediately following arrest. The authors are critical of the lack of on-site health personnel and facilities at police lockups and court holding cells and suggest that reliance on emergency departments to provide care for arrestees is inefficient and costly. They recommend instituting a health screening for all arrestees and providing health facilities and personnel on site for those in need of medications. See also p 619. These findings and recommendations parallel those of an American Medical Association (AMA) study—except that study was reported 20 years ago and the focus was on jails.<sup>2</sup>(Jails are facilities operated by local
Cognitive Function at 3 Years of Age after Fetal Exposure to Antiepileptic Drugs
Authors: Kimford J. Meador, Gus A. Baker, Nancy Browning, Jill Clayton-Smith, Deborah T. Combs-Cantrell, Morris Cohen, Laura A. Kalayjian, Andres Kanner, Joyce D. Liporace, Page B. Pennell, Michael Privitera, David W. Loring
Journal: New England Journal of Medicine (2009)

Fetal exposure of animals to antiepileptic drugs at doses lower than those required to produce congenital malformations can produce cognitive and behavioral abnormalities, but cognitive effects of fetal exposure of humans to antiepileptic drugs are uncertain.
Electrophysiologic effects of partial coronary flow reduction in the exposed canine heart. Effects of ischemia and ischemic-induced regional hypothermia on refractoriness and conduction delay.
Authors: W G Daniel, R H Svenson, T N Masters, F Robicsek
Journal: Circulation (1978)

In the open-chested dog, coronary flow reduction results in a decrese of regional myocardial temperature (T). We assessed the contribution of T decrease to changes in refractoriness and conduction delay attributed to ischemia. The independent effect of regional hypothermia on effective refractory period (ERP) was a linear function of the temperature (ERP = -b T +a) with a -r = 0.97 0.02 in 11 dogs. The effect on conduction time of a ventricular premature beat was a linear function of the dog T at both endocardium (-r = 0.95 +/- 0.02) and epicardium (-r = 0.96 +/- 0.01). A 75% reduction in coronary flow resulted in a mean T decrease of 1.0 +/- 0.3 degrees C. The T decrease was sufficient to mask the effects of ischemia on shortening of the ERP. Furthermore, the conduction delay of ventricular premature beats during 75% coronary flow reduction could be accounted for by the decrease in T alone in five of seven dogs. We conclude that changes in refractoriness and conduction during acute coronary flow reduction in the open-chested dog are due to the composite effects of ischemia and the decrease in regional temperature. The open-chested model may have important limitations in understanding the electrophysiologic effects of acute coronary insufficiency. However, it may have important applications in defining the electrophysiologic environment at the time of coronary artery surgery.
Are patients with COPD psychologically distressed?
Authors: E. J. Wagena, W. A. Arrindell, E. F. M. Wouters, C. P. van Schayck
Journal: European Respiratory Journal (2005)

This study was designed to assess the level of psychological distress in a heterogeneous group of patients with chronic obstructive pulmonary disease (COPD), and compare them with the general population and psychiatric outpatients. A total of 118 patients with COPD, a random sample of 500 subjects from the general population and 500 psychiatric outpatients participated in this study. The Dutch version of the Symptom Checklist-90-Revised was used to assess general psychological distress. The sample of patients with COPD experienced significantly more psychological distress than the general population and significantly less than psychiatric outpatients. Furthermore, no significant association was found between the severity of the pulmonary disease and the level of psychological distress, although patients with severe or very severe COPD appeared to be at increased risk of depression. Lastly, the pattern of psychological complaints seems comparable in depressed patients with COPD and psychiatric outpatients. Once patients with COPD report suffering from depressive symptoms, the level of distress seems to increase to that found in psychiatric outpatients. In conclusion, in clinical settings in which psychological complaints are not routinely assessed, the Beck Depression Inventory and Symptom Checklist-90-Revised are very useful for drawing attention to depression and psychological distress.
Dopaminergic regeneration by neurturin-overexpressing c17.2 neural stem cells in a rat model of Parkinson's disease
Authors: Wei-Guo Liu, Xi-Jing Wang, Guo-Qiang Lu, Biao Li, Gang Wang, Sheng-Di Chen
Journal: Molecular Neurodegeneration (2007)

