tbuckley/cabot-search huggingface dataset:
Adjustment for Comorbidity in Studies on Health Status in ESRD Patients
Authors: Jeannette G. van Manen, Johanna C. Korevaar, Friedo W. Dekker, Elisabeth W. Boeschoten, Patrick M. M. Bossuyt, Raymond T. Krediet
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. Health status can be an important outcome in studies on patients with end-stage renal disease (ESRD). In these studies, adjustment for prognostic factors, such as comorbidity, often has to be made. None of the comorbidity indices that are commonly used in research on ESRD patients has been validated for studies on health status. This study evaluated three existing indices (Khan, Davies, and Charlson) and four indices specifically developed for use in studies on health status. In a large prospective multi-center study (NECOSAD-2), new ESRD patients were included (<i>n</i> = 1041). Comorbidity was assessed at the start of dialysis. Health status was assessed with the physical and mental component summary score of the SF-36 (PCS and MCS), the symptoms dimension of the KDQOL-SF, and the Karnofsky Scale. Patient data were randomly allocated to a modeling or a testing set. The new indices were developed in the modeling set. The three existing indices explained about the same percentage of variance in the PCS (7 to 8%), MCS (1 to 3%), symptoms (2 to 4%), and Karnofsky (10 to 12%). The new indices performed better than the existing indices in the modeling population (13% PCS, 10% MCS, 10% symptoms, 18% Karnofsky), but not in the testing population (8% PCS, 1% MCS, 3% symptoms, 8% Karnofsky). Individual comorbidities explained more variance in PCS (10 to 15%), MCS (1 to 7%), symptoms (6 to 11%), and Karnofsky (11 to 18%) than comorbidity indices. The Khan, Davies, and the Charlson indices will adjust to the same extent for the potential confounding effect of comorbidity in studies with health status as an outcome. Separate comorbidity diagnoses will adjust best for comorbidity. E-mail: j.g.vanmanen@amc.uva.nl
Mitochondrial DNA variation and genetic structure in populations of Drosophila melanogaster.
Authors: L R Hale, R S Singh
Journal: Molecular Biology and Evolution (1987)

The understanding of the genetic structure of a species can be improved by considering together data from different types of genetic markers. In the past, a number of worldwide populations of Drosophila melanogaster have been extensively studied for several such markers, including allozymes, chromosomal inversions, and quantitative characters. Here we present results from a study of restriction-fragment-length polymorphisms of mitochondrial DNA (mtDNA) in 92 isofemale lines from many of the same geographic populations of D. melanogaster. Eleven restriction enzymes were used, of which four revealed restriction-site polymorphism. A total of 24 different haplotypes were observed, of which 18 were unique to single populations. In many populations, the unique haplotypes have reached high frequency without being observed in neighboring populations. A Wagner parsimony tree reveals that mutationally close variants show geographical clumping, suggesting local differentiation of mtDNA in populations. The Old-World and the New-World populations are differentiated, with the predominant Old-World haplotype being virtually absent from the New World. These results contrast with those for the nuclear genes, in which many loci show parallel clines in different continents, and suggest a common origin of D. melanogaster populations in North America.
Relaxin Expression From Tumor-Targeting Adenoviruses and Its Intratumoral Spread, Apoptosis Induction, and Efficacy
Authors: Joo-Hang Kim, Young-Sook Lee, Hoguen Kim, Jing-Hua Huang, A-Rum Yoon, Chae-Ok Yun
Journal: JNCI Journal of the National Cancer Institute (2006)

