tbuckley/cabot-search huggingface dataset:
Psychosocial aspects of patients with focal hyperhidrosis. Marked reduction of social phobia, anxiety and depression and increased quality of life after treatment with botulinum toxin A
Authors: A. Weber, S. Heger, R. Sinkgraven, M. Heckmann, P. Elsner, B. Rzany
Journal: British Journal of Dermatology (2005)

Background Primary focal hyperhidrosis (PFH) is defined as excessive sweating typically localized to specific body areas such as axillae, hands and feet. An association between PFH and anxiety as well as depressive syndromes has been suggested. Objectives To investigate a possible association between PFH and anxiety, depression, social phobia and quality of life, and to study the effect of treatment with botulinum toxin A on these factors. Methods PFH was confirmed clinically and by gravimetry. To measure anxiety and depressive syndromes several German versions of standardized questionnaires were used: State-Trait Anxiety Inventory G Form X2 (STAI), Social Phobia Scale (SPS), Symptom Checklist of Derogatis (SCL-90-R), subscales 'Social Insecurity', 'Depression', 'Anxiety' and 'Phobia', and Hospital Anxiety and Depression Scale (HADS-D). Quality of life was assessed using Skindex. Two analyses were performed. The first analysis included all patients with PFH, the second analysis only patients with PFH who were treated with botulinum toxin A. In the latter group the questionnaires were repeated 2–4 weeks after treatment. Results For the total group at baseline the values for STAI, SCL-90-R, HADS-D and SPS were well within the normal range. However, in the group of patients treated with botulinum toxin A, the mean ± SD SPS score was 17·6 ± 15·5, i.e. above the normal range. Quality of life was impaired, with a mean ± SD Skindex score of 24·3 ± 5·7 at baseline. Treatment with botulinum toxin A led to a significant reduction in all investigated symptoms. Conclusions Despite an impaired quality of life, patients with PFH in general do not show increased symptoms of anxiety, depression or social phobia. Only in the subgroup of patients treated with botulinum toxin A was the SPS increased at baseline. Treatment with botulinum toxin A led to a marked improvement in all factors investigated.
Phase II Trial of Preoperative Chemoradiotherapy Followed by Surgical Resection in Patients With Superior Sulcus Non–Small-Cell Lung Cancers: Report of Japan Clinical Oncology Group Trial 9806
Authors: Hideo Kunitoh, Harubumi Kato, Masahiro Tsuboi, Taro Shibata, Hisao Asamura, Yukito Ichonose, Nobuyuki Katakami, Kanji Nagai, Tetsuya Mitsudomi, Akihide Matsumura, Ken Nakagawa, Hirohito Tada, Nagahiro Saijo
Journal: Journal of Clinical Oncology (2008)

To evaluate the safety and efficacy of preoperative chemoradiotherapy followed by surgical resection for superior sulcus tumors (SSTs).Patients with pathologically documented non-small-cell lung cancer with invasion of the first rib or more superior chest wall were enrolled as eligible; those with distant metastasis, pleural dissemination, and/or mediastinal node involvement were excluded. Patients received two cycles of chemotherapy every 4 weeks as follows; mitomycin 8 mg/m(2) on day 1, vindesine 3 mg/m(2) on days 1 and 8, and cisplatin 80 mg/m(2) on day 1. Radiotherapy directed at the tumor and the ipsilateral supraclavicular nodes was started on day 2 of each course, at the total dose of 45 Gy in 25 fractions, with a 1-week split. Thoracotomy was undertaken 2 to 4 weeks after completion of the chemoradiotherapy. Those with unresectable disease received boost radiotherapy.From May 1999 to November 2002, 76 patients were enrolled, of whom 20 had T4 disease; 75 patients were fully assessable. Chemoradiotherapy was generally well tolerated. Fifty-seven patients (76%) underwent surgical resection, and pathologic complete resection was achieved in 51 patients (68%). There were 12 patients with pathologic complete response. Major postoperative morbidity, including chylothorax, empyema, pneumonitis, adult respiratory distress syndrome, and bleeding, was observed in eight patients. There were three treatment-related deaths, including two deaths owing to postsurgical complications and one death owing to sepsis during chemoradiotherapy. The disease-free and overall survival rates at 3 years were 49% and 61%, respectively; at 5 years, they were 45% and 56%, respectively.This trimodality approach is safe and effective for the treatment of patients with SSTs.
A simplified method for monitoring respiratory impedance during continuous positive airway pressure
Authors: D Navajas, C Duvivier, R Farre, R Peslin
Journal: European Respiratory Journal (2000)

