tbuckley/cabot-search huggingface dataset:
How much to do at the accident scene?
Authors: M. W Cooke
Journal: BMJ (1999)

The argument over how much care to give trauma victims at the scene of an accident reflects the development of the ambulance service Originally the ambulance service simply provided a means of transport to hospital. As such the best policy was to scoop the victim up and run as fast as possible to the hospital, where treatment was started—“scoop and run.” Extended training of ambulance personnel meant that more could be done at the scene. Training, however, was based around learning skills rather than patient assessment, so the skills may have been used without assessment as to whether the timing was correct. The concept of stabilise before transport was developed, forgetting that it may not be possible to stabilise the critically injured patient without surgery. The pendulum swung to overtreating at the scene. Accusations of wasting time appeared and the phrase “stay and play” was adopted. Where are we now in the swing of this pendulum?

Preventable deaths in prehospital care are …
Depression and poor glycemic control: a meta-analytic review of the literature.
Authors: P J Lustman, R J Anderson, K E Freedland, M de Groot, R M Carney, R E Clouse
Journal: Diabetes Care (2000)

OBJECTIVE: Depression is common among patients with diabetes, but its relationship to glycemic control has not been systematically reviewed. Our objective was to determine whether depression is associated with poor glycemic control. RESEARCH DESIGN AND METHODS: Medline and PsycINFO databases and published reference lists were used to identify studies that measured the association of depression with glycemic control. Meta-analytic procedures were used to convert the findings to a common metric, calculate effect sizes (ESs), and statistically analyze the collective data. RESULTS: A total of 24 studies satisfied the inclusion and exclusion criteria for the meta-analysis. Depression was significantly associated with hyperglycemia (Z = 5.4, P &amp;lt; 0.0001). The standardized ES was in the small-to-moderate range (0.17) and was consistent, as the 95% CI was narrow (0.13-0.21). The ES was similar in studies of either type 1 or type 2 diabetes (ES 0.19 vs. 0.16) and larger when standardized interviews and diagnostic criteria rather than self-report questionnaires were used to assess depression (ES 0.28 vs. 0.15). CONCLUSIONS: Depression is associated with hyperglycemia in patients with type 1 or type 2 diabetes. Additional studies are needed to establish the directional nature of this relationship and to determine the effects of depression treatment on glycemic control and the long-term course of diabetes.
Evaluation of the optimal dose of intracoronary adenosine 5′-triphosphate for the measurement of coronary flow velocity reserve
Authors: T. Furuta, H. Yokoi, S. Mori, S. Kakizawa, A. Sugiura, W. Fujiwara, T. Kondo, O. Inami, Y. Abo, Y. Watanabe
Journal: European Journal of Heart Failure (2000)
Postmenopausal Estrogen Use and Coronary Atherosclerosis
Authors: JAY M. SULLIVAN
Journal: Annals of Internal Medicine (1988)

To determine whether estrogen replacement therapy affects the prevalence of severely obstructive coronary arterial lesions defined by selective coronary arteriography.Case-control study.Large, urban, university-affiliated referral hospital.From a consecutive sample of 6452 women having coronary arteriography between 1972 and 1984, 2188 patients were eligible for study; others were excluded because they were nonmenopausal, had congenital heart defects, valvular heart disorders, primary myocardial disease, or no more than mild to moderate coronary artery disease.None.Hospital nurses routinely obtained medication histories. Staff invasive cardiologists interpreted coronary arteriograms. Clinical, laboratory, and angiographic data were abstracted from the cardiac catheterization reports and entered into a computerized registry. Postmenopausal estrogen use for 1444 cases of coronary artery disease (70% stenosis) was compared to that 744 controls (0% stenosis). The odds ratio estimate of the risk of coronary artery disease for estrogen users relative to the risk of coronary artery disease for nonusers was 0.44 (95% confidence interval, 0.29 to 0.67) after adjustment for age, cigarette smoking, diabetes, cholesterol, and hypertension. Postmenopausal estrogen replacement was a significant independent protective factor for coronary artery disease in a multivariate logistic regression model (P = 0.037).The data suggest that postmenopausal estrogen treatment reduces the risk for angiographically significant coronary artery disease.
Vasoconstriction by in situ formed angiotensin II: role of ACE and chymase
Authors: A MaassenVanDenBrink
Journal: Cardiovascular Research (1999)

