tbuckley/cabot-search huggingface dataset:
Birth Weight and Creatinine Clearance in Young Adult Twins
Authors: Marij Gielen, Sara-Joan Pinto-Sietsma, Maurice P Zeegers, Ruth J Loos, Robert Fagard, Peter W de Leeuw, Gaston Beunen, Catherine Derom, Robert Vlietinck
Journal: Journal of the American Society of Nephrology (2005)

Previous studies have shown that low birth weight (LBW) is a risk factor for renal impairment in adult life. The effects of LBW and renal function were studied by using twins, which allows distinguishing among fetoplacental, maternal, and genetic influences. Perinatal data were obtained at birth, and absolute creatinine clearance (not corrected for body surface area) was measured at a mean age of 25.6 yr in 653 individuals. Twins were considered both as individuals and as members of twin pairs. Statistical analyses were performed with and without adjusting for gestational age, zygosity, gender, age, body mass index, glucose level, BP, and smoking status. Creatinine clearance was 4 ml/min lower in twins with LBW (<2500 g) than in twins with a high birth weight (P < 0.04, adjusted). Intrapair birth weight difference correlated positively with the intrapair difference in creatinine clearance equally in monozygotic and dizygotic twins (r = 0.35, P < 0.0001; r = 0.43, P < 0.0001, respectively). This suggests that fetoplacental factors are related to renal function and that genetic factors are less important. There was no significant difference in creatinine clearance between twins who both had LBW as compared with twins who both had a high birth weight. This may suggest that maternal factors, which influence the relation between LBW and renal function, are less important. LBW is related to a lower creatinine clearance at adult age. This relationship is probably due to fetoplacental factors. Surprising, genetic and maternal factors seem less important.
Discrepancies Between Catheter Tip and Tissue Temperature in Cooled-Tip Ablation
Authors: G. Keith Bruce, T. Jared Bunch, Mark A. Milton, Alvaro Sarabanda, Susan B. Johnson, Douglas L. Packer
Journal: Circulation (2005)

Background— It is not known whether catheter tip temperatures with a cooled-tip ablation can be reliably extrapolated to estimate actual tissue temperatures. The relationship between catheter tip temperatures, tissue temperatures, power, and microbubble formation is not known. Methods and Results— Nine dogs underwent 111 radiofrequency energy deliveries at the pulmonary vein ostia with a cooled-tip catheter. Catheter tip and tissue temperatures were markedly discrepant. Catheter tip temperature plateaus at 36°C to 39°C with increasing power, whereas tissue temperature increases to a mean of 75±3°C at 45 W (maximum temperature &gt;100°C). Seventy-two energy deliveries were performed, titrating power to microbubble formation guided by intracardiac echocardiography. Type I and II microbubble formation occurred in 45 (63%) and 19 (26%) ablations, respectively. Type I microbubble emergence occurred at lower powers (21±8 versus 26±4 W; P =0.05), catheter tip temperatures (38±5°C versus 48±10°C; P =0.02), and tissue temperatures (65±19°C versus 81±9°C; P &lt;0.001) than type II microbubble formation. Maximum impedance decreases during ablation before microbubble formation were less with type I microbubble (20±9 versus 37±11 Ω; P &lt;0.001) compared with type II microbubbles. One quarter of type I microbubbles abruptly transitioned to type II microbubbles with significant changes in power or catheter tip temperature. No microbubbles were seen in 19 ablations (26%) despite powers up to 26±9 W and tissue temperatures up to 81±17°C. Conclusions— Catheter tip and tissue temperatures are markedly discrepant during cooled-tip ablation. Type I and II microbubble formation occurs at overlapping power and catheter tip and tissue temperature ranges. Neither the absence of microbubbles nor the presence of type I microbubble formation ensures against excessive tissue heating. The appearance of microbubbles may indicate possible tissue overheating and signal a need to decrease energy.
A CASE OF CARDIAC ASTHMA
Authors: C. Wilson
Journal: BMJ (1913)

