tbuckley/cabot-search huggingface dataset:
Book: The Meat Business: Devouring a Hungry Planet
Authors: M. King
Journal: BMJ (2000)

Eds Geoff Tansey, Joyce D'Silva Earthscan Publications, £12.99, pp 249 ISBN 185383 603 6 Rating: ![Graphic][1]</img>![Graphic][2]</img> “Why don't you eat your sausages?” I asked a little girl. “I don't like eating my friends,” she replied. This book is concerned with how those friends are cared for before they reach the frying pan. It explores the dilemmas that arise as we try to provide healthy and plentiful food for all people in a way that is gentle to animals and the environment. While … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif
Grand Rounds--City Hospital, Nottingham: A complicated case of community acquired pneumonia
Authors: S R Johnson, I D Pavord
Journal: BMJ (1996)

A complicated case ofcommunity acquired pneumonia Beware ofdrug induced side effects in critically il people Community acquired pneumonia is an important cause of morbidity and mortality in young people.Patients needing intensive care often have multiple organ failure and need large doses of different drugs; they are therefore at high risk of side effects of drugs, although these side effects may be difficult to detect.
DNA adduct measurements and tumor incidence during chronic carcinogen exposure in rodents.
Authors: M C Poirier, F A Beland
Journal: Environmental Health Perspectives (1994)

In an attempt to elucidate the relationship between DNA adduct formation and tumorigenesis, DNA adducts were measured in the livers and bladders of mice during chronic exposure to several different doses of 2-acetylaminofluorene (2-AAF) and 4-aminobiphenyl (4-ABP). Continuous oral administration of these compounds for 4 weeks produced an increase in DNA adduct formation during the first 2 weeks, followed by a plateau, which presumably occurred because the rate of adduct removal offset the rate of adduct formation. The quantity of DNA adducts present at equilibrium correlated directly with the carcinogen concentration; therefore, when exposure was continued for 4 weeks, DNA adducts that reflected the plateau level at each dose could be expressed as a function of dose. Liver and bladder DNA adduct profiles thus obtained during administration of multiple doses of 2-AAF (to female mice) and 4-ABP (to male and female mice) were compared to profiles for tumor incidences obtained during lifetime exposures to the same doses. These experiments demonstrated similar profiles for DNA adduct formation and tumorigenesis in liver. In the bladder, DNA adducts were linear, but tumors only appeared at the higher doses in conjunction with cell proliferation. In addition to these aromatic amines, similar data are available for aflatoxin B1, diethylnitrosamine, and (methylnitrosamino)-1-(3-pyridyl)-1-butanone (also known as nicotine-derived nitrosoketone). Of the nine different biological situations (carcinogen/species/sex/organ) for which data are available, correlations between steady-state DNA adduct levels and tumorigenic response at the different doses were linear in five of the nine biological models.(ABSTRACT TRUNCATED AT 250 WORDS)
Tolerogenic maturation of liver sinusoidal endothelial cells promotes B7-homolog 1-dependent CD8+ T cell tolerance
Authors: Linda Diehl, Anna Schurich, Regina Grochtmann, Silke Hegenbarth, Lieping Chen, Percy A. Knolle
Journal: Hepatology (2007)

Liver sinusoidal endothelial cells (LSEC) are unique organ-resident antigen-presenting cells capable of cross-presentation and subsequent tolerization of naïve CD8+ T cells. We investigated the molecular mechanisms underlying this tolerance induction in naive CD8+ T cells. MHC class I–restricted antigen presentation by LSEC led to initial stimulation of naïve CD8+ T cells, which up-regulated CD69, CD25, CD44, and programmed death (PD)-1 and proliferated similar to dendritic cell (DC)–activated CD8+ T cells. Importantly, cognate interaction with naïve CD8+ T cells triggered increased expression of co-inhibitory B7-H1 but not co-stimulatory CD80/86 molecules exclusively on LSEC but not DC. This matured phenotype of B7-H1high CD80/86low was critical for induction of CD8+ T cell tolerance by LSEC: B7-H1–deficient LSEC, that failed to interact with PD-1 on stimulated T cells, were incapable of inducing CD8+ T cell tolerance. Moreover, increased costimulation via CD28 interfered with tolerance induction, indicating that the noninducible low expression levels of CD80/86 on LSEC supported B7-H1–dependent tolerance induction. LSEC-tolerized CD8+ T cells had a distinctive phenotype from naïve and activated T cells with CD25low, CD44high, CD62Lhigh. They also expressed the homeostatic cytokine receptors CD127, CD122, and high levels of Bcl-2, indicating survival rather than deletion of tolerant CD8+ T cells. On adoptive transfer into congenic animals, tolerized CD8+ T cells failed to show specific cytotoxicity in vivo . Conclusion: Cognate interaction of LSEC with naïve CD8+ T cells elicits a unique tolerogenic maturation of LSEC and permissiveness of T cells for tolerogenic signals, demonstrating that LSEC-induced tolerance is an active and dynamic process. (Hepatology 2007.)
Proteomic Profiling of Primary Breast Cancer Predicts Axillary Lymph Node Metastasis
Authors: Taku Nakagawa, Sharon K. Huang, Steve R. Martinez, Andy N. Tran, David Elashoff, Xing Ye, Roderick R. Turner, Armando E. Giuliano, Dave S.B. Hoon
Journal: Cancer Research (2006)

