tbuckley/cabot-search huggingface dataset:
Have Transurethral Resections Contributed to the Increasing Incidence of Prostatic Cancer?
Authors: Richard K. Severson
Journal: JNCI Journal of the National Cancer Institute (1990)

Journal Article Have Transurethral Resections Contributed to the Increasing Incidence of Prostatic Cancer? Get access Richard K. Severson Richard K. Severson Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 82, Issue 20, 17 October 1990, Pages 1597–1599, https://doi.org/10.1093/jnci/82.20.1597 Published: 17 October 1990 Article history Received: 11 September 1990 Accepted: 12 September 1990 Published: 17 October 1990
Clustering of Risk Factors in Parents of Patients With Type 1 Diabetes and Nephropathy
Authors: Lena M. Thorn, Carol Forsblom, Johan Fagerudd, Kim Pettersson-Fernholm, Riika Kilpikari, Per-Henrik Groop
Journal: Diabetes Care (2007)

OBJECTIVE—To assess the impact of parental risk factors for diabetic nephropathy. RESEARCH DESIGN AND METHODS—This cross-sectional study included 2,355 type 1 diabetic patients from the FinnDiane (Finnish Diabetic Nephropathy) study. Diabetic nephropathy was defined as macroalbuminuria (urinary albumin excretion rate &amp;gt;200 μg/min or &amp;gt;300 mg/24 h) or end-stage renal disease. Information was available from 4,676 parents. Parental scores were calculated based on the number of various traits in the parents. RESULTS—Patients with diabetic nephropathy, compared with those without diabetic nephropathy, had a higher prevalence of maternal (41 vs. 35%, P = 0.046) and parental (62 vs. 55%, P = 0.044) hypertension, maternal stroke (7.6 vs. 5.1%, P = 0.044), and maternal (1.4 vs. 0.7%, P = 0.058) and parental (4.3 vs. 2.9%, P = 0.030) type 1 diabetes. If both, compared with none, of the parents had hypertension, the adjusted odds ratio (OR) for diabetic nephropathy in offspring was 1.56 (95% CI 1.13–2.15). The adjusted OR for diabetic nephropathy was 2.13 (1.36–3.33) for the parental hypertension–diabetes score (3–4 vs. 0 points) and 2.13 (1.37–3.33) for the parental hypertension–cardiovascular disease (CVD)–diabetes score (4–6 vs. 0 points). Fathers of patients with diabetic nephropathy, compared with those without diabetic nephropathy, had reduced overall survival (log-rank P = 0.04) and reduced cardiovascular survival (log-rank P = 0.03). CONCLUSIONS—A cluster of parental hypertension, CVD, and diabetes is associated with diabetic nephropathy in type 1 diabetes, as is paternal mortality.
Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration
Authors: Masato Murakami, Chiara Francavilla, Ilaria Torselli, Monica Corada, Luigi Maddaluno, Antonio Sica, Gianluca Matteoli, Iliyan Dimitrov Iliev, Alberto Mantovani, Maria Rescigno, Ugo Cavallaro, Elisabetta Dejana
Journal: Cancer Research (2010)

Abstract Junctional adhesion molecule-A (JAM-A)–null dendritic cells (DCs) are more motile and effective than their wild-type counterpart in promoting contact hypersensitivity reaction. Here, we show that the growth and aggressiveness of pancreatic islet cell carcinoma induced by SV40 T antigen expression in β cells (Rip1Tag2 mice) are significantly reduced in JAM-A–null mice. Because these tumor cells do not express JAM-A, we focused on changes in stroma reactivity. In the absence of JAM-A, tumors showed a small but significant reduction in angiogenesis and a marked increase in the immune reaction with enhanced infiltration of DCs (CD11c+ and MHC-II+) and CD4+ and CD8+ lymphocytes. In contrast, phagocyte number was not affected. DC capacity to produce cytokines was not significantly altered, but transmigration through JAM-A–null endothelial cells was increased as compared with JAM-A–positive endothelium. On adoptive transfer, JAM-A−/− DCs were recruited to tumors at slightly but significantly higher rate than JAM-A+/+ DCs. Ablation of CD4+ and CD8+ cells with specific antibodies abrogated the inhibitory effect of JAM-A deletion on tumor growth and angiogenesis. These findings support the idea that, in the Rip1Tag2 tumor model, abrogation of JAM-A reduces cancer development by increasing antitumor immune response. Cancer Res; 70(5); 1759–65
Skin temperature changes induced by UV irradiation at 254 nm and 300 nm
Authors: A. V. J. CHALLONER, R. E. WOODROUGH
Journal: British Journal of Dermatology (1978)