The forced oscillation technique is useful in detecting changes in upper airway obstruction in patients with sleep apnoea undergoing continuous positive airway pressure (CPAP) ventilation. The aim of this study was to implement and evaluate a method for estimating respiratory impedance (Zrs) from the pressure and flow recorded at the inlet of the CPAP tubing. The method is based on correcting impedance measured at the inlet of the CPAP tubing (Zi) for the effect of the tubing and the exhalation port. The method was evaluated in mechanical analogues and in a healthy subject. Sinusoidal oscillation of 5, 10 and 20 Hz were superimposed on CPAP (5-15 cmH2O). At 5 Hz, the changes in airflow obstruction were substantially underestimated by Zi. Furthermore, Zi exhibited a negative dependence on Zrs at 20 Hz. The assessment of Zrs was greatly improved after correcting Zi for the effects of the CPAP tubing and the exhalation port. Zrs was well estimated at low frequencies, reaching very high values during total occlusion (&gt;60 cmH2O x s x L(-1) at 5-10 Hz). These results indicate that changes in airflow obstruction can be detected using the forced oscillation technique from pressure and flow recorded on the continuous positive airway pressure device. This facilitates the clinical application of the forced oscillation technique for monitoring upper airway patency during sleep.
Effect of Topical Vaginal Androgens in a Woman on the Testosterone Levels of Her Sexual Partner With Prostate Cancer
Authors: Mhd Y. Al-Marrawi, Leah V. Cream, Carol A. Mallon, Sheldon Holder, Monika Joshi, Harold H. Harvey, Giampaolo Talamo, Joseph J. Drabick
Journal: Journal of Clinical Oncology (2015)
Splenectomy and chronic thromboembolic pulmonary hypertension
Authors: X Jais
Journal: Thorax (2005)

<b>Background:</b> An increased prevalence of splenectomy has been reported in patients with idiopathic pulmonary arterial hypertension. Examination of small pulmonary arteries from these subjects has revealed multiple thrombotic lesions, suggesting that thrombosis may contribute to this condition. Based on these findings, we hypothesised that splenectomy could be a risk factor for chronic thromboembolic pulmonary hypertension (CTEPH), a condition defined by the absence of thrombus resolution after acute pulmonary embolism that causes sustained obstruction of the pulmonary arteries and subsequent pulmonary hypertension. <b>Methods:</b> The medical history, clinical characteristics, thrombotic risk factors and haemodynamics of 257 patients referred for CTEPH between 1989 and 1999 were reviewed. In a case-control study the prevalence of splenectomy in patients with CTEPH was compared with that of patients evaluated during the same period for idiopathic pulmonary hypertension (n = 276) or for lung transplantation in other chronic pulmonary conditions (n = 180). <b>Results:</b> In patients with CTEPH, 8.6% (95% CI 5.2 to 12.0) had a history of splenectomy compared with 2.5% (95% CI 0.7 to 4.4) and 0.56% (95% CI 0 to 1.6) in cases of idiopathic pulmonary arterial hypertension and other chronic pulmonary conditions, respectively (p&lt;0.01). <b>Conclusion:</b> Splenectomy may be a risk factor for chronic thromboembolic pulmonary hypertension.
Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients
Authors: I. Godoy, A.O. Campana, R.R.C. Geraldo, C.R. Padovani, S.A.R Paiva
Journal: European Respiratory Journal (2003)