Abstract To determine if protein expression in primary breast cancers can predict axillary lymph node (ALN) metastasis, we assessed differences in protein expression between primary breast cancers with and without ALN metastasis using surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS). Laser capture microdissection was performed on invasive breast cancer frozen sections from 65 patients undergoing resection with sentinel lymph node (SLN) or level I and II ALN dissection. Isolated proteins from these tumors were applied to immobilized metal affinity capture (IMAC-3) ProteinChip arrays and analyzed by SELDI-TOF-MS to generate unique protein profiles. Correlations between unique protein peaks and histologically confirmed ALN status and other known clinicopathologic factors were examined using ANOVA and multivariate logistic regression. Two metal-binding polypeptides at 4,871 and 8,596 Da were identified as significant risk factors for nodal metastasis (P = 0.034 and 0.015, respectively) in a multivariate analysis. Lymphovascular invasion (LVI) was the only clinicopathologic factor predictive of ALN metastasis (P = 0.0038). In a logistic regression model combining the 4,871 and 8,596 Da peaks with LVI, the area under the receiver operating characteristic curve was 0.87. Compared with patients with negative ALN, those with ≥2 positive ALN or non-SLN metastases were significantly more likely to have an increased peak at 4,871 Da (P = 0.016 and 0.0083, respectively). ProteinChip array analysis identified differential protein peaks in primary breast cancers that predict the presence and number of ALN metastases and non-SLN status. (Cancer Res 2006; 66(24): 11825-30)
Effect of secretin on plasma motilin in man.
Authors: P Mitznegg, S R Bloom, W Domschke, W H Haecki, S Domschke, D Belohlavek, E Wunsch, L Demling
Journal: Gut (1977)

Graded doses of 0-1, 0-3, 0-9, and 2-7 clinical units/kg/h of pure synthetic secretin were infused over 60 minute periods in six healthy volunteers. Duodenal bicarbonate output and pH were recorded and plasma secretin and motilin levels were measured by radioimmunoassay. During the infusions plasma motilin fell in a dose dependent manner to a nadir of 35%. This fall was linearly correlated with pancreatic bicarbonate output, whereas a non-linear correlation was observed between plasma motilin and both plasma secretin level and duodenal pH. It is suggested that plasma motilin levels are decreased by secretin-induced pancreatic bicarbonate juice flow. This may be important for the control of motilin secretion initiated by duodenal acidification and the concomitant delay in gastric emptying.
Glioma Virotherapy: Effects of Innate Immune Suppression and Increased Viral Replication Capacity
Authors: Avner Friedman, Jianjun Paul Tian, Giulia Fulci, E. Antonio Chiocca, Jin Wang
Journal: Cancer Research (2006)

Abstract Oncolytic viruses are genetically altered replication-competent viruses that infect, and reproduce in, cancer cells but do not harm normal cells. On lysis of the infected cells, the newly formed viruses burst out and infect other tumor cells. Experiments with injecting mutant herpes simplex virus 1 (hrR3) into glioma implanted in brains of rats show lack of efficacy in eradicating the cancer. This failure is attributed to interference by the immune system. Initial pretreatment with immunosuppressive agent cyclophosphamide reduces the percentage of immune cells. We introduce a mathematical model and use it to determine how different protocols of cyclophosphamide treatment and how increased burst size of the mutated virus will affect the growth of the cancer. One of our conclusions is that the diameter of the cancer will decrease from 4 mm to eventually 1 mm if the burst size of the virus is triple that which is currently available. The effect of repeated cyclophosphamide treatment is to maintain a low density of uninfected cells in the tumor, thus reducing the probability of migration of tumor cells to other locations in the brain. (Cancer Res 2006; 66(4): 2314-9)
SAG/ROC2/Rbx2 Is a Novel Activator Protein-1 Target that Promotes c-Jun Degradation and Inhibits 12-<i>O</i>-Tetradecanoylphorbol-13-Acetate–Induced Neoplastic Transformation
Authors: Qingyang Gu, Mingjia Tan, Yi Sun
Journal: Cancer Research (2007)

