tbuckley/cabot-search huggingface dataset:
Survival Advantage for Adult Hispanic Hemodialysis Patients? Findings from the End-Stage Renal Disease Clinical Performance Measures Project
Authors: Diane L Frankenfield, Michael V Rocco, Sheila H Roman, William M McClellan
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. One-year follow-up mortality in Hispanic and non-Hispanic patients and its association with intermediate outcomes of dialytic care were examined utilizing the Center for Medicare &amp; Medicaid Services' (CMS) ESRD Clinical Performance Measures (CPM) Project and administrative data. Demographic and clinical information was collected on a national random sample of adult in-center hemodialysis (HD) patients for the period of October through December, 1998. Patients were categorized as Hispanic, non-Hispanic White, or non-Hispanic Black. Of 8336 patients 994 (12%) were identified as Hispanic, 3618 (43%) as non-Hispanic White, and 3111 (37%) as non-Hispanic Black. The adjusted 12-mo mortality risk (99% CI) for Hispanics was 0.76 (0.60 to 0.96; <i>P</i> &lt; 0.01) and for non-Hispanic Blacks 0.66 (0.56 to 0.78, <i>P</i> &lt; 0.001) compared with non-Hispanic Whites (referent). Similar 12-mo mortality risks were noted in the groups with diabetes mellitus or hypertension as the causes of ESRD and among patients ≥65 yr. After controlling for demographic and geographic variables, Hispanics compared with the referent group, non-Hispanic Whites, were more likely to have a mean serum albumin ≥4.0/3.7 g/dL (BCG/BCP) (1.5 [1.2 to 1.7]; <i>P</i> &lt; 0.001) and as likely to have a mean Kt/V ≥1.2, mean hemoglobin ≥11 g/dL, and an arteriovenous fistula as their vascular access. These data suggest that adult Hispanic HD patients have a 12-mo survival intermediate to non-Hispanic Blacks and non-Hispanic Whites and experience equivalent or better intermediate outcomes of dialytic care compared with non-Hispanic Whites. E-mail: dfrankenfield@cms.hhs.gov
Psychiatric Disorder and Separation From Military Service: A 10-Year Retrospective Study
Authors: Mark Creamer
Journal: American Journal of Psychiatry (2006)

Objective: This study investigated the association between the onset of psychiatric morbidity and separation from military service over a 10-year period (1991–2001). Method: The prevalence of affective, anxiety, somatic, and substance use disorders was assessed in 2,215 male Australian Navy personnel with the Composite International Diagnostic Interview. Results: The onset of a psychiatric disorder during military service was related to a 19% greater risk of separation overall. The majority of those leaving military service did so in the first year after symptom onset. Personnel who remained in service past this period had no significantly elevated risk of separation in subsequent years. Conclusions: Psychiatric morbidity represents a significant potential cost to defense forces. Improved recognition and early management of mental health problems among military personnel may improve retention rates.
Lateral hypothalamic lesions and norepinephrine turnover in rats.
Authors: T Yoshida, J W Kemnitz, G A Bray
Journal: Journal of Clinical Investigation (1983)

Animals with lateral hypothalamic lesions lost significantly more weight in the 18 h following this lesion than did sham-operated animals or rats with cerebral cortical lesions deprived of food for the same time period. In the acutely fasted sham-operated animals the turnover of norepinephrine in interscapular brown adipose tissue, heart, and pancreas was slowed but in fasted rats with lateral hypothalamic lesions norepinephrine turnover rates were three- to ninefold faster in all three organs. Exposure to the cold (4 degrees C) significantly increased norepinephrine turnover in the interscapular brown adipose tissue, heart, and pancreas of fasted sham-operated rats, but did not further increase the rate of turnover in lateral hypothalamic-lesioned rats. Rats with lesions in the cerebral cortex responded in a fashion similar to that of the sham-operated animals. Gastric erosions and microhemorrhagic gastric mucosa were observed in five of six acutely fasted rats with lateral hypothalamic lesions whereas all sham-operated rats had a normal appearance of the stomach lining. Animals with lateral hypothalamic lesions made 3 wk earlier also showed an increased rate of norepinephrine turnover in the interscapular brown adipose tissue, heart, and pancreas following an 18 h fast. Rats with bilateral lesions in the paraventricular region of the hypothalamus, however, responded similarly to sham-operated animals with a reduction in the turnover in norepinephrine with fasting and an increase in norepinephrine turnover rate after cold exposure even with fasting. These data suggest that lateral hypothalamic lesions produce an acute increase in turnover of norepinephrine, and that this increased turnover persists for up to 3 wk.
Detection of c-Ki-ras Mutation by PCR/RFLP Analysis and Diagnosis of Pancreatic Adenocarcinomas
Authors: T. Urban, S. Ricci, J.-D. Grange, R. Lacave, F. Boudghene, F. Breittmayer, O. Languille, J. Roland, J.-F. Bernaudin
Journal: JNCI Journal of the National Cancer Institute (1993)