Tumour necrosis factor (TNF)‐α has been found to be increased in malnourished chronic obstructive pulmonary disease (COPD) patients; however, the main cause of this phenomenon remains undetermined. In normal subjects, TNF‐α production may be induced by dietary energy deprivation. The aim of this study was to investigate if stable COPD patients present alterations of inflammatory mediators after 48 h of dietary energy restriction. Fourteen COPD patients were admitted to the hospital while receiving an experimental diet with an energy content of approximately one-third of their energy needs. Clinical evaluation, nutritional assessment and serum levels of interleukin (IL)‐6, TNF‐α and C‐reactive protein, and secretion of TNF‐α by peripheral blood monocytes were assessed on admission and after the experimental diet. For reference values of the laboratory parameters, blood was collected from 10 healthy, elderly subjects. COPD patients showed significantly higher serum concentrations of IL‐6 than control subjects, however, the experimental diet was not associated with statistically significant changes in the inflammatory mediators. The findings of this study, although preliminary because of the limited degree and duration of the energy restriction, suggest that the elevated levels of tumour necrosis factor‐α, previously described in undernourished or weight-losing chronic obstructive pulmonary disease patients, may not be linked to a decrease of dietary energy intake.
STROKE/TIA IN PATIENTS WITH PATENT FORAMEN OVALE AND ENDOCARDIAL LEAD DEVICES: DO ECHOCARDIOGRAPHIC VARIABLES PREDICT OUTCOMES?
Authors: Vaibhav Vaidya, Amit Noheria, Christopher DeSimone, Mohammed Shahid, Charles Bruce, Naser Ammash, David Hodge, Joshua Slusser, Paul Friedman
Journal: Journal of the American College of Cardiology (2014)
Metabolic Syndrome
Authors: Kristi Reynolds, Paul Muntner, Vivian Fonseca
Journal: Diabetes Care (2005)

The metabolic syndrome is a cluster of cardiovascular risk factors that is frequently associated with insulin resistance. Although it is synonymous with the “insulin resistance syndrome,” not all patients with the metabolic syndrome will have insulin resistance (1). In 2001, the National Cholesterol Education Program (NCEP) developed operational criteria to make a diagnosis of the metabolic syndrome based on clinical grounds and commonly used laboratory tests that are frequently carried out in an office practice (2). The importance of the metabolic syndrome was further highlighted in 2001 with the approval of an ICD-9 code (277.7) for the metabolic syndrome by the National Center for Health Statistics. Since then, the metabolic syndrome has received considerable attention in the research setting, but its impact in clinical practice is unclear.

In this issue of Diabetes Care , Ford (3) reports that the syndrome is rarely, if ever, recorded as a diagnosis in clinical practice, as assessed from two large national databases. While interesting and important to document, this finding is not surprising for several reasons. First, the analysis was based on data collected in 2002 and 2003, very …
Meralgia paraesthetica--a sports lesion in girl gymnasts.
Authors: J. Macgregor, J. A. Moncur
Journal: British Journal of Sports Medicine (1977)

Investigation into thigh pain in two girl gymnasts has established the likely relationship between the point of impact on the thighs during exercises on the asymmetric bars and mild neuropathy of the lateral femoral cutaenous nerve. The clinical and biomechanical steps taken to elucidate the problem are described. Local infiltration of anaesthetic has confirmed a definitive diagnosis of meralgia paraesthetica in one case.
A role for CD44 in an antigen-induced murine model of pulmonary eosinophilia
Authors: Shigeki Katoh, Nobuhiro Matsumoto, Kumiko Kawakita, Akira Tominaga, Paul W. Kincade, Shigeru Matsukura
Journal: Journal of Clinical Investigation (2003)