Abstract SAG (sensitive to apoptosis gene) was first identified as a stress-responsive protein that, when overexpressed, inhibited apoptosis both in vitro and in vivo. SAG was later found to be the second family member of ROC1 or Rbx1, a RING component of SCF and DCX E3 ubiquitin ligases. We report here that SAG/ROC2/Rbx2 is a novel transcriptional target of activator protein-1 (AP-1). AP-1 bound both in vitro and in vivo to two consensus binding sites in a 1.3-kb region of the mouse SAG promoter. The SAG promoter activity, as measured by luciferase reporter assay, was dependent on these sites. Consistently, endogenous SAG is induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) with an induction time course following the c-Jun induction in both mouse epidermal JB6-Cl.41 and human 293 cells. TPA-mediated SAG induction was significantly reduced in JB6-Cl.41 cells overexpressing a dominant-negative c-Jun, indicating a requirement of c-Jun/AP-1. On the other hand, SAG seemed to modulate the c-Jun levels. When overexpressed, SAG remarkably reduced both basal and TPA-induced c-Jun levels, whereas SAG small interfering RNA (siRNA) silencing increased substantially the levels of both basal and TPA-induced c-Jun. Consistently, SAG siRNA silencing reduced c-Jun polyubiquitination and blocked c-Jun degradation induced by Fbw7, an F-box protein of SCF E3 ubiquitin ligase. Finally, SAG overexpression inhibited, whereas SAG siRNA silencing enhanced, respectively, the TPA-induced neoplastic transformation in JB6-Cl.41 preneoplastic model. Thus, AP-1/SAG establishes an autofeedback loop, in which on induction by AP-1, SAG promotes c-Jun ubiquitination and degradation, thus inhibiting tumor-promoting activity of AP-1. [Cancer Res 2007;67(8):3616–10]
Cryopreservation of tissue-engineered epithelial sheets in trehalose
Authors: Fanfan Chen, Wenjie Zhang, Wei Wu, Yuqing Jin, Lian Cen, James D. Kretlow, Weicheng Gao, Zhenpeng Dai, Jiaming Wang, Guangdong Zhou, Wei Liu, Lei Cui, Yilin Cao
Journal: Biomaterials (2011)
Angiotensin II inhibits interleukin-1β–induced nitric oxide production in cultured rat mesangial cells
Authors: Minoru Kihara, Machiko Yabana, Yoshiyuki Toya, Shunichi Kobayashi, Takayuki Fujita, Tamio Iwamoto, Tomoaki Ishigami, Satoshi Umemura
Journal: Kidney International (1999)
Long-term follow-up of hepatitis C infection in a large cohort of patients with inherited bleeding disorders
Authors: Dietje Elisabeth Fransen van de Putte, Michael Makris, Kathelijn Fischer, Thynn Thynn Yee, Lisa Kirk, Karel Johannes van Erpecum, David Patch, Dirk Posthouwer, Eveline Pauline Mauser-Bunschoten
Journal: Journal of Hepatology (2013)
Prospective randomized controlled trial comparing percutaneous acetic acid injection and percutaneous ethanol injection for small hepatocellular carcinoma
Authors: Kunihiko Ohnishi, Hisashi Yoshioka, Susumu Ito, Kenji Fujiwara
Journal: Hepatology (1998)