Objective: To assess the importance, for vasoconstriction, of in situ angiotensin (Ang) II generation, as opposed to Ang II delivery to AT receptors via the organ bath fluid. Methods: Ang I and II concentration—response curves in human and porcine coronary arteries (HCAs, PCAs) were constructed in relation to estimates of the clearances of Ang I and II (ClAngI, ClAngII) from the organ bath and the release of newly formed Ang II (RAngII) into the bath fluid. HCAs were from 25 heart valve donors (age 5–54 years), and PCAs from 14 pigs (age 3 months). Results: Ang I- and II-evoked constrictions were inhibited by the AT1 receptor antagonist, irbesartan, and were not influenced by the AT2 receptor antagonist, PD123319. In HCAs Ang II was only three times more potent than Ang I, whereas, in the experiments with Ang I, comparison of ClAngI with ClAngII and RAngII indicated that most of the arterially produced Ang II did not reach the bath fluid. Also in PCAs Ang I and II showed similar potency. In HCAs both the ACE inhibitor, captopril, and the chymase inhibitor, chymostatin, inhibited Ang I-evoked vasoconstriction, while only chymostatin had a significant effect on ClAngI. In PCAs Ang I-evoked vasoconstriction was almost completely ACE-dependent. Conclusions: This study points towards the functional importance of in situ ACE- and chymase-dependent Ang II generation, as opposed to Ang II delivery via the circulation. It also indicates that functionally relevant changes in local Ang I–II conversion are not necessarily reflected by detectable changes in circulating Ang II.
Abstract 5267: Mammary stromal fibroblast activity is modulated by HoxC6: impacts on growth and metastatic potential
Authors: Ashley M. Smith, Carola A. Neumann, Carlos S. Moreno, Ioanna G. Maroulakou, Steven A. Rosenzweig, Demetri D. Spyropoulos
Journal: Cancer Research (2010)

Abstract Crosstalk between mammary epithelium and stromal cell types, including fibroblasts and adipocytes is 1) essential for mammary gland development 2) likely impacts breast cancer potential and 3) significantly impacts the growth, invasion and metastasis of tumor cells. Although well recognized, molecular mechanisms important in stromal-epithelial crosstalk are still poorly understood. The purpose of this study is to better elucidate one potentially significant mechanism involving stromal fibroblast to epithelial paracrine signaling in the mammary gland. We previously demonstrated that HoxC6 was required for mammary epithelial cell growth and ductal branching morphogenesis using mouse models and 3-dimensional in vitro culture of human mammary epithelial cell lines. We also demonstrated that constitutive ErbB2/Her2/Neu receptor activation in epithelium of transgenics is sufficient to rescue HoxC6 deficiency in epithelial growth but not branching. Significantly, this model also shows that HoxC6 null stroma facilitates tumor metastasis. Here, we focus attention on stromal fibroblasts (vimentin positive cells) from wild type and HoxC6 null prepubertal mouse thoracic mammary glands (TMGs). When cultured in vitro, HoxC6 null TMG fibroblasts display multiple filopodia and extended cellular processes that could indicate an activated myofibroblast phenotype. In contrast, cultured wild type TMG fibroblasts appear quite similar to mouse embryonic fibroblasts. Quantitative comparisons of gene expression patterns in isolated fibroblasts indicate that HoxC6 null fibroblasts are more activated than wild type fibroblasts. Activation markers studied include alpha smooth muscle actin (ACTA2/SMA), S100A4 (Fsp1) and Wnt1-induced secreted protein 1 (Wisp1). Since estrogens are know to repress HoxC6 expression and are implicated in modulating paracrine stromal-to-epithelial interactions, stromal fibroblasts were isolated and cultured under estrogen-free conditions and treated with 17beta-estradiol, bisphenol A and vitamin D. In addition, stromal fibroblasts were co-cultured with mammary epithelial stem cells and stem-like mammary tumor cells to study the impact of stromal fibroblast HoxC6 status on epithelial cell activities. The results obtained will be discussed as they pertain to stromal-to-epithelial signaling in mammary gland development and in the growth, invasion and metastasis of tumor cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5267.
Appraisal of Vitamin Nutritional Status
Authors: John H. Crandon
Journal: JAMA (1962)