Previous studies established that IL-5-producing CD4(+) T cells play a pivotal role in allergic respiratory inflammation. It was also reported that CD4(+) T cells express higher levels of CD44 in the airway than in peripheral blood of patients with allergic respiratory diseases. We have used experimental pulmonary eosinophilia induced in mice by Ascaris suum (Asc) extract to investigate the role of CD44 in the development of allergic respiratory inflammation. Intraperitoneal administration of anti-CD44 mAb prevented both lymphocyte and eosinophil accumulation in the lung. Anti-CD44 mAb also blocked antigen-induced elevation of Th2 cytokines as well as chemokines (CCL11, CCL17) in bronchoalveolar lavage fluid (BALF). Treatment with anti-CD44 mAb inhibited the increased levels of hyaluronic acid (HA) and leukotriene concentrations in BALF that typically result from antigen challenge. Anti-CD44 mAb also blocked antigen-induced airway hyperresponsiveness. An anti-CD44 mAb (IM7) inhibited the HA-binding ability of splenocytes associated with decreased levels of CD44. Soluble CD44 levels in serum were increased in Asc-challenged IM7-treated mice, but not in KM201-treated mice, compared with Asc-challenged rat IgG-treated mice. Ab's that block CD44-HA binding reduced allergic respiratory inflammation by preventing lymphocyte and eosinophil accumulation in the lung. Thus, CD44 may be critical for development of allergic respiratory inflammation.
Cia25 on rat chromosome 12 regulates severity of autoimmune arthritis induced with pristane and with collagen
Authors: M. Brenner, T. Laragione, A. Mello, P. S Gulko
Journal: Annals of the Rheumatic Diseases (2007)

<b>Background:</b> A genomewide scan in a DA×ACI F2 intercross studied for collagen-induced arthritis (CIA) identified the severity quantitative trait locus <i>Cia25</i> on rat chromosome 12. <i>Cia25</i> co-localises with loci regulating several forms of autoimmune diseases in rats, mice and humans, suggesting a common gene. <b>Objective:</b> To characterise the effects of <i>Cia25</i> on severity of arthritis in congenic rats. <b>Methods:</b> DA.ACI(Cia25) congenic rats were constructed according to a genotype-guided strategy, and tested for pristane-induced arthritis (PIA) and CIA, induced with rat type II collagen (CII). A well-established scoring system previously shown to correlate with histological damage, including cartilage and bone erosions, synovial hyperplasia and synovial inflammation, was used. <b>Results:</b> The introgression of ACI alleles at <i>Cia25</i> into DA background, as in DA.ACI(Cia25) rats, was enough to significantly reduce arthritis severity by 60% in PIA and by 40% in CIA, both in males and females compared with DA rats of the same sex. Levels of IgG anti-CII in male DA.ACI(Cia25) rats were 83% lower than in male DA. Levels of anti-CII in females were not affected by the congenic interval. <b>Conclusions:</b><i>Cia25</i> contains a gene that regulates disease severity in two distinct models of autoimmune arthritis. Although both genders were protected in arthritis studies, only male congenic rats had a dramatic reduction in levels of anti-CII, suggesting the possibility of a second arthritis gene in this interval that operates via the regulation of autoantibodies in a sex-specific manner. The identification of the gene(s) accounting for <i>Cia25</i> is expected to generate novel prognostic biomarkers and targets for therapy.
Changes in the anticitrullinated peptide antibody response in relation to therapeutic outcome in early rheumatoid arthritis: results from the SWEFOT trial
Authors: Alf Kastbom, Kristina Forslind, Sofia Ernestam, Pierre Geborek, Johan A Karlsson, Ingemar F Petersson, Saedis Saevarsdottir, Lars Klareskog, Ronald F van Vollenhoven, Karin Lundberg
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objective</h3> To determine the relationship between changes in antibody levels towards citrullinated peptides derived from different candidate autoantigens and therapeutic outcome in early rheumatoid arthritis (RA). <h3>Methods</h3> Baseline and 3-month serum samples from 316 patients with early RA enrolled in the Swedish Farmacotherapy (SWEFOT) trial were analysed for antibodies against cyclic citrullinated peptides (CCP) and citrullinated peptides derived from vimentin (cVim), fibrinogen (cFib) and α-enolase (CEP-1). At 3-month follow-up, methotrexate monotherapy-inadequate responders were randomised to add-on therapy with sulfasalazine and hydroxychloroquine or infliximab. In these patients, anticitrullinated peptide antibodies (ACPA) were also assessed at 12 and 24 months. The proportion of antibody-positive patients and relative changes in antibody levels were compared across ACPA specificities and related to therapeutic response and radiographic progression. <h3>Results</h3> During the 2-year follow-up, the proportion of patients testing positive declined significantly regarding antibodies to cVim, cFib and CEP-1, while anti-CCP antibody occurrence remained stable over time. Turning anti-cVim antibody negative was most common, and anti-cVim antibody seroreversion during the first three months associated with significantly less 2-year radiographic progression compared with patients who remained positive. Median antibody levels of all tested ACPAs declined uniformly during initial methotrexate therapy and following response to add-on therapy, with no significant relation to treatment regimen or radiographic progression. <h3>Conclusions</h3> The influence of early antirheumatic therapy on ACPA seroreversions was markedly different across specificities, and early disappearance of anti-cVim antibodies associated with better radiological outcome. Thus, these data suggest that the disappearance of particular ACPA reactivities may be beneficial in early RA. <h3>Trial registration number</h3> WHO database at the Karolinska institute: CT20080004; and clinicaltrials.gov: NCT00764725.
Quantitative Trait Loci for Blood Pressure Exist Near the IGF-1, the Liddle Syndrome, the Angiotensin II-Receptor Gene and the Renin Loci in Man
Authors: ZSUZSANNA NAGY, ANDREAS BUSJAHN, SYLVIA BÄHRING, HANS-DIETER FAULHABER, HANS-RÜDIGER GOHLKE, HANS KNOBLAUCH, MAGDA ROSENTHAL, BERTRAM MÜLLER-MYHSOK, HERBERT SCHUSTER, FRIEDRICH C. LUFT
Journal: Journal of the American Society of Nephrology (1999)