To assess whether ultrasound-guided percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small hepatocellular carcinoma (HCC), 60 patients with one to four HCCs smaller than 3 cm were entered onto a randomized controlled trial. Thirty-one and 29 patients, respectively, were treated by percutaneous acetic acid injection using 50% acetic acid or by percutaneous ethanol injection using absolute ethanol. There were no significant differences in age, sex ratio, Child-Pugh class, size of tumors, or number of tumors between the two groups. When there was no evidence of viable HCC from biopsy, plain and helical dynamic computed tomography, or angiography, the treatment was considered successful and was discontinued. All original tumors were treated successfully by either therapy. However, 8% of 38 tumors treated with percutaneous acetic acid injection and 37% of 35 tumors treated with percutaneous ethanol injection developed a local recurrence ( P &lt; .001) during the follow-up periods of 29 ± 8 months and 23 ± 10 months, respectively. The 1- and 2-year survival rates were 100% and 92% in percutaneous acetic acid injection and 83% and 63% in percutaneous ethanol injection ( P = .0017). A multivariate analysis of prognostic factors revealed that treatment was an independent predictor of survival. The risk ratio of percutaneous acetic acid injection versus percutaneous ethanol injection was 0.120 (range, 0.027-0.528; P = .0050). In conclusion, percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small HCC.
Abnormal cation transport in uremia. Mechanisms in adipocytes and skeletal muscle from uremic rats.
Authors: W Druml, R A Kelly, R C May, W E Mitch
Journal: Journal of Clinical Investigation (1988)

The cause of the abnormal active cation transport in erythrocytes of some uremic patients is unknown. In isolated adipocytes and skeletal muscle from chronically uremic chronic renal failure rats, basal sodium pump activity was decreased by 36 and 30%, and intracellular sodium was increased by 90 and 50%, respectively, compared with pair-fed control rats; insulin-stimulated sodium pump activity was preserved in both tissues. Lower basal NaK-ATPase activity in adipocytes was due to a proportionate decline in [3H]ouabain binding, while in muscle, [3H]ouabain binding was not changed, indicating that the NaK-ATPase turnover rate was decreased. Normal muscle, but not normal adipocytes, acquired defective Na pump activity when incubated in uremic sera. Thus, the mechanism for defective active cation transport in CRF is multifactorial and tissue specific. Sodium-dependent amino acid transport in adipocytes closely paralleled diminished Na pump activity (r = 0.91), indicating the importance of this defect to abnormal cellular metabolism in uremia.
Human hematopoietic precursors in long-term culture: single CD34+ cells that lack detectable T cell, B cell, and myeloid cell antigens produce multiple colony-forming cells when cultured with marrow stromal cells.
Authors: R G Andrews, J W Singer, I D Bernstein
Journal: The Journal of Experimental Medicine (1990)

CD34+ human marrow cells not expressing T cell-, B cell-, and myeloid cell-associated antigens (TBM-) were cloned by two-color cell sorting into culture wells containing irradiated marrow stromal cells. After 4 wk of culture, 3.7 +/- 2.1% of these cells generated colony-forming cells (CFC), with each of these cells generating 6.3 +/- 5.3 CFC. This was not due to the 0.5 +/- 0.5% CFC present in the purified CD34+ TBM- cells, as less than 1% of CFC persist in these cultures. This is the first demonstration that single immature precursor cells in human long-term cultures generate multiple CFC progeny. The immature nature of these clonable CD34+ TBM- precursors suggests their candidate status as human hematopoietic stem cells.
Antigenic, Adjuvant and Permeability Enhancing Properties of Melittin in Mice
Authors: L. S. Kind, C. Ramaika, E. Allaway
Journal: Allergy (1981)

Melittin, a mast cell lytic agent which comprises 50% of the protein content of bee venom, may be responsible for some of the severe reactions produced by bee stings in allergic and non-allergic individuals. We therefore investigated some of the biologic properties of this molecule in mice and found that repeated intradermal injections of melittin without adjuvant induced IgE formation in mice. In addition, melittin as well as another surfactant, saponin, were potent adjuvants for IgE formation in mice when mixed with ovalbumin (Ov). Titres of 1280 and 2560 to ovalbumin were produced in CBA mice after two injections of melittin and Ov or saponin and Ov. Melittin was also shown to have an enhancing effect on the vascular permeability induced by an antigen antibody interaction in mouse skin. Evan's blue dye was injected intravenously into ovalbumin-sensitized mice which had been injected intradermally with ovalbumin alone, melittin alone or a mixture of melittin and ovalbumin. The amount of local extravasation of dye was significantly greater in the area injected with the melittin and ovalbumin mixture than the amount of dye obtained from the skin site injected with melittin alone plus that extracted from the site injected with ovalbumin alone.
Empirical modeling of an in vitro activity of polychlorinated biphenyl congeners and mixtures.
Authors: D J Svendsgaard, T R Ward, H A Tilson, P R Kodavanti
Journal: Environmental Health Perspectives (1997)