Abstract Background Genetically engineered neural stem cell (NSC) lines are promising vectors for the treatment of neurodegenerative diseases, particularly Parkinson's disease (PD). Neurturin (NTN), a member of the glial cell line-derived neurotrophic factor (GDNF) family, has been demonstrated to act specifically on mesencephalic dopaminergic neurons, suggesting its therapeutic potential for PD. In our previous work, we demonstrated that NTN-overexpressing c17.2 NSCs exerted dopaminergic neuroprotection in a rat model of PD. In this study, we transplanted NTN-c17.2 into the striatum of the 6-hydroxydopamine (6-OHDA) PD model to further determine the regenerative effect of NTN-c17.2 on the rat models of PD. Results After intrastriatal grafting, NTN-c17.2 cells differentiated and gradually downregulated nestin expression, while the grafts stably overexpressed NTN. Further, an observation of rotational behavior and the contents of neurotransmitters tested by high-performance liquid chromatography showed that the regenerative effect of the NTN-c17.2 group was significantly better than that of the Mock-c17.2 group, and the regenerative effect of the Mock-c17.2 group was better than that of the PBS group. Further research through reverse-transcriptase polymerase chain reaction assays and in vivo histology revealed that the regenerative effect of Mock-c17.2 and NTN-c17.2 cell grafts may be attributed to the ability of NSCs to produce neurotrophic factors and differentiate into tyrosine hydroxylase-positive cells. Conclusion The transplantation of NTN-c17.2 can exert neuroregenerative effects in the rat model of PD, and the delivery of NTN by NSCs may constitute a very useful strategy in the treatment of PD.
Autoimmune hepatitis in the elderly
Authors: D R PARKER, J G C KINGHAM
Journal: Gut (1998)

Autoimmune hepatitis in the elderlyEDITOR,-We were interested to read Professor James' comments on autoimmune hepatitis (AIH) in his review of parenchymal liver disease in the elderly (Gut 1997;41:430-2).He described an unpublished series of patients with AIH, 20% of whom were over 65 years of age 1 at presentation.We recently published an 11-year follow up of patients with type I AIH from an unselected population in South Wales. 2 Forty one patients were identified according to the AIH group criteria.The median age was 62 years and 23 (56%) patients were over 60 years of age at presentation; the usual presentation was an acute icteric hepatitis.Response to immunosuppression in the over-60's was gratifying and prompt and the five year survival rate compared favourably with that of our series as a whole.Our experience is similar to that of the Newcastle group, and it now seems clear that AIH should no longer be regarded primarily as a disease of the young.Indeed, our unselected series suggests that AIH is primarily a disease of the elderly.The diagnosis should be considered in any patient presenting with acute icteric hepatitis whatever his or her age.
Multiple Genetic Loci Modulate Lung Adenocarcinoma Clinical Staging
Authors: Elisa Frullanti, Antonella Galvan, Felicia S. Falvella, Giacomo Manenti, Francesca Colombo, Alberto Vannelli, Matteo Incarbone, Marco Alloisio, Mario Nosotti, Luigi Santambrogio, Anna Gonzalez-Neira, Ugo Pastorino, Tommaso A. Dragani
Journal: Clinical Cancer Research (2011)

Abstract Purpose: The main prognostic factor of lung cancer patient outcome is clinical stage, a parameter of tumor aggressiveness. Our study was conducted to test whether germ line variations modulate individual differences in clinical stage. Experimental Design: We conducted a case-only genome-wide association study (GWAS) using a 620,901 single-nucleotide polymorphism (SNP) array in a first series of 600 lung adenocarcinoma (ADCA) patients and in a replication series of 317 lung ADCA patients. Results: GWAS identified 54 putatively associated SNPs, 3 of which were confirmed in the replication series. Joint analysis of the two series pointed to 22 statistically associated (P &amp;lt; 0.01) genetic variants that together explained about 20% of the phenotypic variation in clinical staging (P &amp;lt; 2 × 10−16) and showed a statistically significant difference in overall survival (P = 8.0 × 10−8). The strongest statistical association was observed at rs10278557 (P = 1.1 × 10−5), located in the mesenchyme homeobox 2 (MEOX2) gene. Conclusion: These data point to the role of germ line variations involving multiple loci in modulating clinical stage and, therefore, prognosis in lung ADCA patients. Clin Cancer Res; 17(8); 2410–6. ©2011 AACR.
Enhanced TLR-mediated NF-IL6–dependent gene expression by Trib1 deficiency
Authors: Masahiro Yamamoto, Satoshi Uematsu, Toru Okamoto, Yoshiharu Matsuura, Shintaro Sato, Himanshu Kumar, Takashi Satoh, Tatsuya Saitoh, Kiyoshi Takeda, Ken J. Ishii, Osamu Takeuchi, Taro Kawai, Shizuo Akira
Journal: The Journal of Experimental Medicine (2007)