Abstract. Blood pressure (BP) is heritable and finding quantitative trait loci that influence BP is an important step in identifying genes responsible for BP regulation. Sixty-six pairs of dizygotic (DZ) twin subjects and their parents were used in a sib-pair analysis to look for linkage of selected candidate genes to the quantitative trait BP. Microsatellite markers were tested in the vicinity of the gene loci for insulin-like growth factor-1 (IGF-1), Liddle syndrome, autosomal-dominant hypertension with brachydactyly, angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, renin, and lipoprotein lipase. BP was measured in a standardized manner. Heart size was determined echocardiographically. Significant linkage was found at the IGF-1, Liddle syndrome, and AT 1 receptor gene for systolic BP. Linkage for diastolic BP was found at the autosomal-dominant hypertension with brachydactyly locus. Both systolic and diastolic BP were linked to the renin gene locus. The linkage was most consistent for the IGF-1 gene locus and systolic BP. Linkage was also found between the IGF-1 gene locus and posterior cardiac wall thickness, septal thickness, and left ventricular mass index. It is suggested that these quantitative trait loci may be important for the subsequent detection of allelic variants for elevated BP. Furthermore, these results linking the IGF-1 gene locus to both BP and cardiac dimensions underscore the importance of the IGF-1 gene as a candidate gene for cardiovascular disease.
Eltrombopag for the treatment of children with persistent and chronic immune thrombocytopenia (PETIT): a randomised, multicentre, placebo-controlled study
Authors: James B Bussel, Purificación Garcia de Miguel, Jenny M Despotovic, John D Grainger, Julián Sevilla, Victor S Blanchette, Lakshmanan Krishnamurti, Philip Connor, Michèle David, Koh B Boayue, Dana C Matthews, Michele P Lambert, Lisa M Marcello, Malini Iyengar, Geoffrey W Chan, Karen D Chagin, Dickens Theodore, Christine K Bailey, Kalpana K Bakshi
Journal: The Lancet Haematology (2015)
Familial aggregation and heritability of adult lung function: results from the Busselton Health Study
Authors: L.J. Palmer, M.W. Knuiman, M.L. Divitini, P.R. Burton, A.L. James, H.C. Bartholomew, G. Ryan, A.W. Musk
Journal: European Respiratory Journal (2001)