The use of oncolytic adenoviruses as cancer gene therapy is limited by their uneven penetration and distribution in tumors. We investigated whether the expression of the cell matrix-degradative protein relaxin by adenovirus could improve adenovirus distribution and penetration in tumors.We generated relaxin-expressing, replication-incompetent (dl-lacZ-RLX) and -competent (Ad-deltaE1B-RLX) adenoviruses by inserting a relaxin gene into the E3 adenoviral region. Controls were parental adenoviruses (dl-lacZ and Ad-deltaE1B) and phosphate-buffered saline (PBS) (vehicle). Replication-incompetent viruses, which do not lyse cells, were used to assess transduction efficiency. Viral spread in tumor spheroids, made by dissecting tumor tissue into homogeneous fragments, was assessed by reporter gene (i.e., lacZ) expression. Tumor growth inhibition was assessed by injecting adenoviruses into xenograft tumors in athymic mice (n = 8 or 9). Overall survival was assessed by the Kaplan-Meier method. Extracellular matrix was examined with Masson's trichrome staining. Therapeutic efficacy was evaluated by assessing spontaneous pulmonary metastasis in the B16BL6 melanoma mouse model and growth inhibition of orthotopically implanted hepatoma (n = 4-6). All statistical tests were two-sided.In tumor spheroids and established solid tumors in vivo, transduction with dl-lacZ-RLX, compared with parental virus or vehicle, elicited higher transduction efficiency and viral spread throughout the tumor mass. Infection with Ad-deltaE1B-RLX, compared with parental virus, elicited greater viral persistence and spread, leading to increased survival (e.g., 100%, 95% confidence interval [CI] = 63.1% to 100%, for C33A tumor-bearing mice treated with Ad-deltaE1B-RLX, and 50%, 95% CI = 15.7% to 84.3%, for C33A tumor-bearing mice treated with Ad-deltaE1B). Infection with Ad-deltaE1B-RLX substantially decreased the collagen content of tumor tissue but not of adjacent normal tissue, compared with noninfected tissues. Intratumoral injection of Ad-deltaE1B-RLX inhibited the formation of lung metastases in mice (PBS = 268 mg of metastatic tumor per mouse and Ad-deltaE1B-RLX = 10 mg; difference = 258 mg, 95% CI = 94 to 426; P = .003, Mann-Whitney test). Systemic treatment with Ad-deltaE1B-RLX completely inhibited the growth of Hep1 hepatocellular carcinomas (PBS = 20.2 mg of tumor per mouse and Ad-deltaE1B-RLX = 0 mg; difference = 20.2 mg, 95% CI = 3.7 to 36.7; P = .004, Mann-Whitney test).Extracellular matrix degradation by relaxin expressed by adenoviruses increased viral distribution and tumor penetration, inhibited tumor growth and metastasis, and increased survival of mice.
Risk Factors Associated With The Development Of Asthma and Allergic Rhinitis Among Adolescents Living In São Paulo – Brazil
Authors: Fernanda Patini Furlan, Djanira Andrade, Danielli Christinni Bichuete-Silva, Tessa Rachel Tranquilini Gonçalves, Inês Camelo Nunes, Dirceu Sole
Journal: Journal of Allergy and Clinical Immunology (2014)
Methoxyflurane as an anaesthetic agent in aversive pleural procedures
Authors: Alice Cottee, Tajalli Saghaie, Philip Corke, Matthew Peters
Journal: European Respiratory Journal (2014)

Introduction   Rapid-onset, adequate analgesia in pleural procedures is important but commonly not achieved. Standard sedation as a supplement to local anesthesia(LA) carries the risk of respiratory depression. Methoxyflurane (Penthrox) is self-administered using a whistle-device and is used in Australia in trauma and before some procedures. Patients can self-titrate inhalation against pain during a procedure.   Aim   To assess the efficacy and tolerability of methoxyflurane during pleural procedures.   Method   Consecutive consenting patients undergoing chest tube insertion or medical pleuroscopy were recruited. Subjects inhaled methoxyflurane prior to standard LA infiltration and during the procedure. Supplementary IV opiate analgesia was administered as needed. Patient and operator questionnaires regarding efficacy and tolerance of methoxyflurane were conducted after the procedure and the dose of opiate required recorded. Pain and anxiety were rated by subjects from 0(none)-10(worst imaginable). Operators rated pain in the same way.   Results   16 ICC insertions, 2 pleuroscopies and 4 tunneled pleural catheter procedures were studied. Mean age was 72(range 43-94). Mean(SEM) score was 2.9(0.5) for pain during and 1.7(0.5) for pain after procedure. Mean(SEM) anxiety was 4.5(0.6). Mean operator pain score was 2.3(0.2). No patient required opiate analgesia. Cough was seen in 35%. No patient became sedated. Renal function was unaffected. 77% of patients would use methoxyflurane in future procedures.   Conclusion   Methoxyflurane provided effective analgesia and was well tolerated. Its rapid onset provides adequate anaesthesia prior to LA infiltration. Further studies should compare this approach with current standard practice.
Biochemical and Immunologic Characterization of Galactosyltransferase Purified From the Ascites of Ovarian Cancer Patients&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: S K Chatterjee, M Bhattacharya, J J Barlow
Journal: JNCI Journal of the National Cancer Institute (1985)