Toll-like receptors (TLRs) recognize a variety of microbial components and mediate downstream signal transduction pathways that culminate in the activation of nuclear factor κB (NF-κB) and mitogen-activated protein (MAP) kinases. Trib1 is reportedly involved in the regulation of NF-κB and MAP kinases, as well as gene expression in vitro. To clarify the physiological function of Trib1 in TLR-mediated responses, we generated Trib1-deficient mice by gene targeting. Microarray analysis showed that Trib1-deficient macrophages exhibited a dysregulated expression pattern of lipopolysaccharide-inducible genes, whereas TLR-mediated activation of MAP kinases and NF-κB was normal. Trib1 was found to associate with NF-IL6 (also known as CCAAT/enhancer-binding protein β). NF-IL6–deficient cells showed opposite phenotypes to those in Trib1-deficient cells in terms of TLR-mediated responses. Moreover, overexpression of Trib1 inhibited NF-IL6–dependent gene expression by down-regulating NF-IL6 protein expression. In contrast, Trib1-deficient cells exhibited augmented NF-IL6 DNA-binding activities with increased amounts of NF-IL6 proteins. These results demonstrate that Trib1 is a negative regulator of NF-IL6 protein expression and modulates NF-IL6–dependent gene expression in TLR-mediated signaling.
THE ROLE OF ANTI-INFLAMMATORY DRUGS IN THE PREVENTION AND TREATMENT OF ALZHEIMER'S DISEASE
Authors: John C. S. Breitner, M.D., M.P.H
Journal: Annual Review of Medicine (1996)

Risk factor intervention is a useful strategy for prevention of poorly understood diseases. Fifteen studies have examined the relation of glucocorticoid and nonsteroid antiinflammatory treatments and onset or progression of Alzheimer's disease (AD). Fourteen of these studies suggest that such treatments (especially nonsteroidal agents) prevent or ameliorate symptoms of AD. Abundant circumstantial evidence implicates inflammation in the pathogenesis of AD. Inhibition of cyclooxygenases, the central action of nonsteroidal antiinflammatory drugs (but not a prominent effect of steroids), limits inflammation, but it may also alter neural metabolic pathways, resulting in cell death from excitotoxicity or oxidative stress. Randomized controlled trials are needed to determine whether steroids, nonsteroidal antiinflammatory drugs, or both can prevent or treat the symptoms of AD.
Characterization of a swelling-activated anion conductance in homozygous typing cell hepatoma cells
Authors: K Bodily, Y Wang, R Roman, A Sostman, J G Fitz
Journal: Hepatology (1997)

Liver cell volume and intracellular ion concentrations are maintained within a narrow physiologic range by regulated changes in membrane ion permeability. These studies of homozygous HTC hepatoma cells, a model liver cell line, evaluate the relationship between cell volume and membrane ion permeability, and assess the possibility that cell swelling allows the efflux of the intracellular osmolite taurine through the opening of a conductive pathway. Cell swelling induced by exposure to hypotonic solutions (203 mOsm) caused a rapid increase in cell volume, followed by recovery toward basal values. Volume recovery was inhibited by Cl- depletion or by exposure to the putative Cl- channel blocker 5-nitro-2-(3-phenylpropyl-amino) benzoic acid (NPPB) (25 micromol/L). Swelling increased the efflux rates of 36Cl (181% +/- 15%, P < .01) and 125I (310% +/- 21%, P < .01). In whole cell patch clamp recordings, cell swelling induced by 1) exposure to hypotonic solution or 2) intracellular perfusion with hypertonic sucrose-containing solutions activated an anion-selective current which was outwardly rectified and showed time-dependent inactivation at depolarizing potentials. The current density at -80 mV increased proportionally with increases in the transmembrane osmotic gradient from basal values of -1 pA/pF to maximal values of 70 pA/pF with 100 mmol/L sucrose in the pipette. Basal taurine permeability was low, but cell swelling increased the efflux of [1,2-3H]taurine to 1,587% +/- 172% of basal levels (P < .05). Intracellular perfusion with hypertonic solutions activated currents carried by anionic taurine, with an estimated taurine/Cl- permeability ratio of .88 +/- .17 for whole cell currents. These studies demonstrate that the HTC membrane anion permeability is closely coupled to changes in cell volume, and that the recovery from swelling depends upon activation of anion-selective conductance pathways permeable to both Cl- and taurine.
A monoclonal antibody (MUM1p) detects expression of the MUM1/IRF4 protein in a subset of germinal center B cells, plasma cells, and activated T cells
Authors: Brunangelo Falini, Marco Fizzotti, Alessandra Pucciarini, Barbara Bigerna, Teresa Marafioti, Marcello Gambacorta, Roberta Pacini, Cristina Alunni, Laura Natali–Tanci, Barbara Ugolini, Carla Sebastiani, Giorgio Cattoretti, Stefano Pileri, Riccardo Dalla-Favera, Harald Stein
Journal: Blood (2000)
Altered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington disease
Authors: John Labbadia, Helen Cunliffe, Andreas Weiss, Elena Katsyuba, Kirupa Sathasivam, Tamara Seredenina, Ben Woodman, Saliha Moussaoui, Stefan Frentzel, Ruth Luthi-Carter, Paolo Paganetti, Gillian P. Bates
Journal: Journal of Clinical Investigation (2011)

