tbuckley/cabot-search huggingface dataset:
Philadelphia chromosome in essential thrombocythemia?
Authors: R. Sarode, N. Marwaha, R. K. Gupta, G. Garewal, Scott Murphy
Journal: American Journal of Hematology (1989)

We have read with interest the article "Clinical Presentation and Natural History of Patients with Essential Thrombocythemia and the Philadelphia Chromosome" by Stoll et al. [l].We were surprised to note that the authors have taken Polycythemia Vera Study Group (PVSG) criteria laid down in 1982 [2], for diagnosing essential thrombocythemia (ET), and not the latest PVSG criteria proposed in 1986 [3].The latter recommendations include "absence of Philadelphia (Ph') chromosome" as the only criterion to exclude the diagnosis of chronic granulocytic leukemia (CGL).Going through the case histories, it is quite evident that all six cases are CGL in early stages with marked thrombocytosis (platelet counts more than 1,OOO X 109/L).On follow-up, case 1 showed a typical picture of CGL going into blast crisis, case 3 developed an accelerated phase of CGL, and cases 4 and 6 had low leukocyte alkaline phosphatase typical of CGL.The morphology of megakaryocytes described in the paper is more like CGL than ET.Moreover, in terminal stages 5/6 cases went into blast crisis, which is the usual terminal event in CGL, but very rare in ET.We have seen three cases with such presentation where platelet counts were more than 1,OOO x 109/L with not very high leukocyte counts, but having Ph' chromosome.The clinical course of these patients was like CGL.In cases of CGL who had undergone bone marrow transplantation (BMT) as a mode of therapy, it was documented on regular follow-up that the Ph' chromosome appeared 2-4 months before the hematological onset of relapse of CGL [4].In the same study other patients who have Ph' chromosome 9 to 18 months post-BMT are still alive without hematological features of CGL.This supports the view that Ph' chromosome appears much before the hematological abnormalities.Moreover, six patients described in this paper appear to be identical to 617 cases described by Murphy et al.[3].The latter study excluded a diagnosis of ET in these patients solely on the basis of presence of Ph' chromosome.In conclusion, cases described by Stoll et al. are CGL in early stages of evolution with marked thrombocytosis, as the follow-up showed that these cases developed a characteristic picture of either chronic phase, accelerated phase, or blast crisis of CGL.
SENSORY DEPRIVATION AND SCHIZOPHRENIA: SOME CLINICAL AND THEORETICAL SIMILARITIES
Authors: NORMAN ROSENZWEIG
Journal: American Journal of Psychiatry (1959)

It would seem, in fact, that we now have an experimental model of the schizophrenic syndrome superior to the "model psychoses" induced with mescaline or LSD. Not only will perceptual interference reproduce more closely the primary symptoms of schizophrenia, but these disturbances are caused entirely by external manipulation, without the confusion of a toxic psychosis. While of course we cannot assume that approaches such as these will give us valid answers to all our questions, I believe we have here an important instrument to help us bridge the gap between the laboratory and the clinic.
Systematic review of noninvasive positive pressure ventilation in severe stable COPD
Authors: M. A. Kolodziej, L. Jensen, B. Rowe, D. Sin
Journal: European Respiratory Journal (2007)