Galactosyltransferase appears to be a promising marker for ovarian carcinoma. For an understanding of its role in this cancer, the enzyme was purified from the ascites of ovarian cancer patients, and its biochemical and immunologic properties were studied. For adequate recovery and stability, Triton X-100 (0.01%) was necessary in all the buffers used for the purification of this enzyme. Immunoglobulins were not detectable in this preparation, which showed a single band in sodium dodecyl sulfatepolyacrylamide gel electrophoresis. Electrophoresis under nondenaturing conditions resolved the enzyme into two to three active components. An antiserum in rabbits, however, produced a single precipitin line suggesting a single determinant. By chromatography in concanavalin A-Sepharose 4B, the enzyme can be resolved into two components (F-1 and F-2). Purified galactosyltransferase and components F-1 and F-2 all catalyzed the transfer of galactose from UDP-galactose to alkali-stable β-N-glycosidic acceptors, as well as to alkali-labile β-O-glycosidic mucin-type acceptors. In addition, they catalyzed the N-acetyllactosamine synthetase reaction and, in the presence of α-lactalbumin, the lactose synthetase reaction. Galactosyltransferase and components F-1 and F-2 differed in their sensitivity to α-lactalbumin-induced inhibition of N-acetyllactosamine synthesis. Galactosyltransferase in the malignant ascites exists as different isoforms, which do not differ significantly in major biochemical and immunologic properties.
Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome, severe pneumonia, and controls
Authors: T. T Bauer
Journal: Thorax (2000)

<h3>BACKGROUND</h3> The inflammatory response has been widely investigated in patients with acute respiratory distress syndrome (ARDS) and pneumonia. Studies investigating the diagnostic values of serum cytokine levels have yielded conflicting results and only little information is available for the differential diagnosis between ARDS and pneumonia. <h3>METHODS</h3> Clinical and physiological data, serum concentrations of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and quantitative cultures of lower respiratory tract specimens were obtained from 46 patients with ARDS and 20 with severe pneumonia within 24 hours of the onset of the disease and from 10 control subjects with no inflammatory lung disease. Cytokine concentrations were compared between groups and determinants in addition to the diagnosis were tested. <h3>RESULTS</h3> Serum TNF-α levels were significantly higher in ARDS patients (67 (57) pg/ml) than in patients with severe pneumonia (35 (20) pg/ml; p = 0.031) or controls (17 (8) pg/ml; p = 0.007). For IL-1β and IL-6 the observed differences were not statistically significant between patients with ARDS (IL-1β: 34 (65) pg/ml; IL-6: 712 (1058) pg/ml), those with severe pneumonia (IL-1β: 3 (4) pg/ml, p = 0.071; IL-6: 834 (1165) pg/ml, p = 1.0), and controls (IL-1β: 6 (11) pg/ml, p = 0.359; IL-6: 94 (110) pg/ml, p = 0.262). TNF-α (standardised coefficient β = 0.410, p&lt;0.001) and IL-1β (standardised coefficient β = 0.311, p = 0.006) were most strongly associated with the degree of lung injury, even when the diagnostic group was included in the statistical model. <h3>CONCLUSIONS</h3> Serum TNF-α levels were higher in patients with ARDS than in those with severe pneumonia or in control subjects. Multivariate results suggest that the levels of systemic TNF-α and IL-1β reflect the severity of the lung injury rather than the diagnosis.
Molecular Signatures Predict Outcomes of Breast Cancer
Authors: Joyce A. O'Shaughnessy
Journal: New England Journal of Medicine (2006)