The c-Ki-ras oncogene (also known as KRAS2) is activated by point mutations involving codon 12 in 72%-100% of primary pancreatic adenocarcinomas, but the gene is not activated in nonneoplastic tissues. Therefore, the detection of c-Ki-ras mutations can facilitate the diagnosis of pancreatic adenocarcinomas, which are not always identified with current tests. Detection is usually performed by oligonucleotide hybridization combined with polymerase chain reaction (PCR), RNAse mismatch cleavage assay, or non-isotopic mismatched PCR, methods that are not feasible for routine screening of large numbers of samples because they are time consuming and/or expensive.Our purpose was to evaluate a rapid, non-radioactive method of detection of a mutation in codon 12 of the c-Ki-ras gene in pancreatic tumor samples obtained by fine-needle aspiration for diagnostic screening.Twenty consecutive patients (15 with pancreatic adenocarcinoma, one with pancreatic cystadenocarcinoma, one with endocrine islet cell tumor, and three with chronic pancreatitis) were selected for this study. A sample of pancreatic tissue from each patient with a tumor or pancreatitis was obtained and evaluated by fine-needle aspiration biopsy under computerized tomography scan or ultrasound guidance using a two-needle coaxial technique. Pancreatic DNA from each of these samples was evaluated by PCR amplification and restriction fragment length polymorphism (RFLP) analysis with nucleotide substitution in PCR primers, creating BstNI restriction patterns that distinguished mutated from normal alleles. The accuracy of the PCR/RFLP assay was validated with DNA from SW480 and HT29 colonic carcinoma cell lines with known mutated and wild-type c-Ki-ras gene sequences. Sensitivity was tested with a series of titration experiments.PCR/RFLP analysis can detect a mutation present in 1% of cells. No amplification could be performed in four (20%) samples because of the absence of cells in the aspirated sample. In the 16 samples adequate for PCR/RFLP analysis, a c-Ki-ras gene mutation was detected in 11 (92%) of 12 adenocarcinomas. Overall, diagnosis was obtained by pathologic (cytomorphologic) examination alone in 13 samples (81%). The presence of malignant cells and/or mutated c-Ki-ras gene was detected in 12 of 12 adenocarcinomas but not in chronic pancreatitis or islet cell tumor.Screening of pancreatic tissue samples obtained by fine-needle aspiration for c-Ki-ras mutation using PCR/RFLP analysis combined with pathologic examination could facilitate diagnosis of pancreatic tumors.
Randomized Trial of Fenretinide to Prevent Second Breast Malignancy in Women With Early Breast Cancer
Authors: U. Veronesi, G. De Palo, E. Marubini, A. Costa, F. Formelli, L. Mariani, A. Decensi, T. Camerini, M. R. Del Turco, M. G. Di Mauro, M. G. Muraca, M. Del Vecchio, C. Pinto, G. D'Aiuto, C. Boni, T. Campa, A. Magni, R. Miceli, M. Perloff, W. F. Malone, M. B. Sporn
Journal: JNCI Journal of the National Cancer Institute (1999)