To the Editor:—  In a recent issue ( JAMA  180 :49 [April 7] 1962) an article by Dr. William Pearson entitled, Biochemical Appraisal of the Vitamin Nutritional Status in Man, under the aegis of the Council on Foods and Nutrition, contains 2 statements with respect to ascorbic acid deficiency which demand comment:   In the statement, If an adult consumes a diet free of ascorbic acid... clinical signs of scurvy do not appear until approximately  weeks, the 10  should be changed to 18 to 23 weeks (providing the adult is otherwise normal).  The statement,  means that all individuals with clinical scurvy have serum ascorbic acid levels that are nearly zero, requires the qualifying phrase, providing there has been no recent intake of the vitamin! This is an important and easily overlooked qualification. For example, 2 years ago, at Boston City Hospital, a patient entered in the late
Better staff engagement improves NHS care, says report
Authors: J. Wise
Journal: BMJ (2014)

A new report calls on healthcare organisations to increase staff engagement by making support for staff central to their strategies—and this in turn will improve the care of patients, productivity, and financial performance, it says.1

The report, by the Point of Care Foundation, an independent charity formed as a result of work carried out by the healthcare think tank the King’s Fund, said that patients’ satisfaction with services was higher in NHS trusts with better ratings of staff health and wellbeing.

The report drew …
Evidence for linkage of a candidate chromosome 1 region to human systemic lupus erythematosus.
Authors: B P Tsao, R M Cantor, K C Kalunian, C J Chen, H Badsha, R Singh, D J Wallace, R C Kitridou, S L Chen, N Shen, Y W Song, D A Isenberg, C L Yu, B H Hahn, J I Rotter
Journal: Journal of Clinical Investigation (1997)

Genetic susceptibility confers significant risk for systemic lupus erythematosus (SLE). The MHC region and other polymorphic loci have been associated with SLE. Because more compelling evidence for an involvement of a genetic locus includes linkage, we tested a candidate region homologous to a murine SLE susceptibility region in 52 SLE-affected sibpairs from three ethnic groups. We analyzed seven microsatellite markers from the human chromosome 1q31-q42 region corresponding to the telomeric end of mouse chromosome 1, the region where specific manifestations of murine lupus, including glomerulonephritis and IgG antichromatin, have been mapped. Comparing the mean allele sharing in affected sibpairs of each of these seven markers to their expected values of 0.50, only the five markers located at 1q41-q42 showed evidence for linkage (P = 0.0005-0.08). Serum levels of IgG antichromatin also showed evidence for linkage to two of these five markers (P = 0.04), suggesting that this phenotype is conserved between mice and humans. Compared to the expected random distribution, the trend of increased sharing of haplotypes was observed in affected sibpairs from three ethnic groups (P < 0.01). We concluded that this candidate 1q41-q42 region probably contains a susceptibility gene(s) that confers risk for SLE in multiple ethnic groups.
p50–NF-κB Complexes Partially Compensate for the Absence of RelB: Severely Increased Pathology in <i>p50−</i>/−<i>relB−</i>/−Double-knockout Mice
Authors: Falk Weih, Stephen K. Durham, Debra S. Barton, William C. Sha, David Baltimore, Rodrigo Bravo
Journal: The Journal of Experimental Medicine (1997)

RelB-deficient mice (relB−/−) have a complex phenotype including multiorgan inflammation and hematopoietic abnormalities. To examine whether other NF-κB/Rel family members are required for the development of this phenotype or have a compensatory role, we have initiated a program to generate double-mutant mice that are deficient in more than one family member. Here we report the phenotypic changes in relB−/− mice that also lack the p50 subunit of NFκB (p50−/−). The inflammatory phenotype of p50−/−relB−/− double-mutant mice was markedly increased in both severity and extent of organ involvement, leading to premature death within three to four weeks after birth. Double-knockout mice also had strongly increased myeloid hyperplasia and thymic atrophy. Moreover, B cell development was impaired and, in contrast to relB−/− single knockouts, B cells were absent from inflammatory infiltrates. Both p50−/− and heterozygous relB−/+ animals are disease-free. In the absence of the p50, however, relB−/+ mice (p50−/−relB−/+) had a mild inflammatory phenotype and moderate myeloid hyperplasia. Neither elevated mRNA levels of other family members, nor increased κB-binding activities of NF-κB/Rel complexes could be detected in single- or double-mutant mice compared to control animals. These results indicate that the lack of RelB is, in part, compensated by other p50-containing complexes and that the “classical” p50-RelA–NF-κB activity is not required for the development of the inflammatory phenotype.
Natural Killer Cells and Bone Marrow Transplantation
Authors: W. J. Murphy, C. W. Reynolds, P. Tiberghien, D. L. Longo
Journal: JNCI Journal of the National Cancer Institute (1993)