Breast cancer is classified and managed largely on the basis of anatomy — in contrast with lymphoma, which has been classified and treated according to grade for more than 20 years. Tumor size and the degree of involvement of the axillary nodes are used to estimate the risk of systemic micrometastases at diagnosis and, accordingly, whether systemic adjuvant therapy, which improves overall survival in largely unselected populations, is needed.1 A routine question faced by oncologists is, which of the two thirds of patients with hormone-receptor–positive breast cancer require systemic adjuvant chemotherapy to decrease their chance of recurrence? Although there are . . .
Abstract 10415: Lipoprotein-Associated Phospholipase A2 is Not Associated With Impairments in Endothelial Function: The Multi-Ethnic Study of Atherosclerosis
Authors: Parveen K Garg, Robyn Mcclelland, Nancy S Jenny, Michael H Criqui, Kiang Liu, Joseph Polak, Neal Jorgensen, Mary Cushman
Journal: Circulation (2010)

Objectives: Higher levels of Lipoprotein-associated phospholipase A2 (Lp-PLA2) are associated with risk of cardiovascular events, but mechanisms underlying this are not well understood. Considering...
Focal glycogenosis of the liver in disorders of ureagenesis: Its occurrence and diagnostic significance
Authors: K Badizadegan, A R Perez-Atayde
Journal: Hepatology (1997)

Metabolic disorders of ureagenesis can cause a Reye-like syndrome with potentially fatal hyperammonemia in children. A mechanistically heterogeneous subset of these disorders shares the biochemical end-result of impaired mitochondrial citrulline production. These include deficiencies of the mitochondrial enzymes, ornithine transcarbamylase (OTC) and carbamyl-phosphate synthase (CPS), as well as dibasic aminoacidurias hyperammonemia-hyperornithinemia-homocitrullinuria (HHH) and lysinuric protein intolerance (LPI). In this report, we present histopathology of the liver in 10 children with defects of ureagenesis, including 6 with OTC deficiency, 3 with CPS deficiency, and 1 with HHH. The liver showed diffuse microvesicular steatosis, marked periportal nuclear glycogen, and variable portal fibrosis with occasional delicate portal-to-portal bridging. Discrete aggregates of distended hepatocytes with central nuclei and nonvacuolated clear cytoplasm were present in 5 of the 10 children, including two 2 OTC deficiency, 2 with CPS deficiency, and 1 with HHH. Similar aggregates had been previously noted in the liver of some children with OTC deficiency or LPI, but their nature and diagnostic significance had so far remained unknown. Using special stains on frozen tissue sections and electron microscopy, we show that the hepatocytes in these aggregates have little or no cytoplasmic neutral fat, but contain excessive free cytoplasmic glycogen, morphologically mimicking a glycogen storage disease. In our experience, hepatocellular aggregates of this nature do not occur in Reye syndrome or in any of its metabolic mimics other than the subset of defects listed above. Identification of these aggregates on liver biopsy can potentially narrow the differential diagnosis of a Reye-like syndrome with diffuse hepatocellular steatosis.
Hailey-Hailey disease responsive to topical calcitriol
Authors: S.M. Rajpara, C.M. King
Journal: British Journal of Dermatology (2005)

Journal Article Hailey–Hailey disease responsive to topical calcitriol Get access S.M. Rajpara, S.M. Rajpara Department of Dermatology, Royal Liverpool and Broadgreen Hospitals NHS Trust, Liverpool, U.K. E‐mail: sanjaysunil@yahoo.com; sanjay.rajpara@nhs.net Search for other works by this author on: Oxford Academic Google Scholar C.M. King C.M. King Department of Dermatology, Royal Liverpool and Broadgreen Hospitals NHS Trust, Liverpool, U.K. E‐mail: sanjaysunil@yahoo.com; sanjay.rajpara@nhs.net Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 152, Issue 4, 1 April 2005, Pages 816–817, https://doi.org/10.1111/j.1365-2133.2005.06489.x Published: 01 April 2005
Circulating peripheral blood plasma cells as a prognostic indicator in patients with primary systemic amyloidosis
Authors: Animesh Pardanani, Thomas E. Witzig, Georgene Schroeder, Edwin A. McElroy, Rafael Fonseca, Angela Dispenzieri, Martha Q. Lacy, John A. Lust, Robert A. Kyle, Philip R. Greipp, Morie A. Gertz, S. Vincent Rajkumar
Journal: Blood (2003)
p38 Regulates Cyclooxygenase-2 in Human Mammary Epithelial Cells and Is Activated in Premalignant Tissue
Authors: Mona L. Gauthier, Curtis R. Pickering, Caroline J. Miller, Colleen A. Fordyce, Karen L. Chew, Hal K. Berman, Thea D. Tlsty
Journal: Cancer Research (2005)