BACKGROUND: Fenretinide, a vitamin A analogue, has been shown to inhibit breast carcinogenesis in preclinical studies. We determined the efficacy of fenretinide in preventing a second breast malignancy in women with breast cancer. METHODS: We randomly assigned 2972 women, aged 30-70 years, with surgically removed stage I breast cancer or ductal carcinoma in situ to receive for 5 years either fenretinide orally (200 mg/day) or no treatment. The primary end point was the incidence of contralateral breast cancer or ipsilateral breast cancer 7 years after randomization. Other end points considered post hoc were the same outcomes stratified by menopausal status, incidence of distant metastases, overall mortality, and tumors in other organs. The hazards of breast cancer occurrence were determined by Cox proportional hazards regression analysis. Statistical tests were two-sided. RESULTS: At a median observation time of 97 months, there were no statistically significant differences in the occurrence of contralateral breast cancer (P = .642) or ipsilateral breast cancer (P = .177) between the two arms. However, an interaction was detected between fenretinide treatment and menopausal status in both outcomes (P for interaction in both outcomes = .045), with a possible beneficial effect in premenopausal women (contralateral breast cancer: adjusted hazard ratio [HR] = 0.66, and 95% confidence interval [ CI] = 0.41-1.07; ipsilateral breast cancer: adjusted HR = 0.65, and 95% CI = 0.46-0.92) and an opposite effect in postmenopausal women (contralateral breast cancer: adjusted HR = 1.32, and 95% CI = 0.82-2.15; ipsilateral breast cancer: adjusted HR = 1.19, and 95% CI = 0.75-1.89). There were no statistically significant differences between the two arms in tumors in other organs, incidence of distant metastasis, and all-cause mortality. CONCLUSIONS: Fenretinide treatment of women with breast cancer for 5 years appears to have no statistically significant effect on the incidence of second breast malignancies overall, although a possible benefit was detected in premenopausal women. These studies, particularly the post hoc analyses, are considered exploratory and need to be confirmed.
Brief Overview of Preclinical and Clinical Studies in the Development of Intraperitoneal Radioimmunotherapy for Ovarian Cancer
Authors: Ruby F. Meredith, Donald J. Buchsbaum, Ronald D. Alvarez, Albert F. LoBuglio
Journal: Clinical Cancer Research (2007)

Abstract Due to the generally slow and incomplete transit of i.p. infused agents into the circulation, treating disease confined to the peritoneal cavity with chemotherapy, biologics, and/or radionuclides provides a pharmacologic advantage. A higher i.p. concentration can be achieved than could be tolerated by systemic administration. An advantage of i.p. versus i.v. administration for localization of radiolabeled antibodies to small peritoneal surface disease has been shown in animal model and human biopsy studies (1, 2). A recent phase III Gynecologic Oncology Group chemotherapy trial has confirmed a survival advantage for i.p. delivery among women undergoing initial therapy for advanced ovarian cancer (3). Although the therapy was more difficult to tolerate such that 60% of patients randomized to the i.p. arm did not complete the entire regimen, there was a 16-month survival advantage. I.p. radionuclide therapy has been used in treatment of ovarian cancer for more than three decades, but side effects have been problematic in non–tumor-targeted 32P therapy (4). Efforts to improve specificity have used a number of antigens expressed on ovarian cancer cells as targets for selective delivery of radionuclide-conjugates. Mouse models and cell culture have been prominent for preclinical study of agents and strategies in the development of i.p. targeted radionuclide therapy for ovarian cancer. Animal studies, which have directed clinical trials, have shown clear improvement in survival with various modifications including combination chemotherapy, pretargeting, and combination of antibodies over simply delivery of a radiolabeled antibody via i.p. route.
The Nongenomic Actions of Aldosterone
Authors: John W. Funder
Journal: Endocrine Reviews (2005)

Aldosterone has physiological effects to regulate fluid and electrolyte homeostasis across epithelia and proinflammatory effects on a variety of nonepithelial cells in the context of inappropriate salt status. These effects are mediated by mineralocorticoid receptors, members of a large family of nuclear transcription factors, by DNA-directed, RNA-mediated protein synthesis. Rapid effects of aldosterone, insensitive to actinomycin D or cycloheximide and thus clearly nongenomic, have been convincingly documented in a variety of epithelial and nonepithelial tissues. Despite strenuous attempts, isolation of a nonclassical membrane receptor for aldosterone has proven unsuccessful, and rapid nongenomic effects mediated by classical mineralocorticoid receptors are increasingly recognized in the kidney, heart, and vascular wall. The mechanism of rapid nongenomic actions of aldosterone may vary between tissues in terms of pathways; in addition, what remains to be established is the physiological role of aldosterone action via such rapid nongenomic mechanisms and how they might synergize with the longer time course genomic actions of mineralocorticoids.
Numerical, morphological and phenotypic changes in Langerhans cells in the course of murine graft-versus-host disease
Authors: K. Asagoe, K. Takahashi, T. Yoshino, E. Kondo, R. Tanaka, J. Arata, T. Akagi
Journal: British Journal of Dermatology (2001)