Huntington disease (HD) is a devastating neurodegenerative disorder for which there are no disease-modifying treatments. Previous studies have proposed that activation of the heat shock response (HSR) via the transcription factor heat shock factor 1 (HSF1) may be of therapeutic benefit. However, the effect of disease progression on the HSR and the therapeutic potential of this pathway are currently unknown. Here, we used a brain-penetrating HSP90 inhibitor and physiological, molecular, and behavioral readouts to demonstrate that pharmacological activation of HSF1 improves huntingtin aggregate load, motor performance, and other HD-related phenotypes in the R6/2 mouse model of HD. However, the beneficial effects of this treatment were transient and diminished with disease progression. Molecular analyses to understand the transient nature of these effects revealed altered chromatin architecture, reduced HSF1 binding, and impaired HSR accompanied disease progression in both the R6/2 transgenic and HdhQ150 knockin mouse models of HD. Taken together, our findings reveal that the HSR, a major inducible regulator of protein homeostasis and longevity, is disrupted in HD. Consequently, pharmacological induction of HSF1 as a therapeutic approach to HD is more complex than was previously anticipated.
A low polymorphic mouse H-2 class I gene from the Tla complex is expressed in a broad variety of cell types.
Authors: C Transy, S R Nash, B David-Watine, M Cochet, S W Hunt, L E Hood, P Kourilsky
Journal: The Journal of Experimental Medicine (1987)

We have previously described the isolation of pH-2d-37, a cDNA clone that encodes a so far unknown, poorly polymorphic, class I surface molecule. We report here the isolation of the corresponding gene, its nucleotide sequence, and its localization in the Tla region of the murine MHC. Using a RNase mapping assay, we have confirmed that the second domain coding region of the 37 gene displays very limited polymorphism, and that the gene is transcribed in a broad variety of cell types, in contrast to the genes encoding the known Qa and TL antigens. Possible functions are discussed.
Circumflex femoral vein thrombosis misinterpreted as acute hamstring strain
Authors: Stergios G Papastergiou, Nikolaos E Koukoulias, Ioannis Tsitouridis, Constantinos Natsis, Constantinos A Parisis
Journal: British Journal of Sports Medicine (2007)

The case of a 24-year-old female professional, long-distance runner who presented with acute proximal posterior thigh pain is reported. History and clinical findings were consistent with acute hamstring strain but MRI demonstrated circumflex femoral vein thrombosis. This is the first case of proximal posterior thigh pain caused by circumflex femoral vein thrombosis reported in the literature. Doctors dealing with sports injuries should be aware of this clinical entity that mimics hamstring strain.
Regulatory T Cells Specific for the Same Framework 3 Region of the Vβ8.2 Chain Are Involved in the Control of Collagen II–induced Arthritis and Experimental Autoimmune Encephalomyelitis
Authors: Vipin Kumar, Fatema Aziz, Eli Sercarz, Alexander Miller
Journal: The Journal of Experimental Medicine (1997)