The present systematic review examined the effectiveness of bilevel noninvasive positive pressure ventilation (NIPPV) in the management of chronic respiratory failure (CRF) due to severe stable chronic obstructive pulmonary disease (COPD). Randomised controlled trials (RCTs) and non-RCTs (crossover design) of adults with severe stable COPD and CRF receiving bilevel NIPPV via nasal, oronasal or total face mask were identified from electronic databases and manual screening of journals and reference lists. Respiratory function (gas exchange, lung function, ventilatory/breathing pattern, respiratory muscle function and work of breathing) and health-related outcomes (dyspnoea, functional status, exercise tolerance, health-related quality of life (HRQOL), morbidity and mortality) were assessed. In total, 15 studies met the inclusion criteria: six RCTs and nine non-RCTs. RCTs did not find improved gas exchange with bilevel NIPPV, while non-RCTs did. Lung hyperinflation and diaphragmatic work of breathing were reduced in a nonrandomised subset. HRQOL and dyspnoea, the least studied outcomes, showed improvement with bilevel NIPPV. In a subset of individuals on maximal medical treatment regimes for severe stable chronic obstructive pulmonary disease, bilevel noninvasive positive pressure ventilation may have an adjunctive role in the management of chronic respiratory failure through attenuation of compromised respiratory function and improvement in health-related outcomes.
Prognostic features of residual pleural thickening in parapneumonic pleural effusions
Authors: D. Jiménez Castro, G. Díaz, E. Pérez-Rodríguez, R.W. Light
Journal: European Respiratory Journal (2003)

The objective of the study was the identification of predictive factors for the development of residual pleural thickening (RPT) in patients with parapneumonic effusion. The design of the prospective study involved investigating patients with parapneumonic pleural effusions diagnosed between March 1991 and December 2000 in the respiratory department of Hospital Ramón y Cajal (Madrid, Spain) which is a 1,500 tertiary-care hospital. The clinical and radiological characteristics and measurements of microbiological and biochemical variables in the pleural fluid taken from the patients were studied. RPT was defined in a posteroanterior chest radiograph as pleural thickening of ≥10 mm measured at the lateral chest wall at the level of an imaginary line, tangent to the diaphragmatic dome. A total of 48 of the 348 patients studied (13.79%) were found to have RPT. Among the factors studied, only presence of pus in the pleural space, Fine classes IV and V, temperature ≥38°C and delayed resolution of pleural effusions after diagnosis (&gt;15 days) were independently associated with the risk of RPT. This study showed that significant residual pleural thickening was not a common complication of parapneumonic pleural effusions. There are certain risk factors for the development of residual pleural thickening. However, this complication was not associated with long-term functional repercussions in the series of patients involved in this study.
Donor and recipient family histories of hypertension influence renal impairment and blood pressure during acute rejections.
Authors: E Guidi, M G Cozzi, E Minetti, G Bianchi
Journal: Journal of the American Society of Nephrology (1998)