Bone marrow transplantation is currently used in the treatment of a variety of neoplastic and nonneoplastic diseases. However, significant obstacles still limit the efficacy of this procedure. These include the occurrence of graft-versus-host disease, the failure of the marrow to engraft, the susceptibility of patients to opportunistic infections during the period of immunodeficiency after transplantation before full recovery of immune function, and finally, the recurrence of the cancer. Natural killer (NK) cells are lymphoid cells responsible for mediating a variety of immunologic and homeostatic functions. Initially described almost 20 years ago, the full range of functions carried out by these enigmatic cells continues to unfold. NK cells may be both beneficial and deleterious in bone marrow transplantation, depending on their genotype and activation status. Resting host-derived NK cells appear capable of mediating resistance to both autologous and allogeneic bone marrow cell grafts. At the other end of the spectrum, the transfer of activated NK cells of donor type appears to produce multiple beneficial effects during both syngeneic and allogeneic bone marrow transplantation. Here, we review and attempt to reconcile the literature concerning the basic biology of NK cells and their effects on hematopoiesis, both in vitro and in vivo. We also discuss the current issues in bone marrow transplantation and the potential role NK cells may play in determining the outcome of the marrow graft, the occurrence of graft-versus-host disease, and the generation of a graft-versus-tumor response when bone marrow transplantation is used for the treatment of cancer. [J Natl Cancer Inst 85:1475–1482, 1993]
S-adenosylmethionine protects against acetaminophen hepatotoxicity in two mouse models
Authors: Gary P. Bray, Michael J. Tredger, Roger Williams
Journal: Hepatology (1992)

Because S-adenosylmethionine promotes synthesis of hepatic glutathione in chronic liver disease and is well tolerated in man, we investigated its use as an antidote to acetaminophen hepatotoxicity in two mouse models. In C57Bl6 mice, deaths were abolished by S-adenosylmethionine given within 1 hr of 3.3 mmol/kg body wt acetaminophen (0 of 32 vs. 13 of 49, p less than 0.005) and reduced if given 2 to 5 hours after acetaminophen administration (4 of 42 vs. 13 of 49, p less than 0.01). Mixed disulfate/tosylate salt of S-adenosylmethionine abolished mortality in C3H mice given 2 mmol/kg body wt acetaminophen (0 of 24 vs. 4 of 18; p less than 0.05). In both mouse models, S-adenosylmethionine reduced depletion of plasma (median = 20.8 mumol/L vs. 14.6 mumol/L) and liver glutathione (198% vs. 100%; p less than 0.05), liver damage and release of AST after acetaminophen administration. Pretreatment with buthionine sulfoximine, which inhibits glutathione synthesis, abolished the beneficial effect of S-adenosylmethionine on survival and plasma glutathione level. S-adenosylmethionine reduces acetaminophen hepatotoxicity by metabolism of the active moiety to glutathione. This benefit may last as long as 5 hr after acetaminophen ingestion.
Utility of the “bear claw”, or over-the-scope clip (OTSC) system, to provide endoscopic hemostasis for bleeding posterior duodenal ulcers
Authors: K. Mönkemüller, J. Toshniwal, M. Zabielski, K. Vormbrock, H. Neumann
Journal: Endoscopy (2012)

The "bear claw", or over-the-scope clip (OTSC) system (Ovesco Endoscopy, Tübingen, Germany), is an innovative clipping device made of superelastic biocompatible nitinol [1] [2] [3]. This device was developed to close wall defects of the luminal gastrointestinal tract, such as perforations, anastomotic leaks, and fistulas [1] [2]. The use of the "bear claw" in humans is still limited, but due to the excellent capabilities of the "bear claw" to close large mucosal defects, more reports on its efficacy are being published [2] [3]. Here we present the use of the "bear claw" to provide hemostasis of large ulcers of the posterior duodenal wall.
The role of the Thomsen-Friedenreich antigen as a tumor-associated molecule.
Authors: W Dippold, A Steinborn, K H Meyer zum Büschenfelde
Journal: Environmental Health Perspectives (1990)