Recent evidence indicates that chronic autoimmune disease can result from breakdown of regulation and subsequent activation of self-reactive T cells. In many murine autoimmune disease systems and in the Lewis rat, antigen-specific T cells utilizing the T cell receptor (TCR) Vβ8.2 gene segment play a major role. In the myelin basic protein–induced experimental autoimmune encephalomyelitis (EAE) model in H-2u mice, we had shown that T cells recognizing a peptide determinant within the framework 3 region of the Vβ8.2 chain have a critical role in influencing the course of the disease. Here, we report experiments in another disease system, collagen II (CII)–induced arthritis (CIA) in DBA/1LacJ (H-2q) mice, indicating a remarkably parallel control circuit to that found for EAE. A critical role is played by CII-specific Vβ8.2bearing T cells in the CIA system, which we have confirmed. Animals treated with the superantigen SEB before CII administration are significantly protected from CIA. Next, we tested the ability of peptides encompassing the entire Vβ8.2 chain to induce proliferative responses. Only TCR peptide B5 (amino acids 76–101), a regulatory peptide in EAE, induced proliferation. B5 was then used to vaccinate DBA/1LacJ mice and was shown to reduce greatly the severity and incidence of CIA as measured by joint inflammation or histology. Furthermore, similar protection was found when B5 was administered after CII immunization. It was shown that there is physiological induction of a proliferative response to B5 during CIA and that the determinant within B5 is produced from a single chain TCR construct containing the entire Vβ8.2 chain. Finally, the regulation of CIA is discussed in the context of other experimental autoimmune diseases, especially EAE, with emphasis on what appear to be strikingly common mechanisms.
Phylogenetic Assessment of Introns and SINEs Within the Y Chromosome Using the Cat Family Felidae As a Species Tree
Authors: J Pecon-Slattery, A J Pearks Wilkerson, W J Murphy, S J O'Brien
Journal: Molecular Biology and Evolution (2004)

The cat family Felidae was used as a species tree to assess the phylogenetic performance of genes, and their embedded SINE elements, within the nonrecombining region of the Y chromosome (NRY). Genomic segments from single-copy X-Y homologs SMCY, UBE1Y, and ZFY (3,604 bp) were amplified in 36 species of cat. These genes are located within the X-degenerate region of the NRY and are thought to be molecular "fossils" that ceased conventional recombination with the X chromosome early within the placental mammal evolution. The pattern and tempo of evolution at these three genes is significant in light of the recent, rapid evolution of the family over approximately 12 Myr and provides exceptional support for each of the eight recognized felid lineages, as well as clear diagnostic substitutions identifying nearly all species. Bootstrap support and Bayesian posterior probabilities are uniformly high for defining each of the eight monophyletic lineages. Further, the preferential use of specific target-site motifs facilitating SINE insertion is empirically supported by sequence analyses of SINEs embedded within the three genes. Target-site insertion is thought to explain the contradiction between intron phylogeny and results of the SMCY SINE phylogeny that unites distantly related species. Overall, our data suggest X-degenerate genes within the NRY are singularly powerful markers and offer a valuable patrilineal perspective in species evolution.
Percutaneous Aortic Valve Implantation Retrograde From the Femoral Artery
Authors: John G. Webb, Mann Chandavimol, Christopher R. Thompson, Donald R. Ricci, Ronald G. Carere, Brad I. Munt, Christopher E. Buller, Sanjeevan Pasupati, Samuel Lichtenstein
Journal: Circulation (2006)

Background— Percutaneous aortic valve implantation by an antegrade transvenous approach has been described but is problematic. Retrograde prosthetic aortic valve implantation via the femoral artery has potential advantages. Percutaneous prosthetic aortic valve implantation via the femoral arterial approach is described and the initial experience reported. Methods and Results— The valve prosthesis is constructed from a stainless steel stent with an attached trileaflet equine pericardial valve and a fabric cuff. After routine aortic balloon valvuloplasty, a 22F or 24F sheath is advanced from the femoral artery to the aorta. A steerable, deflectable catheter facilitates manipulation of the prosthesis around the aortic arch and through the stenotic valve. Rapid ventricular pacing is used to reduce cardiac output while the delivery balloon is inflated to deploy the prosthesis within the annulus. Percutaneous aortic prosthetic valve implantation was attempted in 18 patients (aged 81±6 years) in whom surgical risk was deemed excessive because of comorbidities. Iliac arterial injury, seen in the first 2 patients, did not recur after improvement in screening and access site management. Implantation was successful in 14 patients. After successful implantation, the aortic valve area increased from 0.6±0.2 to 1.6±0.4 cm 2 . There were no intraprocedural deaths. At follow-up of 75±55 days, 16 patients (89%) remained alive. Conclusions— This initial experience suggests that percutaneous transarterial aortic valve implantation is feasible in selected high-risk patients with satisfactory short-term outcomes.