A previous historical prospective observational study, double blinded for knowledge of kidney donors' family history of hypertension, included 85 transplanted patients with stable renal function, not treated with cyclosporine, who were followed-up for an average of 8 yr and carefully characterized for the presence or absence of hypertension in the donor and recipient families. The recipients without a family history of hypertension, but grafted with a kidney coming from a "hypertensive" family, developed hypertension much more frequently than recipients grafted with a kidney coming from a "normotensive" family, or recipients with familial hypertension in whom the origin of the kidney did not influence the prevalence of hypertension after transplantation. In this second study of the same patients, it was found that these recipients with a "normotensive" family and a "hypertensive" kidney showed a greater increase of diastolic BP (P = 0.005) and a greater degree of acute renal damage (P = 0.004) during acute rejections than all of the other recipients. This extension study shows that a grafted kidney can transmit not only chronic hypertension, but also susceptibility to a greater rise in BP and more severe kidney impairment after an acute insult.
Localization and Regulation of the ATP6V0A4 (a4) Vacuolar H+-ATPase Subunit Defective in an Inherited Form of Distal Renal Tubular Acidosis
Authors: Paul A. Stehberger, Nicole Schulz, Karin E. Finberg, Fiona E. Karet, Gerhard Giebisch, Richard P. Lifton, John P. Geibel, Carsten A. Wagner
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. Vacuolar-type H+-ATPases (V-H+-ATPases) are the major H+-secreting protein in the distal portion of the nephron and are involved in net H+ secretion (bicarbonate generation) or H+ reabsorption (net bicarbonate secretion). In addition, V-H+-ATPases are involved in HCO3− reabsorption in the proximal tubule and distal tubule. V-H+-ATPases consist of at least 13 subunits, the functions of which have not all been elucidated. Mutations in the accessory ATP6V0A4 (a4 isoform) subunit have recently been shown to cause an inherited form of distal renal tubular acidosis in humans. Here, the localization of this subunit in human and mouse kidney was studied and the regulation of expression and localization of this subunit in mouse kidney in response to acid-base and electrolyte intake was investigated. Reverse transcription-PCR on dissected mouse nephron segments amplified a4-specific transcripts in proximal tubule, loop of Henle, distal convoluted tubule, and cortical and medullary collecting duct. a4 protein was localized by immunohistochemistry to the apical compartment of the proximal tubule (S1/S2 segment), the loop of Henle, the intercalated cells of the distal convoluted tubule, the connecting segment, and all intercalated cells of the entire collecting duct in human and mouse kidney. All types of intercalated cells expressed a4. NH4Cl or NaHCO3 loading for 24 h, 48 h, or 7 d as well as K+ depletion for 7 and 14 d had no influence on a4 protein expression levels in either cortex or medulla as determined by Western blotting. Immunohistochemistry, however, demonstrated a subcellular redistribution of a4 in response to the different stimuli. NH4Cl and K+ depletion led to a pronounced apical staining in the connecting segment, cortical collecting duct, and outer medullary collecting duct, whereas NaHCO3 loading caused a stronger bipolar staining in the cortical collecting duct. Taken together, these results demonstrate a4 expression in the proximal tubule, loop of Henle, distal tubule, and collecting duct and suggest that under conditions in which increased V-H+-ATPase activity is required, a4 is regulated by trafficking but not protein expression. This may allow for the rapid adaptation of V-H+-ATPase activity to altered acid-base intake to achieve systemic pH homeostasis. The significance of a4 expression in the proximal tubule in the context of distal renal tubular acidosis will require further clarification.
Screening for Asymptomatic Carotid Artery Stenosis
Authors: George W. Weyer, Andrew M. Davis
Journal: JAMA (2015)

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Investigating Protein-Coding Sequence Evolution with Probabilistic Codon Substitution Models
Authors: M. Anisimova, C. Kosiol
Journal: Molecular Biology and Evolution (2008)

This review is motivated by the true explosion in the number of recent studies both developing and ameliorating probabilistic models of codon evolution. Traditionally parametric, the first codon models focused on estimating the effects of selective pressure on the protein via an explicit parameter in the maximum likelihood framework. Likelihood ratio tests of nested codon models armed the biologists with powerful tools, which provided unambiguous evidence for positive selection in real data. This, in turn, triggered a new wave of methodological developments. The new generation of models views the codon evolution process in a more sophisticated way, relaxing several mathematical assumptions. These models make a greater use of physicochemical amino acid properties, genetic code machinery, and the large amounts of data from the public domain. The overview of the most recent advances on modeling codon evolution is presented here, and a wide range of their applications to real data is discussed. On the downside, availability of a large variety of models, each accounting for various biological factors, increases the margin for misinterpretation; the biological meaning of certain parameters may vary among models, and model selection procedures also deserve greater attention. Solid understanding of the modeling assumptions and their applicability is essential for successful statistical data analysis.
Alternating combination chemotherapy and levamisole improves survival in multiple myeloma: a Southwest Oncology Group Study.
Authors: S E Salmon, A Haut, J D Bonnet, M Amare, J K Weick, B G Durie, D O Dixon
Journal: Journal of Clinical Oncology (1983)