The Thomsen-Friedenreich antigen (Gal-GalNAc) represents a tumor-associated molecule, which is assumed to be one of the few chemically well-defined antigens with a proven association with malignancy. In order to analyze the role of the carbohydrate structure Gal-GalNAc for gastrointestinal tumors, we immunized Balb/c mice with MCF-7 breast tumor cells together with synthetic Gal-GalNAc linked to a BSA carrier. One monoclonal antibody (82-A6) was established which recognizes the Thomsen-Friedenreich antigen according to the biochemical and serological analysis presented here. In contrast to the studies performed in the past, immunohistochemical results using this antibody 82-A6 did not exhibit a reactivity clearly restricted to tumors. Preliminary biochemical analysis revealed that the T-determinant is detectable in the high-molecular weight range (about 1000 kD), suggesting that the Gal-GalNAc epitope is found on mucinlike glycoproteins. Tumor restriction of Thomsen-Friedenreich antigen may therefore be determined either by the protein backbone or by the beta-glycosidic linkage of the carbohydrate structure to the protein.
546. Gene Therapy of Ovarian Cancer by IAI.3B Promoter Driven Oncolytic Adenovirus
Authors: Katsuyuki Hamada, Toshiro Shirakawa, Akinobu Gotoh
Journal: Molecular Therapy (2005)

To explore the potential use of IAI.3B promoter isolated from ovarian cancer cells in gene therapy for ovarian cancer, we created a replication-selective adenovirus, AdE3-IAI.3B, driven by the IAI.3B promoter. Ovarian cancer cells has 100-fold higher levels of IAI.3B mRNA than other cancer and normal cells. Transient transfection experiments showed that the DNA segment located at -1816 bp resulted in preferential expression in ovarian cancer cells with negligible expression in other cancer and normal cells. The promoter activity of IAI.3B is almost the same as that of cytomegalovirus and an order of magnitude higher than those of midkine and cyclooxygenase-2 in ovarian cancer cells. We inserted the IAI.3B promoter into the E1A promoter region of adenovirus to make an oncolytic adenovirus specific for ovarian cancer therapy. This oncolytic adenovirus, AdE3-IAI.3B specifically replicated only in ovarian cancer cells but not in other cancer and normal cells. AdE3-IAI.3B expressed E1A protein only in ovarian cancer cells but not in other cancer and normal cells. AdE3-IAI.3B lysed ovarian cancer cells but not other cancer and normal cells. From these results, AdE3-IAI.3B might provide a potential for the development of ovarian cancer gene therapy.
Primary mucosa-associated lymphoid tissue (MALT) lymphoma of the trachea: a case of surgical resection and long term survival
Authors: K Okubo
Journal: Thorax (2004)

Primary malignant lymphoma of the trachea is rare. The case history is presented of a 44 year old woman with a mucosa-associated lymphoid tissue (MALT) lymphoma of the trachea who was treated with a tracheal resection and reconstruction. The patient has been free from the disease for 53 months, which confirms the favourable prognosis of MALT lymphoma following local treatment.
Are addictions “biases and errors” in the rational decision process?
Authors: Elias L. Khalil
Journal: Behavioral and Brain Sciences (2008)

Abstract Redish et al. view addictions as errors arising from the weak access points of the system of decision-making. They do not analytically distinguish between addictions, on the one hand, and errors highlighted by behavioural decision theory, such as over-confidence, representativeness heuristics, conjunction fallacy, and so on, on the other. Redish et al.'s decision-making framework may not be comprehensive enough to capture addictions.
Retinal ganglion cells express a cGMP-gated cation conductance activatable by nitric oxide donors
Authors: Iqbal Ahmad, Trese Leinders-Zufall, Jeffery D. Kocsis, Gordon M. Shepherd, Frank Zufall, Colin J. Barnstable
Journal: Neuron (1994)

We have identified a putative cGMP-gated cation conductance in rat retinal ganglion cells. Both in situ hybridization and polymerase chain reaction amplification detected transcripts in ganglion cells that were highly homologous to the cGMP-gated cation channel expressed in rod photoreceptors. Whole-cell patch-clamp recordings detected a current stimulated by cGMP due to activation of nonselective cation channels. This current had a reversal potential near 0 mV, showed some outward rectification, and could be blocked by Cd2+. The current could also be activated by a phosphodiesterase inhibitor and the nitric oxide donors sodium nitroprusside and S-nitrosocysteine. We propose that nitric oxide released from an identified subpopulation of amacrine cells may activate this channel to modulate ganglion cell activity.
104 SOMATIC MUTATIONS ACTIVATING STAT3 IN INFLAMMATORY HEPATOCELLULAR ADENOMAS
Authors: C. Pilati, M.P. Bihl, M. Amessou, K. Poussin, C. Balabaud, J. Tran Van Nhieu, V. Paradis, J.C. Nault, T. Izard, P. Bioulac-Sage, J. Zucman-Rossi
Journal: Journal of Hepatology (2011)