In the course of graft-versus-host disease (GVHD) or diseases that histologically mimic GVHD (e.g. toxic epidermal necrolysis, Stevens-Johnson syndrome), it is known that epidermal Langerhans cells (LCs) are depleted from the epidermis. However, the mechanism and significance of LC depletion is not well known.To investigate the numerical, morphological and phenotypic changes in LCs and apoptosis of LCs in the course of GVHD using a non-irradiated mouse GVHD model.BALB/c nu/nu mice and C57BL/6 mice were used as recipients and donors, respectively. Recipient mice were injected with T-cell-enriched donor spleen cells. Skin samples were harvested at various times after the inoculation. The numerical and morphological changes were examined by an immunofluorescence study of epidermal sheets. Apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling method and flow cytometric analysis using annexin V. Phenotypic change was studied by flow cytometric analysis of epidermal cell suspensions. The mixed epidermal cell lymphocyte reaction (MELR) was performed to examine functional changes in the epidermal cells.Five days after inoculation, a graft-versus-host reaction occurred. Epidermal LCs began to decrease from the sixth day. On the fifth day, the LCs became larger and had prominent dendrites. Immediately before the LCs began to decrease, many LCs became round in shape, with scanty dendrites. LC apoptosis was not observed in the epidermis either on the fifth or seventh day. Phenotypically, the expression of CD40, CD80, CD86 and major histocompatibility complex class II antigen on the LCs was upregulated on the fifth and seventh day. Epidermal cells from GVHD mice showed an increased allostimulatory capacity in the secondary MELR.These results suggest that at early GVHD onset, most LCs may not undergo apoptosis in the epidermis but are phenotypically activated, resulting in further activation of alloreactive T cells and aggravation of the disease.
Circulating tumor DNA as an early marker of therapeutic response in patients with metastatic colorectal cancer
Authors: J. Tie, I. Kinde, Y. Wang, H.L. Wong, J. Roebert, M. Christie, M. Tacey, R. Wong, M. Singh, C.S. Karapetis, J. Desai, B. Tran, R.L. Strausberg, L.A. Diaz, N. Papadopoulos, K.W. Kinzler, B. Vogelstein, P. Gibbs
Journal: Annals of Oncology (2015)
Sedation and analgesia practices in neonatal intensive care units (EUROPAIN): results from a prospective cohort study
Authors: Ricardo Carbajal, Mats Eriksson, Emilie Courtois, Elaine Boyle, Alejandro Avila-Alvarez, Randi Dovland Andersen, Kosmas Sarafidis, Tarja Polkki, Cristina Matos, Paola Lago, Thalia Papadouri, Simon Attard Montalto, Mari-Liis Ilmoja, Sinno Simons, Rasa Tameliene, Bart van Overmeire, Angelika Berger, Anna Dobrzanska, Michael Schroth, Lena Bergqvist, Hugo Lagercrantz, Kanwaljeet J S Anand
Journal: The Lancet Respiratory Medicine (2015)
Cell-free circulating DNA in Hodgkin's and non-Hodgkin's lymphomas
Authors: S. Hohaus, M. Giachelia, G. Massini, G. Mansueto, B. Vannata, V. Bozzoli, M. Criscuolo, F. D'Alò, M. Martini, L.M. Larocca, M.T. Voso, G. Leone
Journal: Annals of Oncology (2009)
Human cytolytic cell clones lacking surface expression of T cell receptor alpha/beta or gamma/delta. Evidence that surface structures other than CD3 or CD2 molecules are required for signal transduction.
Authors: G Pantaleo, M R Zocchi, S Ferrini, A Poggi, G Tambussi, C Bottino, L Moretta, A Moretta
Journal: The Journal of Experimental Medicine (1988)

We have analyzed the transmembrane signaling operating in human cytolytic lymphocytes lacking surface expression of the CD3/TCR complex. Peripheral blood lymphocytes were fractionated into CD3+ and CD3- on the FACS and cloned under limiting conditions in the presence of PHA and IL-2. Approximately 90% CD3+ and 10% CD3- cells underwent clonal expansion. Clones obtained from the CD3- fraction belonged to two main phenotypic groups: CD2+ CD7+ and CD2- CD7+. Several clones were expanded and analyzed for surface phenotype and function. All of the five clones selected for detailed analysis did not express CD4, CD8, and CD28 antigens and did not release IL-2, whereas they displayed cytolytic activity against NK-sensitive, NK-resistant, and fresh tumor target cells. After stimulation with anti-CD2 mAbs or PHA a rapid increase in [Ca2+]i was detected in CD3- CD2+ CD7+ clones. This increment was caused by the release of Ca2+ from intracellular stores and by the influx from the extracellular compartment. Signaling in response to PHA did not appear to be dependent upon surface expression of CD2 molecules since antibody-induced modulation of CD2 did not prevent PHA-induced signal transduction. Similarly, in CD3- CD2- CD7+ clones [Ca2+]i increments and inositol phosphate formation occurred after stimulation with PHA. These data indicate that the functional PHA-binding structures, expressed in both groups of CD3- clones, are distinct from CD3/TCR complex and CD2 molecules.
Response to Comment on: Saisho et al. β-Cell Mass and Turnover in Humans: Effects of Obesity and Aging. Diabetes Care 2013;36:111–117
Authors: Yoshifumi Saisho, Alexandra E. Butler, Erica Manesso, Peter C. Butler
Journal: Diabetes Care (2013)