this tinme wvithotit anyv rigors.The uteruis througlhouit this attack appeared (quite normal.The temperature again fell, but rose olnce more on the twenty-second day.Pyelitis (B.coli).I lhad examinied the uirine regularly every otlher day, anid found othlinlg amiss save a considerable quantitv of utrates; the acetone had gradually diminished, and was by inow scarcely to be (letected.At this stage, htowever, a turbid deposit appeared, after solution of urates, whiclh under the microscope was fotuni(d to consist of pus wvith a few gran-ular casts; a catlheter specimen'was-drawn off into a sterile bottle, and from the pus ai pure cuilture of B..coli was obtained.The. patienit was given uirotropine and bland fluids, and it was hIolped that the condlition would turn out to be pure pyelitis an(l not pyelonephritis; this was, fortunately, the case, despite thie lprsencc of casts, aind though there was a further relapse on the thirt--third dav the temperature settled down for good on thte thirty-sixth; three weeks later the urine was com- pletelv free from pus or albumen.The patient is now in good lhealth and steadily recovering her normal vigour.
The role of 3D structure and protein conformation on the innate and adaptive immune responses to silk-based biomaterials
Authors: Maumita Bhattacharjee, Elke Schultz-Thater, Emanuele Trella, Sylvie Miot, Sanskrita Das, Marko Loparic, Alok R. Ray, Ivan Martin, Giulio C. Spagnoli, Sourabh Ghosh
Journal: Biomaterials (2013)
Postmenopausal hormone therapy and asthma onset in the E3N cohort
Authors: I. Romieu, A. Fabre, A. Fournier, F. Kauffmann, R. Varraso, S. Mesrine, B. Leynaert, F. Clavel-Chapelon
Journal: Thorax (2010)

<h3>Background</h3> Epidemiological studies have suggested that female hormones might play a role in asthma and that menopausal hormone therapy (MHT or hormone replacement therapy (HRT)) might increase the risk of asthma in postmenopausal women. The only prospective study addressing this issue reports an increase in the risk of developing asthma which was similar for oestrogen alone and oestrogen/progestagen treatment. <h3>Methods</h3> The association between the use of different types of MHT and the risk of asthma onset in postmenopausal women was investigated prospectively from 1990 to 2002 by biennial questionnaires as part of the French E3N cohort study. Asthma onset was considered to be the time of medical diagnosis of asthma cases occurring during the follow-up of women who were asthma free at baseline. Cox proportional hazards models were used, adjusting for potential confounding factors. <h3>Results</h3> Among 57 664 women free of asthma at menopause, 569 incident cases of asthma were identified during 495 448 years of follow-up. MHT was related to an increased risk of asthma onset (HR=1.20, 95% CI 0.98 to 1.46) among recent users. The increase in risk of asthma onset was only significant among women reporting the use of oestrogen alone (HR=1.54, 95% CI 1.13 to 2.09) particularly in never smokers (HR=1.80, 95% CI 1.15 to 2.80) and women reporting allergic disease prior to asthma onset (HR=1.86, 95% CI 1.18 to 2.93). A small increase in the risk of asthma onset associated with the use of oestrogen/progestagen was also observed in these subgroups. <h3>Conclusion</h3> Postmenopausal use of oestrogen alone was associated with an increased rate of newly diagnosed asthma in menopausal women.
The sleeping brain and the neural basis of emotions
Authors: Roumen Kirov, Serge Brand, Vasil Kolev, Juliana Yordanova
Journal: Behavioral and Brain Sciences (2012)

Abstract In addition to active wake, emotions are generated and experienced in a variety of functionally different states such as those of sleep, during which external stimulation and cognitive control are lacking. The neural basis of emotions can be specified by regarding the multitude of emotion-related brain states, as well as the distinct neuro- and psychodynamic stages (generation and regulation) of emotional experience.
Ceramide accumulation during oxidant renal tubular injury
Authors: R A Zager, D S Conrad, K Burkhart
Journal: Journal of the American Society of Nephrology (1998)