Skin temperatures 24 h after irradiation at both 254 and 300 nm have been examined using the technique of thermography. Increases in skin temperature have been recorded at both wavelengths but the magnitude of these differences after 254 nm irradiation is influenced by the ambient temperature. The apparent disagreement between two groups of observers working in the field of UV erythema may well have been explained.
Endothelial Dysfunction and Oxidative Stress During Estrogen Deficiency in Spontaneously Hypertensive Rats
Authors: Sven Wassmann, Anselm T. Bäumer, Kerstin Strehlow, Martin van Eickels, Christian Grohé, Katja Ahlbory, Renate Rösen, Michael Böhm, Georg Nickenig
Journal: Circulation (2001)

Background —Postmenopausal estrogen deficiency is associated with an increased cardiovascular risk, hypertension, and oxidative stress. Angiotensin type 1 (AT 1 ) receptor regulation is involved in the pathogenesis of atherosclerosis. To characterize vascular function, oxidative stress, and AT 1 receptor regulation during estrogen deficiency, ovariectomized spontaneously hypertensive rats (SHR) were investigated in comparison with sham-operated animals and with ovariectomized rats receiving estrogen replacement therapy with 17β-estradiol. Methods and Results —Arterial blood pressure was similar in all 3 groups investigated. Five weeks after ovariectomy, endothelial dysfunction in aortic rings was observed, which was reversed by estrogen replacement therapy. Estrogen deficiency led to an enhanced vasoconstriction by angiotensin II. Vascular superoxide production was significantly increased compared with that in sham-operated rats, as measured by lucigenin chemiluminescence assays. Estrogen substitution normalized the production of free radicals in the vessel wall. Vascular AT 1 receptor expression was significantly upregulated by estrogen deficiency, as shown by quantitative reverse transcription–polymerase chain reaction, whereas endothelial NO synthase mRNA expression and NO release were unchanged. Five-week treatment of the animals with the AT 1 receptor antagonist irbesartan prevented endothelial dysfunction in ovariectomized rats and normalized the vascular production of free radicals. Conclusions —In SHR, estrogen deficiency leads to increased vascular free radical production and enhanced angiotensin II–induced vasoconstriction via increased vascular AT 1 receptor expression, resulting in endothelial dysfunction. Estrogen replacement therapy and AT 1 receptor antagonism prevent these pathological changes. Therefore, estrogen deficiency–induced AT 1 receptor overexpression and oxidative stress may play an important role in cardiovascular diseases associated with menopause.
Development of a risk adjustment mortality model using the American College of Cardiology–National Cardiovascular Data Registry (ACC–NCDR) experience: 1998–2000
Authors: Richard E Shaw, H.Vernon Anderson, Ralph G Brindis, Ronald J Krone, Lloyd W Klein, Charles R McKay, Peter C Block, Leslee J Shaw, Kathleen Hewitt, William S Weintraub
Journal: Journal of the American College of Cardiology (2002)
Reduced Dose and Intermittent Treatment with Lapatinib and Trastuzumab for Potent Blockade of the HER Pathway in HER2/<i>neu</i>-Overexpressing Breast Tumor Xenografts
Authors: Mothaffar F. Rimawi, Lisa S. Wiechmann, Yen-Chao Wang, Catherine Huang, Ilenia Migliaccio, Meng-Fen Wu, Carolina Gutierrez, Susan G. Hilsenbeck, Grazia Arpino, Suleiman Massarweh, Robin Ward, Robert Soliz, C. Kent Osborne, Rachel Schiff
Journal: Clinical Cancer Research (2010)