We thank Gargani et al. (1) for their interest in our article reporting β-cell mass in age-matched obese ( n = 61) and lean ( n = 53) human pancreas samples. In that study, we reported an ∼50% greater β-cell mass (0.8 to 1.2 g) in obese humans compared with lean humans (2). We acknowledged that our study was cross-sectional and so we could provide no time course for the difference we reported. In the interesting report that Gargani et al. direct us to, we note their approach to the question of human islet adaptation to dietary insulin resistance. They implanted 400 human islet equivalents under the renal capsule in immunodeficient mice and then …
Renin Concentration of Normotensive and Hypertensive Dog Kidney
Authors: Herman E. Schmid, Leonard Graham, Betsy B. Brennan, George E. Wakerlin
Journal: Circulation Research (1962)

This report relates blood pressure, serum antirenin titer, and renal renin concentration in normotensive, acute and chronic experimental renal hypertensive, and spontaneous hypertensive dogs sacrificed at different levels of neutralizing antibody (antirenin) produced by injections of hog kidney extracts containing renin. Sufficient levels of antirenin can prevent or lower the blood pressure elevations secondary to partial constriction of the renal arteries in the dog. A highly significant relationship and correlation was found between increasing titer of antirenin and renal renin concentrations in both normotensive and hypertensive dogs. Two dogs not developing antirenin, although injected for many months with hog renins, did not have a renal renin concentration above control level. Goats treated with hog renin developed high antirenin titers but did not have an increase in renal renin. The goat differs from the dog, as does the monkey and man, in that antirenin produced from hog or dog renins does not neutralize the endogenous renin of the animal. It is concluded that the increase in renal renin found in these experiments is related directly to the presence of antirenin which is capable of neutralizing the endogenous renin of the experimental animal.
Transfection With a Dominant-Negative Inhibitor of Monocyte Chemoattractant Protein-1 Gene Improves Cardiac Function After 6 Hours of Cold Preservation
Authors: Noriyoshi Kajihara, Shigeki Morita, Takahiro Nishida, Hideki Tatewaki, Masataka Eto, Kensuke Egashira, Hisataka Yasui
Journal: Circulation (2003)

Background— Monocyte chemoattractant protein-1 (MCP-1), a potent chemotactic factor for monocytes, is induced during ischemia-reperfusion. As monocytes might play an important causative role in reperfusion injury, we investigated if inhibition of monocyte activation could attenuate ischemia-reperfusion injury and thereby improve cardiac preservation. To inhibit monocyte activation, we transfected a dominant-negative inhibitor of MCP-1 (7ND) gene in an animal model. Methods and Results— We used an isolated rabbit heart preparation perfused with support-rabbit blood and transfected 7ND genes to skeletal muscle of the support rabbits (n=7) using electroporation technique; causing an elevation of serum 7ND level to 20±7 pg/mL at 5 days after transfection. Animals receiving empty plasmid served as controls (n=7). Five days after transfection, hearts from other rabbits were excised, stored in UW solution for 6hours, and perfused with blood from transfected support rabbits. The 7ND group showed better cardiac output (128.7±17.9 versus 81.6±19.8 mL/min; P &lt;0.01), lower serum CK-MB levels (5.0±1.8 versus 11.1±2.9 ng/mL; P &lt;0.01), lower serum IL-1β levels (257.2±23.2 versus 311.2±37.4pg/mL; P &lt;0.05), and lower serum TNF-α levels (19.0±8.4 versus 35.1±13.0pg/mL; P &lt;0.05). The numbers of infiltrating cells in myocardium were significantly reduced in the 7ND group. Conclusions— Inhibition of MCP-1 with 7ND gene transfection reduced cytokine activation, attenuated myocardial damage, and improved cardiac function after 6 hours of preservation. These results show that MCP-1 plays an important role in ischemia-reperfusion injury.