Ceramide is an important signaling molecule that is typically generated via sphingomyelinase (SMase)-mediated sphingomyelin (SM) hydrolysis. Although diverse forms of renal injury elicit ceramide accumulation, the molecular determinants of this change and its contribution to tissue damage are poorly defined. The present study uses iron (Fe/hydroxyquinoline)-mediated injury of cultured human proximal tubular (HK-2) cells to gain additional insights into these issues. A 4-h Fe exposure doubled ceramide levels in the absence of cell death. This was independent of de novo synthesis, since ceramide synthase inhibition (with fumonisin B1) had no effect. Oxidant stress directly suppressed, rather than stimulated, SMase activity by: (1) decreasing SMase levels; (2) depleting SMase-stimulating glutathione; and (3) increasing SM resistance to SMase attack. Fe suppressed cell sphingosine levels (3 to 4 times ceramide/sphingosine ratio increments), suggesting a possible ceramidase block. Fe did not directly affect HK-2 ceramidase levels. However, arachidonic acid (C20:4) accumulation, a consequence of oxidant-induced phospholipase A2 (PLA2) activation, markedly suppressed ceramidase and stimulated SMase activity. Exogenous C20:4, as well as PLA2 (in doses simulating Fe-induced deacylation) recapitulated Fe's ceramide-generating effect. Because C20:4 is directly cytotoxic, it was hypothesized that ceramide might offset some of C20:4's adverse effects. Supporting this possibility were the following: (1) C20:4 exacerbated Fe toxicity; (2) this was abrogated by ceramide treatment; and (3) ceramide blunted Fe-mediated cell death. Conclusions: (1) ceramide accumulation during acute cell injury can be an adaptive response to PLA2 activation/C20:4 generation; (2) C20:4-induced ceramidase inhibition, coupled with SMase stimulation, may trigger this result; and (3) these ceramide increments may exert a "biostat" function, helping to offset C20:4/PLA2- and "catalytic" iron-mediated tubular cell death.
CD59 protects glomerular endothelial cells from immune-mediated thrombotic microangiopathy in rats.
Authors: M Nangaku, C E Alpers, J Pippin, S J Shankland, K Kurokawa, S Adler, B P Morgan, R J Johnson, W G Couser
Journal: Journal of the American Society of Nephrology (1998)

CD59 is a cell membrane-bound complement regulatory protein on glomerular cells that inhibits C5b-9 assembly and insertion. This report describes a recently developed model of immune thrombotic microangiopathy (TMA) induced by the renal artery perfusion of anti-glomerular endothelial cell (anti-GEN) antibody. To examine the role of CD59 in protecting the GEN from immune-mediated injury, rats underwent selective renal artery perfusion with F(ab')2 fragments of anti-CD59 monoclonal antibody to block CD59 activity or control mouse IgG followed by anti-GEN antibody or control goat IgG. Neutralization of CD59 in normal rats did not result in any significant functional or histologic changes. Perfusion with anti-CD59 did not change deposition of the pathogenic anti-GEN IgG used to induce the TMA model. However, neutralization of CD59 in the TMA model resulted in more C5b-9 formation in glomeruli, accompanied by increased platelet and fibrin deposition, more severe endothelial injury, and reduced renal function compared with the animals perfused with control F(ab')2 fragments. These results demonstrate directly that CD59 serves a protective role for GEN in this TMA model of rats, and confirm that C5b-9 formation has a critical pathogenic role in the mediation of the disease. CD59 may play an important role in protecting glomerular endothelium from other complement-mediated types of injury.
Measurement of Serum Levels of Macrophage Inhibitory Cytokine 1 Combined with Prostate-Specific Antigen Improves Prostate Cancer Diagnosis
Authors: David A. Brown, Carsten Stephan, Robyn L. Ward, Mathew Law, Mark Hunter, Asne R. Bauskin, Janaki Amin, Klaus Jung, Eleftherios P. Diamandis, Garret M. Hampton, Pamela J. Russell, Graham G. Giles, Samuel N. Breit
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Current serum testing for the detection of prostate cancer (PCa) lacks specificity. On diagnosis, the optimal therapeutic pathway is not clear and tools for adequate risk assessment of localized PCa progression are not available. This leads to a significant number of men having unnecessary diagnostic biopsies and surgery. A search for novel tumor markers identified macrophage inhibitory cytokine 1 (MIC-1) as a potentially useful marker. Follow-up studies revealed MIC-1 overexpression in local and metastatic PCa whereas peritumoral interstitial staining for MIC-1 identified lower-grade tumors destined for recurrence. Consequently, we sought to assess serum MIC-1 measurement as a diagnostic tool. Experimental Design: Using immunoassay determination of serum MIC-1 concentration in 1,000 men, 538 of whom had PCa, we defined the relationship of MIC-1 to disease variables. A diagnostic algorithm (MIC-PSA score) based on serum levels of MIC-1, total serum prostate-specific antigen, and percentage of free prostate-specific antigen was developed. Results: Serum MIC-1 was found to be an independent predictor of the presence of PCa and tumors with a Gleason sum ≥7. We validated the MIC-PSA score in a separate population and showed an improved specificity for diagnostic blood testing for PCa over percentage of free prostate-specific antigen, potentially reducing unnecessary biopsies by 27%. Conclusions: Serum MIC-1 is an independent marker of the presence of PCa and tumors with a Gleason sum of ≥7. The use of serum MIC-1 significantly increases diagnostic specificity and may be a future tool in the management of PCa.
Phase III Trial of Two Versus Four Additional Cycles in Patients Who Are Nonprogressive After Two Cycles of Platinum-Based Chemotherapy in Non–Small-Cell Lung Cancer
Authors: Joon Oh Park, Sang-We Kim, Jin Seok Ahn, Cheolwon Suh, Jung Shin Lee, Joung Soon Jang, Eun Kyung Cho, Sung Hyun Yang, Jin-Hyuk Choi, Dae Seog Heo, Suk Young Park, Sang Won Shin, Myung Ju Ahn, Jong Seok Lee, Young Ho Yun, Jae-Won Lee, Keunchil Park
Journal: Journal of Clinical Oncology (2007)