Previously untreated patients with multiple myeloma were entered on a randomized clinical trial to determine whether the use of alternating combination chemotherapy, including vincristine, doxorubicin, alkylating agents, and prednisone (160 patients) was more effective than conventional chemotherapy with melphalan and prednisone (77 patients), and whether the addition of the immunomodulating agent levamisole to maintenance chemotherapy enhanced the survival of patients achieving remission. The treatment groups were well matched for all major factors. The more aggressive chemotherapy was more effective at inducing remission, with a significantly higher proportion of patients achieving at least 75% tumor mass regression (53% with alternating combinations versus 32% with melphalan-prednisone, p = 0.002). Furthermore, the median survival was increased to 43 months with alternating combination chemotherapy as compared to 23 months with melphalan-prednisone (p = 0.004). After six to 12 months of induction therapy, 84 patients achieving remission were rerandomized to receive maintenance chemotherapy alone or with the addition of levamisole. The survival from the start of maintenance therapy was longer in patients receiving the added levamisole than with chemotherapy alone (p = 0.01). These findings support the use of aggressive multiagent chemotherapy for remission induction in patients with advanced-stage multiple myeloma.
The thymus leukemia antigen binds human and mouse CD8.
Authors: M Teitell, M F Mescher, C A Olson, D R Littman, M Kronenberg
Journal: The Journal of Experimental Medicine (1991)

The thymus leukemia antigen (TLA) is a class Ib, or 'nonclassical' class I molecule, one of several encoded within the Tla locus of the mouse major histocompatibility complex (MHC). It structurally resembles the H-2K, D, and L class I transplantation antigens, which present processed peptides to cytotoxic T lymphocytes (CTLs). Although their function(s) are unknown, there has been recent speculation concerning the possibility that class Ib molecules may present antigens to T cells that express gamma delta T cell antigen receptors (TCRs). In this report, using both a cell-cell adhesion assay and adhesion of T lymphocyte clones to purified plate-bound TLA, we provide evidence that TLA can bind to both human and mouse CD8. We also show that a chimeric class I molecule containing the peptide antigen binding site of Ld and the alpha 3 domain, transmembrane, and cytoplasmic segments of TLA, can support a CD8-dependent immune response by CTLs. These results demonstrate for the first time binding of a class Ib molecule to CD8 with a functional outcome, as is observed for the class I transplantation antigens. The capacity to interact with CD8 has been conserved despite the extensive sequence divergence of TLA in the peptide antigen binding site, suggesting this interaction is highly significant. TLA is expressed by epithelial cells in the mouse small intestine. As these epithelial cells are in close contact with intestinal intraepithelial lymphocytes that are nearly all CD8+, and many of which express the gamma delta TCR, the data are consistent with the hypothesis that TLA is involved in antigen presentation, perhaps to gamma delta-positive lymphocytes in this site.
Ankylosing hyperostosis. I. Clinical and radiological features.
Authors: J Harris, A R Carter, E N Glick, G O Storey
Journal: Annals of the Rheumatic Diseases (1974)

Ankylosing hyperostosis is a condition in which new bone is laid down on the right antero-lateral aspect of the dorsal vertebrae and across the intervertebral spaces forming spurs or bridges.The lumbar and cervical spines, pelvis, hips, and knees may also be involved.There is no single approved name for this condition.Oppenheimer (1942) described 'Calcifi- cation and ossification of vertebral ligaments'.Forestier and Rotes-Querol (1950) named it 'senile ankylosing hyperostosis of the spine', but in later works (Forestier and Lagier, 1971) the adjective 'senile' was omitted when the condition was described in younger patients.Smith, Pugh, and Polley (1955) described 'physiologic vertebral ligamentous calcifi- cation' and Haijkova, Streda, and Skrha (1965) 'hyperostotic spondylosis'.Beardwell (1969) termed this condition 'ankylosing vertebral hyperostosis ' and Julkunen, Heinonen, and Py6rala (1971) referred to 'hyperostosis of the spine'.Bywaters and Forestier (1967) presented a revised system for nomenclature of spinal diseases at the 6th European Congress of Rheumatology.They advised that this condition be named 'ankylosing hyperostosis', and this is the terminology which we have adopted.
A novel integrin 5 1 binding domain in module 4 of connective tissue growth factor (CCN2/CTGF) promotes adhesion and migration of activated pancreatic stellate cells
Authors: R Gao
Journal: Gut (2005)