Decreased spirometric indices are characteristic of asthma and other respiratory diseases. The aim of this study was to investigate the genetic and environmental components of variance of forced expiratory volume in one second (FEV 1 ) and forced vital capacity (FVC) measured in adulthood in an Australian population-based sample of 468 Caucasian nuclear families. The inter-relationships of the genetic determinants of these traits with asthma and atopic rhinitis were also investigated. Serial cross-sectional studies were conducted in the town of Busselton in Western Australia between 1966 and 1981 and follow-up of previous attendees was undertaken in 1995. Data from each subject included in this study were from a single survey in adulthood (25–60 yrs of age) when the subject was as close to age 45 yrs as possible. Multivariate analysis suggested that FEV 1 and FVC levels were associated with age, sex, height, tobacco smoke exposure, asthma and atopic rhinitis. After adjustment for relevant covariates, FEV 1 levels had a narrow-sense heritability ( h 2 N ) of 38.9% (SE 9.1 %). FVC levels had an h 2 N of 40.6% (SE 8.9%). Extended modelling demonstrated little overlap in the genetic determinants of asthma or atopic rhinitis and either FEV 1 or FVC levels. The results of this study were consistent with the existence of important genetic determinants of adult lung function that are independent of asthma or other atopic disease, cigarette smoking, height, age or sex.
Functional, Molecular, and Biochemical Characterization of Streptozotocin-Induced Diabetes
Authors: DONALD T. WARD, S. KAM YAU, ANDREW P. MEE, E. BARBARA MAWER, CHRISTOPHER A. MILLER, HUGH O. GARLAND, DANIELA RICCARDI
Journal: Journal of the American Society of Nephrology (2001)

Abstract. Altered divalent cation homeostasis with bone mineral loss, hypercalciuria, and hypomagnesemia have been associated consistently with human diabetes mellitus. This study investigated functional, molecular, and biochemical determinants that accompany this condition in chronically (2 wk) streptozotocin (STZ)-diabetic rats. Catheterized, conscious, diabetic rats on servo-controlled fluid replacement exhibited an increased GFR (+70%) and a substantially raised urinary calcium output (+568%) when compared with control rats. In addition, fractional calcium reabsorption was reduced, indicating that the hypercalciuria was not due solely to an osmotic effect but may involve an actual tubular defect. The expression of proteins involved in renal distal Ca 2+ and water transport in STZ-diabetic rats were then studied by Western analysis and immunofluorescence microscopy to investigate the molecular basis of the hypercalciuria. Extracellular Ca 2+ -sensing receptor abundance was reduced to 52% of control in STZ-diabetes, whereas thiazide-sensitive NaCl cotransporter expression was increased by 192%. Subcutaneous insulin implant rectified both functional and molecular parameters. The levels of calbindin D 28k , plasma membrane Ca 2+ ATPase, and aquaporin 1 in whole kidney and of aquaporin 2 in inner medulla were unchanged in diabetic and/or insulin replacement. Blood levels of 1,25(OH) 2 D 3 were reduced in diabetes as were levels of osteocalcin, a marker of bone formation. It is concluded that diabetic hypercalciuria in rats involves elevated GFR with raised urinary output, reduced Ca 2+ reabsorption, and impaired bone deposition. Changes in Ca 2+ -sensing receptor and NaCl cotransporter protein expression could account for the altered divalent cation homeostasis seen during diabetes mellitus.