Purpose This trial was conducted to determine the optimal duration of chemotherapy in Korean patients with advanced non–small-cell lung cancer (NSCLC). Patients and Methods Patients with stages IIIB to IV NSCLC who had not progressed after two cycles of chemotherapy were randomly assigned to receive either four (arm A) or two (arm B) more cycles of third-generation, platinum-doublet treatment. Results Of the 452 enrolled patients, 314 were randomly assigned to the groups. One-year survival rates were 59.0% in arm A and 62.4% in arm B, and the difference of 3.4% (95% CI, −8.0 to 4.8) met the predefined criteria for noninferiority. The median time to progression (TTP), however, was 6.2 months (95% CI, 5.7 to 6.7 months) in arm A and 4.6 months (95% CI, 4.4 to 4.8 months) in arm B, the difference of which is statistically significant (P = .001). The frequencies of hematologic and nonhematologic toxicities were similar in the two arms. Conclusion This study confirms the noninferiority of overall survival with four cycles compared with six cycles of chemotherapy for the first-line treatment of advanced NSCLC and supports the current American Society of Clinical Oncology guidelines. Notably, patients receiving six cycles of chemotherapy compared with four cycles showed a favorable TTP, suggesting that further investigation of the new strategies of maintenance therapy with less toxic agents after three to four cycles of induction chemotherapy might be warranted to improve survival, with consideration of both ethnicity and pharmacogenomic signatures.
IgG and IgM anti-snRNP reactivity in sequentially obtained serum samples from patients with connective tissue diseases.
Authors: U Nyman, I Lundberg, E Hedfors, M Wahren, I Pettersson
Journal: Annals of the Rheumatic Diseases (1992)

Sequentially obtained serum samples from 30 patients with connective tissue disease positive for antibody to ribonucleoprotein (RNP) were examined to determine the specificities of IgG and IgM antibodies to snRNP during the disease course using immunoblotting of nuclear extracts. The antibody patterns were correlated with disease activity. The patterns of antibody to snRNP of individual patients were mainly stable during the study but changes in levels of antibody to snRNP were seen corresponding to changes in clinical activity. These results indicate that increased reactivity of serum IgM antibodies against the B/B' proteins seems to precede a clinically evident exacerbation of disease whereas IgG antibody reactivity to the 70 K protein peaks at the time of a disease flare.
SIDE EFFECTS OF SYSTEMIC ADRENAL STEROTD THERAPY. *
Authors: B. E. C. NORDTN
Journal: British Journal of Dermatology (1960)

Journal Article SIDE EFFECTS OF SYSTEMIC ADRENAL STEROTD THERAPY. Get access B. E. C. NORDTN, M.D., M.R.C.P. B. E. C. NORDTN, M.D., M.R.C.P. Lecturer in Medicine, University of Glasgow, Gardiner Institute, Western Infirmary, Glasgow, W.I Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 72, Issue 1, 1 January 1960, Pages 40–47, https://doi.org/10.1111/j.1365-2133.1960.tb13812.x Published: 01 January 1960
Delayed Neutrophil Elastase Inhibition Prevents Subsequent Progression of Acute Lung Injury Induced by Endotoxin Inhalation in Hamsters
Authors: KAZUHITO KAWABATA, TETSUYA HAGIO, SHIGERU MATSUMOTO, SHINTARO NAKAO, SHINICHIRO ORITA, YOSHIYA AZE, HIROYUKI OHNO
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