We have shown that incomplete blockade of the human epidermal growth factor (HER) pathway is a mechanism of resistance to treatment with trastuzumab (T) in HER2-overexpressing tumor xenografts. We now investigate whether the addition of lapatinib (L), a dual HER1/2 kinase inhibitor, to T results in more potent inhibition of the pathway and therefore inhibition of tumor growth, and whether reduced dose and intermittent treatment with the combination is equally effective.Nude mice bearing HER2-overexpressing MCF7/HER2-18 or BT-474 xenograft tumors were treated with L and T, alone or in various combinations with other HER inhibitors. L + T for short duration (14 and 42 days), intermittent administration (14 days on/off), and reduced dosing (half dose) was also investigated. Inhibition of tumor growth, downstream signaling, proliferation, and induction of apoptosis were assessed. All statistical tests were two-sided.L + T was the most effective regimen in both MCF7/HER2-18 and BT-474 xenografts with complete regression (CR) of tumor observed in all mice. Intermittent and reduced dose treatment (½ dose) resulted in high rates of CR and low rates of tumor recurrence that were comparable to full dose continuous treatment. L + T resulted in significantly reduced downstream signaling and proliferation, and increased apoptosis.L + T is a potent and effective combination even when given in reduced dose or intermittent schedule potentially resulting in lower toxicity and reduced cost if translated to patients. These findings warrant timely clinical testing.
Hand bone densitometry: a more sensitive standard for the assessment of early bone damage in rheumatoid arthritis
Authors: G. Haugeberg, M. J Green, P. G Conaghan, M. Quinn, R. Wakefield, S. M Proudman, S. Stewart, E. Hensor, P. Emery
Journal: Annals of the Rheumatic Diseases (2007)

<h3>Objective:</h3> To examine the role of hand dual-energy <i>x</i> ray absorptiometry (DEXA) compared with radiography in the assessment of bone involvement in patients with early rheumatoid arthritis (RA) who have active disease. <h3>Methods:</h3> The study population (n = 79) had RA of &lt;12 months’ duration and were selected for poor prognostic features. Clinical data and bone mineral density (BMD) data were collected at baseline, 24 and 48 weeks. Hand radiographs were performed at baseline and 48 weeks. Bone damage analyses were performed for the group and individuals using the smallest detectable change (SDC) method. <h3>Results:</h3> At baseline, mean disease duration was 8.5 months, erythrocyte sedimentation rate was 34.3 mm/hour, C-reactive protein was 40.2 mg/l, Health Assessment Questionnaire score was 1.35 and 81% of patients were positive for rheumatoid factor. Mean (95% CI) hand BMD loss was 2.5% (−3.5 to −1.5) at 24 weeks and 2.6% (−3.8 to −1.5) at 48 weeks. Individual hand bone loss exceeding the SDC was seen in 46.8% at 24 weeks and in 58.2% at 48 weeks. In the subgroup of 58 patients who had undergone radiography, radiographic joint damage score evaluated by the Sharp–van der Heijde method increased from 4.8 to 10.6 (p = 0.001). Individual hand bone loss in this subgroup exceeding the SDC was seen in 50.0% at 24 weeks and in 56.9% at 48 weeks, whereas at 48 weeks only 22.4% had deteriorated in modified Sharp score. <h3>Conclusion:</h3> The study results indicate that hand DEXA is a more sensitive tool than radiology (radiographic joint-damage scores), for measuring disease-related bone damage in early RA.
Acute changes in arginine vasopressin, sweat, urine and serum sodium concentrations in exercising humans: does a coordinated homeostatic relationship exist?
Authors: T Hew-Butler, T D Noakes, S J Soldin, J G Verbalis
Journal: British Journal of Sports Medicine (2008)

The parallel response of sweat rate and urine production to changes in plasma osmolality and volume support a role for arginine vasopressin (AVP) as the main endocrine regulator of both excretions. A maximal test to exhaustion and a steady-state run on a motorised treadmill were both completed by 10 moderately trained runners, 1 week apart. Sweat, urine and serum sodium concentrations ([Na + ]) were evaluated in association with the plasma concentrations of cytokines, neurohypophyseal and natriuretic peptides, and adrenal steroid hormones. When data from both the high-intensity and steady-state runs were combined, significant linear correlations were noted between: sweat [Na + ] versus postexercise urine [Na + ] (r=0.80; p&lt;0.001), postexercise serum [Na + ] versus both postexercise urine [Na + ] (r=0.56; p&lt;0.05) and sweat [Na + ] (r=0.64; p&lt;0.01) and postexercise urine [Na + ] versus postexercise plasma arginine vasopressin concentration ([AVP] P ) (r=0.48; p&lt;0.05). A significant positive correlation was noted between postexercise [AVP] P and sweat [Na + ] during the steady-state condition only (r=0.66; p&lt;0.05). These correlations suggest that changes in serum [Na + ] during exercise may evoke corresponding changes in sweat and urine [Na + ], which are likely regulated coordinately by changes in [AVP] P to preserve body fluid homeostasis.
Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in cancer promotion.
Authors: W R Adey
Journal: Environmental Health Perspectives (1990)