The immediate-early gene, cyclooxygenase-2 (COX-2), is induced in a variety of inflammatory and neoplastic processes and is believed to play an important role in tumorigenesis. In this study, we identify an important upstream regulatory pathway of COX-2 expression in variant human mammary epithelial cells (vHMEC), which has been shown to exhibit phenotypes important for malignancy. We find that the stress-activated kinase, p38, is phosphorylated and activated in vHMEC compared with HMEC and is responsible for the expression of COX-2 in vHMEC as cells grow in culture. Furthermore in this capacity, p38 acts to stabilize the COX-2 transcript rather than activate COX-2 transcription. Inhibition of p38 kinase, using a chemical inhibitor, down-regulates COX-2 and decreases cell survival. Examination of archived tissue from women with ductal carcinoma in situ reveals epithelial cells that not only overexpress COX-2 but also have an abundance of activated phospho-p38 in the nucleus and cytoplasm, mirroring the expression observed in vitro. These epithelial cells are found within premalignant lesions as well as in fields of morphologically normal tissue that surround the lesions. In contrast, low phospho-p38 staining was observed in the majority of normal tissue obtained from reduction mammoplasty. These data help define the regulation of COX-2 expression in early carcinogenesis and provide alternative candidates for targeted prevention of COX-2-induced phenotypes and breast cancer.
Jehovah's Witnesses
Authors: J. Lowell Dixon
Journal: JAMA (1981)

Physicians face a special challenge in treating Jehovah's Witnesses. Members of this faith have deep religious convictions against accepting homologous or autologous whole blood, packed RBCs, WBCs, or platelets. Many will allow the use of (non-blood-prime) heart-lung, dialysis, or similar equipment if the extracorporeal circulation is uninterrupted. Medical personnel need not be concerned about liability, for Witnesses will take adequate legal steps to relieve liability as to their informed refusal of blood. They accept nonblood replacement fluids. Using these and other meticulous techniques, physicians are performing major surgery of all types on adult and minor Witness patients. A standard of practice for such patients has thus developed that accords with the tenet of treating the "whole person." (<i>JAMA</i>1981;246:2471-2472)
Knife and Gun Clubs of America
Authors: Laurence J. Purdy
Journal: JAMA (1992)

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Molecular Heterogeneity in Acute Renal Allograft Rejection Identified by DNA Microarray Profiling
Authors: Minnie Sarwal, Mei-Sze Chua, Neeraja Kambham, Szu-Chuan Hsieh, Thomas Satterwhite, Marilyn Masek, Oscar Salvatierra
Journal: New England Journal of Medicine (2003)

The causes and clinical course of acute rejection vary, and it is not possible to predict graft outcome reliably on the basis of available clinical, pathological, and genetic markers. We hypothesized that previously unrecognized molecular heterogeneity might underlie some of the variability in the clinical course of acute renal allograft rejection and in its response to treatment.We used DNA microarrays in a systematic study of gene-expression patterns in biopsy samples from normal and dysfunctional renal allografts. A combination of exploratory and supervised bioinformatic methods was used to analyze these profiles.We found consistent differences among the gene-expression patterns associated with acute rejection, nephrotoxic effects of drugs, chronic allograft nephropathy, and normal kidneys. The gene-expression patterns associated with acute rejection suggested at least three possible distinct subtypes of acute rejection that, although indistinguishable by light microscopy, were marked by differences in immune activation and cellular proliferation. Since the gene-expression patterns pointed to substantial variation in the composition of immune infiltrates, we used immunohistochemical staining to define these subtypes further. This analysis revealed a striking association between dense CD20+ B-cell infiltrates and both clinical glucocorticoid resistance (P=0.01) and graft loss (P<0.001).Systematic analysis of gene-expression patterns provides a window on the biology and pathogenesis of renal allograft rejection. Biopsy samples from patients with acute rejection that are indistinguishable on conventional histologic analysis reveal extensive differences in gene expression, which are associated with differences in immunologic and cellular features and clinical course. The presence of dense clusters of B cells in a biopsy sample was strongly associated with severe graft rejection, suggesting a pivotal role of infiltrating B cells in acute rejection.