Connective tissue growth factor (CCN2) is upregulated in pancreatic fibrosis and desmoplastic pancreatic tumours. CCN2 interacts with integrin alpha5beta1 on pancreatic stellate cells (PSC) in which it stimulates fibrogenesis, adhesion, migration, and proliferation.To determine the structural domain(s) in CCN2 that interact with integrin alpha5beta1 to regulation PSC functions.Primary activated rat PSC were tested for their adherence to isoforms of CCN2 comprising modules 1-4 (CCN2(1-4)), modules 3-4 (CCN2(3-4)), module 3 alone (CCN2(3)), or module 4 alone (CCN2(4)). Adhesion studies were performed in the presence of EDTA, divalent cations, anti-integrin alpha5beta1 antibodies, CCN2 synthetic peptides, or heparin, or after pretreatment of the cells with heparinase, chondroitinase, or sodium chlorate. CCN2 integrin alpha5beta1 binding was analysed in cell free systems. The ability of CCN2(1-4), CCN2(3-4), or CCN2(4) to stimulate PSC migration was evaluated in the presence of anti-integrin alpha5beta1 or heparin.PSC adhesion was stimulated by CCN2(1-4), CCN2(3-4), or CCN2(4) and supported by Mg2+ but not Ca2+. CCN2(4) supported PSC adhesion or migration were blocked by anti-integrin alpha5beta1 antibodies or by treatment of cells with heparinase or sodium chlorate. A direct interaction between CCN2(4) and integrin alpha5beta1 was demonstrated in cell free assays. The sequence GVCTDGR in module 4 mediated the binding between CCN2(4) and integrin alpha5beta1 as well as CCN2(4) mediated PSC adhesion and migration.A GVCTDGR sequence in module 4 of CCN2 is a novel integrin alpha5beta1 binding site that is essential for CCN2 stimulated functions in PSC and which represents a new therapeutic target in PSC mediated fibrogenesis.
Effects of Antipsychotic Medications on Psychosocial Functioning in Patients With Chronic Schizophrenia: Findings From the NIMH CATIE Study
Authors: Marvin S. Swartz, Diana O. Perkins, T. Scott Stroup, Sonia M. Davis, George Capuano, Robert A. Rosenheck, Fred Reimherr, Mark F. McGee, Richard S.E. Keefe, Joseph P. McEvoy, John K. Hsiao, Jeffrey A. Lieberman
Journal: American Journal of Psychiatry (2007)

Objective: This study examined the relative effects of the second-generation antipsychotic drugs and an older representative agent on psychosocial functioning in patients with chronic schizophrenia. Method: Consenting patients were enrolled in the NIMH Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) project. In phase 1, patients were randomly assigned to receive olanzapine, perphenazine, quetiapine, risperidone, or ziprasidone for up to 18 months. Clozapine was included for patients who chose this pathway after discontinuing phase 1 due to inefficacy; all other patients received another second-generation antipsychotic. Psychosocial functioning was assessed using the Quality of Life Scale. Results: Psychosocial functioning modestly improved for the one-third of phase 1 patients who reached the primary Quality of Life Scale analysis endpoint of 12 months (average effect size 0.19 SD units). Although for several of the drugs individually there were significant changes from baseline, overall there were no significant differences between the different agents. Results were similar at 6 and 18 months. There were no significant differences among the treatment groups in the amount of change in the Quality of Life Scale total score or subscale scores at 6, 12, or 18 months. Patients treated with clozapine in the efficacy pathway made comparable gains. Early treatment discontinuations, especially among patients most impaired at baseline, limited the ability to achieve more substantial functional gains. Conclusions: All antipsychotic treatment groups in all phases made modest improvements in psychosocial functioning. There were no differences among them after 6, 12, or 18 months. More substantial improvements would likely require more intensive adjunctive psychosocial rehabilitation interventions.