The goal of this research is to predict an in vitro activity of polychlorinated biphenyl (PCB) congeners and their mixtures and to describe the relationship between this activity and chemical structure. The test system used multiple PCB concentrations on each cell culture plate in a repeated measures design, which improved precision for comparing between concentration levels. A weighted regression that accounted for this experimental design feature was used in fitting a nonlinear dose-response exponential model to the PCB concentration-activity data from an in vitro test system in which 3H-phorbol ester binding was measured in cerebellar granule cells exposed to different PCB congeners to test for their effects on protein kinase C translocation. The model allowed for the minimum level to be less than control, a common slope, and the estimation of the log of the concentration that produces an activity 50% above the control activity (E50) for 36 congeners and 3 commercial mixtures. Next, a weighted logistic regression using a second order response model in the variables Clortho, Clpara, and Clmeta was used to relate the estimated log E50s to indicators of chemical structure. This model was preferred over models that might seem more mechanistically based because in internal validation, it attained a smaller PRESS statistic (the sum of squares between all observed and predicted observations) than other models. Evidently, this second order model makes more efficient use of parameters than other models considered. Plots of the predictions of the logistic second order response model versus log Kow confirm the usual pattern that congeners with intermediate levels of log Kow are the more active. The data of three commercial mixtures were included in this regression by assuming a common combination index (ratio of observed E50 to predicted E50, assuming dose addition). The logistic model suggests that congeners with one, two, or three chlorine substitutions at the ortho position are more active than other congeners. Also, congeners with log Kow between 5.2 and 6.6 are generally more active. The estimated combination index indicated that the joint action of PCB congeners in the three commercial mixtures was less than dose additive. The error sum of squares was significantly large, which may indicate a lack of fit of the logistic model. Empirical Bayes estimates (EBE) are weighted averages of model predictions and observations of E50s and can be better estimates than the fitted model when there is a lack of fit. The PRESS statistic for the EBE indicated larger prediction error than for the logistic model, but the EBE provided better estimates of commercial mixture E50s based on dose addition. This may indicate that the logistic model is not incorporating all the information in the single congener data needed to predict mixtures.
The effect of universal health insurance on health care utilization in Taiwan. Results from a natural experiment
Authors: S. H. Cheng
Journal: JAMA (1997)

The government of Taiwan introduced universal health insurance to cover all citizens in 1995. This national health insurance program was proposed to assure the accessibility to health care at reasonable cost. Evaluation of the consequences, including health care utilization and expenditure, is crucial for policy adjustment.To evaluate the effect of Taiwan's national health insurance on health care utilization.Cohort survey conducted before and after the implementation of the national health insurance program.A total of 1021 randomly selected Taiwanese adults.Physician visits in the 2 weeks prior to the survey and hospital admissions and emergency department visits in the immediate past year.After the introduction of universal health insurance, the newly insured consumed more than twice the amount of outpatient physician visits (0.21 vs 0.48, P<.05) and hospital admissions (0.04 vs 0.11, P<.05) than before universal health insurance was implemented, bringing them to the same amount of health care contacts as the previously insured group. The newly insured also experienced an insignificant increase in emergency department visits. In contrast, the previously insured group had a small but statistically significant increase in outpatient visits (0.48 vs 0.59, P<.05) and insignificant changes in hospital admissions and emergency department visits.The universal health insurance removed some barriers to health care for those newly insured. The copayment design in the insurance scheme seemed to have an insignificant effect on curbing medical care utilization. Taiwanese health policy analysts should seriously consider the growth of health care expenditures since the implementation of universal health insurance.
Fetal Proteins in Ataxia-Telangiectasia
Authors: Kathleen E. Richkind
Journal: JAMA (1982)

Ataxia-telangiectasia (AT) is a genetic disorder of unknown pathogenesis, with primary effects on the immune and nervous systems. The presence of a fetal-like thymus and elevated alpha-fetoprotein (alpha FP) levels in patients with AT suggests that suppressed mesodermal development may be a factor in the development of this disease. We investigated this hypothesis by using electrophoretic and quantitative analyses to test for the presence of other fetal proteins in mesodermal tissues. With the exceptions of alpha FP and carcinoembryonic antigen, all other proteins assessed in these patients were present at levels or in isozymic patterns characteristic of a normal, nonfetal state.