Studies of environmental electromagnetic (EM) field interactions in tissues have contributed to a new understanding of both normal growth and the biology of cancer in cell growth. From cancer research comes a floodtide of new knowledge about the disruption of communication by cancer-promoting chemicals with an onset of unregulated growth. Bioelectromagnetic research reveals clear evidence of joint actions at cell membranes of chemical cancer promoters and environmental electromagnetic fields. The union of these two disciplines has resulted in the first major new approach to tumor formation in 75 years, directing attention to dysfunctions in inward and outward streams of signals at cell membranes, rather than to damage DNA in cell nuclei, and to synergic actions of chemical pollutants and environmental electromagnetic fields. We are witnesses and, in great measure, participants in one of the great revolutions in the history of biology. In little more than a century, we have moved from organs, to tissues, to cells, and finally to the molecules that are the elegant fabric of living tissues. Today, we stand at a new frontier. It may be more difficult to comprehend, but it is far more significant; for it is at the atomic level, rather than the molecular, that physical, rather than chemical, processes appear to shape the flow of signals that are at the essence of living matter. To pursue these problems in the environment and in the laboratory, our needs for further research with appropriate budgets are great.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma Carotenoids and Recurrence-Free Survival in Women With a History of Breast Cancer
Authors: Cheryl L. Rock, Shirley W. Flatt, Loki Natarajan, Cynthia A. Thomson, Wayne A. Bardwell, Vicky A. Newman, Kathy A. Hollenbach, Lovell Jones, Bette J. Caan, John P. Pierce
Journal: Journal of Clinical Oncology (2005)

Purpose Previous studies suggest that diet may affect recurrence or survival rates in women who have been diagnosed with breast cancer. The purpose of this study was to examine the relationship between plasma carotenoid concentration, as a biomarker of vegetable and fruit intake, and risk for a new breast cancer event in a cohort of women with a history of early-stage breast cancer. Methods Participants were 1,551 women previously treated for breast cancer who were randomly assigned to the control arm of a diet intervention trial between March 1995 and November 2000. Outcome events were probed during semiannual interviews and verified by medical record review. During the period under study, 205 women had a recurrence or new primary breast cancer. Plasma carotenoid concentrations were measured in baseline blood samples. Hazard ratios (HR) and 95% CIs by quartiles of plasma carotenoids were computed, controlling for tumor stage, grade, and hormone receptor status; chemotherapy and tamoxifen therapy; clinical site; age at diagnosis; body mass index; and plasma cholesterol concentration. Results Women in the highest quartile of plasma total carotenoid concentration had significantly reduced risk for a new breast cancer event (HR, 0.57; 95% CI, 0.37 to 0.89), controlled for covariates influencing breast cancer prognosis. Conclusion Plasma carotenoids are a biologic marker of intake of vegetables and fruit, so this observation supports findings from previous studies that have linked increased vegetable and fruit intake with greater likelihood of recurrence-free survival in women who have been diagnosed with early-stage breast cancer.
Reply: Fibrosis in liver as a predictive marker for hepatitis C virus therapy
Authors: Salvatore Petta, Antonio Craxì
Journal: Hepatology (2010)

We thank Dr. Altınbas and colleagues for their interest in our recent article.1 They pointed out that in our study population fibrosis was not a driver of low sustained virological response (SVR) as in other studies. We are fully aware that advanced fibrosis and cirrhosis in particular strongly affect the likelihood of SVR, as shown also in a large-scale study.2 We have in fact included in our study a cohort of consecutive patients with a histological diagnosis of genotype 1 chronic hepatitis C and a low prevalence of cirrhosis (less than 10%) because at our center patients with clinical evidence of cirrhosis are excluded from biopsy according to current guidelines.3 Hence, the small number of subjects with cirrhosis in our study does not allow us to point out the inverse relationship between fibrosis and SVR. In contrast, the absence of a major factor of unresponsiveness, such as severe fibrosis, allowed us to explore in this highly homogeneous cohort of patients with genotype 1 chronic hepatitis C the impact on SVR of metabolic factors, such as steatosis, and vitamin D, a promising mediator of liver damage and immune response modulation. The lack of an association in our study between SVR and age, sex, and body mass index, also underlined by Altınbas and colleagues, is likely due to differences in demographic, anthropometric, biochemical, and histological features. Accordingly, all these negative predictors have not been identified together in phase III trials of pegylated interferon and ribavirin,4-6 probably because of heterogeneity in the enrolled populations. Salvatore Petta*, Antonio Craxì*, * Operating Unit of Gastroenterology, University of Palermo, Palermo, Italy.
Induction of Cyclooxygenase-2 and Activation of Nuclear Factor-κB in Myocardium of Patients With Congestive Heart Failure
Authors: Samuel C. Y. Wong, Mitsumasa Fukuchi, Peter Melnyk, Ian Rodger, Adel Giaid
Journal: Circulation (1998)