To define the role of neutrophil elastase (NE) in the progression of acute lung injury (ALI), we examined the effects of post-treatment with a specific NE inhibitor, sivelestat sodium hydrate (sivelestat), on ALI induced by endotoxin (ET) inhalation in hamsters. Inhalation of ET (300 microg/ml, 30 min) in conscious hamsters increased inflammatory cell count, protein concentration, and hemorrhage in bronchoalveolar lavage fluid (BALF) that peaked 24 h after ET inhalation. These changes were significant 2 h after ET inhalation and paralleled the increase in NE activity in BALF. When intravenously infused from 2 to 24 h post-ET inhalation, sivelestat (0.03 to 3 mg/kg/h) dose-dependently attenuated changes in these BALF parameters at 24 h post-ET inhalation in a manner dependent on the inhibition of NE activity in BALF. Histopathological analysis also indicated that sivelestat prevented the progression of lung inflammation such as alveolar neutrophil infiltration and hemorrhage. In contrast, dexamethasone (3 mg/kg, intravenously) was not effective in this model when administered 2 h after ET inhalation, although it was highly effective when applied before ET. We conclude that delayed inhibition of NE activity with sivelestat prevents subsequent progression of ALI in hamsters after ET inhalation. Thus NE may play an important role in the progression of ALI.
The Agents of Biological Warfare
Authors: LTC Peter Vogel
Journal: JAMA (1997)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Preoperative Chemoradiotherapy for Esophageal or Junctional Cancer
Authors: P. van Hagen, M.C.C.M. Hulshof, J.J.B. van Lanschot, E.W. Steyerberg, M.I. van Berge Henegouwen, B.P.L. Wijnhoven, D.J. Richel, G.A.P. Nieuwenhuijzen, G.A.P. Hospers, J.J. Bonenkamp, M.A. Cuesta, R.J.B. Blaisse, O.R.C. Busch, F.J.W. ten Kate, G.-J. Creemers, C.J.A. Punt, J.T.M. Plukker, H.M.W. Verheul, E.J. Spillenaar Bilgen, H. van Dekken, M.J.C. van der Sangen, T. Rozema, K. Biermann, J.C. Beukema, A.H.M. Piet, C.M. van Rij, J.G. Reinders, H.W. Tilanus, A. van der Gaast
Journal: New England Journal of Medicine (2012)

The role of neoadjuvant chemoradiotherapy in the treatment of patients with esophageal or esophagogastric-junction cancer is not well established. We compared chemoradiotherapy followed by surgery with surgery alone in this patient population.
Impaired Tamoxifen Metabolism Reduces Survival in Familial Breast Cancer Patients
Authors: William G. Newman, Kristen D. Hadfield, Ayshe Latif, Stephen A. Roberts, Andrew Shenton, Christopher McHague, Fiona Lalloo, Sacha Howell, D. Gareth Evans
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Tamoxifen has been the mainstay adjuvant hormonal treatment for breast cancer for many years. Conversion of tamoxifen to its active metabolite, endoxifen, is reduced by low activity of the cytochrome P450 enzyme, CYP2D6. We examined the effect of reduced CYP2D6 activity on the response to tamoxifen in patients with familial early-onset breast cancer. Experimental Design: We conducted a case note review and genotyping for the CYP2D6*3, CYP2D6*4, CYP2D6*5, and CYP2D6*41 alleles in 115 patients (47 BRCA1, 68 BRCA2) with familial breast cancer who had been treated with 20-mg tamoxifen following surgery. Results: Eight (7%) individuals had genotypes consistent with poor metabolizer status, and 4 (3.5%) individuals took CYP2D6 inhibitor drugs concomitant with their tamoxifen and were also considered poor metabolizer. Time to tumor recurrence, disease-free survival, and overall survival were reduced in the patient group with poor metabolizer CYP2D6 activity. However, a significant effect was confined to patients with BRCA2 mutations with a worse overall survival (median survival, 7 versus 28 years; P = 0.008; adjusted hazard ratio, 9.7). Conclusions: Poor metabolizer status for CYP2D6 predicts worse overall survival in patients with familial breast cancer. Therefore, CYP2D6 inhibitor drugs should not be prescribed concomitantly with tamoxifen. Prospective studies should be undertaken to establish the effect of CYP2D6 status on outcome in familial breast cancer patients treated with tamoxifen.
A history of smoking is inversely correlated with the incidence of gemcitabine-induced neutropenia
Authors: M. Kanai, S. Morita, S. Matsumoto, T. Nishimura, E. Hatano, S. Yazumi, T. Sasaki, H. Yasuda, T. Kitano, A. Misawa, H. Ishiguro, K. Yanagihara, I. Ikai, R. Doi, M. Fukushima
Journal: Annals of Oncology (2009)