Chronic heart failure is associated with induction of secondary inflammatory mediators, including prostanoids. The latter exert diverse functional and morphological effects on cardiac myocytes. Induction of cyclooxygenase (COX), the enzyme responsible for generating prostanoids, requires activation of nuclear factor-kappaB (NF-kappaB). The aim of the present study was to determine the expression of COX-2 and activation of NF-kappaB in the failing human heart.Myocardial tissue from 27 patients with end-stage heart failure (various etiologies: ischemic heart disease, n=16; idiopathic dilated cardiomyopathy, n=10; and valvular heart disease, n=1), 2 septic patients, and 8 normal control subjects was immunostained with antisera to COX-2 and NF-kappaB. Western blotting was performed and showed high anti-COX-2 antibody specificity and the presence of COX-2 protein in the sample tissues. In situ hybridization and immunohistochemistry showed little or no expression of COX-2 and NF-kappaB in the control hearts. In contrast, there was abundant expression of COX-2 mRNA and protein in myocytes and inflammatory cells in areas of fibrotic scar compared with regions of normal morphology in all cases of heart failure, except the cases with sepsis, which showed an abundance of COX-2 throughout the myocardium. Sites of NF-kappaB activation were associated with those of COX-2 expression.We demonstrate induction of COX-2 and activation of NF-kappaB in the myocardium of failing human hearts. Induction of both molecules appears to be associated with the presence of inflammation and scar formation.
Effect of Pravastatin on Loss of Renal Function in People with Moderate Chronic Renal Insufficiency and Cardiovascular Disease
Authors: Marcello Tonelli, Lemuel Moyé, Frank M. Sacks, Thom Cole, Gary C. Curhan
Journal: Journal of the American Society of Nephrology (2003)

Limited data suggest that HMG-CoA reductase inhibitors (statins) may slow loss of renal function in individuals with chronic renal insufficiency. This study was conducted to determine whether pravastatin reduced rates of loss of renal function in people with moderate chronic renal insufficiency. This was a post hoc subgroup analysis of a randomized double-blind placebo controlled trial. Data were analyzed from the CARE study (a randomized trial of pravastatin versus placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol < 240 mg/dl). Participants with estimated GFR (MDRD-GFR) < 60 ml/min per 1.73 m(2) body surface area at baseline were considered to have moderate chronic renal insufficiency. Multivariate regression was used to calculate rates of decline in MDRD-GFR for individuals receiving pravastatin and placebo, controlling for prospectively determined covariates that might influence rates of renal function loss. Change in renal function could be calculated in 3384 individuals, of whom 690 (20.4%) had MDRD-GFR < 60 ml/min per 1.73 m(2) and were eligible for inclusion. Among all individuals with MDRD-GFR < 60 ml/min per 1.73 m(2)), the MDRD-GFR decline in the pravastatin group was not significantly different from that in the placebo group (0.1 ml/min per 1.73 m(2)/yr slower; 95% CI, -0.2 to 0.4; P = 0.49). However, there was a significant stepwise inverse relation between MDRD-GFR before treatment and slowing of renal function loss with pravastatin use, with more benefit in those with lower MDRD-GFR at baseline (P = 0.04). Rate of change in MDRD-GFR in the pravastatin group was 0.6 ml/min per 1.73 m(2)/yr slower than placebo (95% CI, -0.1 to 1.2; P = 0.07) in those with MDRD-GFR < 50 ml/min, and 2.5 ml/min per 1.73 m(2)/yr slower (95% CI, 1.4 to 3.6 slower; P = 0.0001) in those with MDRD-GFR < 40 ml/min per 1.73 m(2)/yr. Pravastatin also reduced rates of renal loss to a greater extent in participants with than without proteinuria at baseline (P = 0.006). It is concluded that pravastatin may slow renal function loss in individuals with moderate to severe kidney disease, especially those with proteinuria. These findings require confirmation by a large randomized trial conducted specifically in people with chronic renal insufficiency.