tbuckley/cabot-search huggingface dataset:
Xanthine oxidase inhibition attenuates kupffer cell production of neutrophil chemoattractant following ischemia-reperfusion in rat liver
Authors: Fujio Matsumura, Yasuo Yamaguchi, Mataro Goto, Osamu Ichiguchi, Eiji Akizuki, Teishi Matsuda, Kazutoshi Okabe, Jian Liang, Hajime Ohshiro, Takeshi Iwamoto, Shinwa Yamada, Katsutaka Mori, Michio Ogawa
Journal: Hepatology (1998)

We investigated the effects of the xanthine oxidase inhibitor, BOF–4272, on the production of cytokine–induced neutrophil chemoattractant (CINC) following reperfusion injury in rat liver. Ischemia was induced for 30 minutes by portal vein occlusion. Animals were pretreated with intravenous injection of BOF–4272 (1 mg/kg) or heparin (50 U/kg) 5 minutes before vascular clamp. Both BOF–4272 and heparin limited increases in the chemoattractant compared with nonpretreated rats. Pretreatment with BOF–4272 plus heparin resulted in an additive effect. Most cells immunostained for chemoattractant were macrophages in sinusoids. In vitro chemoattractant production by Kupffer cells isolated from animals pretreated with heparin or BOF–4272 was significantly lower than by Kupffer cells from nonpretreated animals. Expression of transcripts in liver for chemoattractant peaked 3 hours after reperfusion in nonpretreated animals, while pretreatment with heparin or BOF–4272 significantly decreased chemoattractant mRNA levels. In vitro chemoattractant transcription and production could be induced in naive Kupffer cells by hypoxanthine and xanthine oxidase, but BOF–4272 prevented these increases. We conclude that Kupffer cells release chemoattractant in response to oxygen radicals reducible by xanthine oxidase inhibition.
Five-Year Prospective Study of Glomerular Filtration Rate and Albumin Excretion Rate in Normofiltering and Hyperfiltering Normoalbuminuric NIDDM Patients
Authors: Sandra Pinho Silveiro, Rogerio Friedman, Mirela Jobim De Azevedo, Luis Henrique Canani, Jorge Luiz Gross
Journal: Diabetes Care (1996)

OBJECTIVE To evaluate the evolution of glomerular filtration rate (GFR) and albumin excretion rate (AER) of normofiltering (NF) and hyperfiltering (HF) normoalbuminuric NIDDM patients. RESEARCH DESIGN AND METHODS A longitudinal study of 32 normoalbuminuric (AER &amp;lt; 20 μg/min) NIDDM patients and 20 age-, sex-, and BMI-matched normal individuals was done. Subjects had their GFR (51Cr-labeled EDTA single-injection method) measured at entry and after 40 and 60 months. At entry, 13 NIDDM patients had GFR values above the upper limit of the normal range in our laboratory (&amp;gt; 137 ml · min−1 x 1.73 m−2) and were considered as HF. In NIDDM patients, the 24-h AER (radioimmunoassay), HbA1c, urinary urea, and mean arterial blood pressure (MBP) were analyzed at entry and after 40 and 60 months. RESULTS There was a significant decline of GFR in NIDDM patients and normal subjects at 60 months. The decline was significantly greater in HF patients (−0.61 ml · min−1.month−1; P = 0.001) than in NF (−0, 18) and control subjects (−0, 14); the rate of change in NF and control subjects was the same (P &amp;gt; 0.05). In stepwise multiple regression analysis, with GFR decline as the dependent variable and GFR and AER at baseline, age and change in MBP, change in urinary urea, change in HbA1c, and change in therapy as independent variables, only baseline GFR (R2 = 0.19, P = 0.002) and age (R2 = 0.31, P = 0.048) were significantly related to the outcome. At 60 months, AER raised &amp;gt; 20 μg/min in three HF and in four NF patients. In logistic regression analysis, only higher initial AER (although still in the normal range; P = 0.037) and an increase in urinary urea (P = 0.021) were significantly related to the later development of microalbuminuria. CONCLUSIONS The GFR of normoalbuminuric NIDDM patients declines significantly over 60 months. This decline is associated to baseline GFR and age. HF NIDDM patients show a faster decline in GFR than NF patients, whose GFR falls at a rate that is compatible with the age-related change observed in normal control subjects. The development of microalbuminuria is related to higher baseline AER and to increases in urinary urea and is similar in NF (4 of 19) and HF (3 of 13) NIDDM patients (P &amp;gt; 0.05).
Shared idiotypic determinants on B and T lymphocytes reactive against the same antigenic determinants. II. Determination of frequency and characteristics of idiotypic T and B lymphocytes in normal rats using direct visualization.
Authors: H Binz, H Wigzell
Journal: The Journal of Experimental Medicine (1975)

Anti-idiotypic antibodies made against the antigen-binding receptors of T lymphocytes for a given antigen (Ag-B locus antigens in rats) can be shown to react with IgG antibodies of the same antigen-binding reactivity. Using such anti-idiotypic antibodies, normal Lewis T lymphocytes of B and T type can be visualized by the use of anti-(Lewis-anti-DA) antibodies. Visualization was made possible by the use of direct fluorescent antibody tests or by autoradiography. Using the first technique and naked eye observations 6.2% of normal Lewis T lymphocytes expressed idiotypic markers signifying anti-DA reactivity, whereas anti-DA-reactive B lymphocytes as measured by this approach was in the order of 1.1%. Autoradiography was purified normal Lewis T lymphocytes gave similar figures. When comparing the intensity of fluorescence at the single cell level using quantitative cytofluorometry anti-idiotypic antibodies reactive with T lymphocytes gave a similar degree of intensity as was obtained using anti-Ig antibodies against B lymphocytes.
Emergency admissions to a general medical unit: A survey of the accompanying letters, with recommendations
Authors: P. K. Barnes, R. W. Hoile
Journal: BMJ (1969)

Letters of referral accompanied 166 out of 188 emergency admissions to a general medical unit over a four-month period. Of these, 129 contained useful information concerning past medical history, emergency treatment given, drugs taken, and provisional diagnosis. It is suggested that general practitioners should adopt some format based on essential criteria when writing letters of referral, so that important information is not overlooked.
Rodent models to study the relationships between mammals and their bacterial inhabitants
Authors: Rodrigo Bibiloni
Journal: Gut Microbes (2012)

Laboratory rodents have been instrumental in helping researchers to unravel the complex interactions that mammals have with their microbial commensals. Progress in defining these interactions has also been possible thanks to the development of culture-independent methods for describing the microbiota associated to body surfaces. Understanding the mechanisms that govern this relationship at the molecular, cellular, and ecological levels is central to both health and disease. The present review of rodent models commonly used to investigate microbial-host "conversations" is focused on those complex bacterial communities residing in the lower gut. Although many types of pathology have been studied using gnotobiotic animals, only the models relevant to commensal bacteria will be described.
Abstract 5527: Short-chain glucosylceramide improves doxorubicin delivery in spontaneous mouse breast carcinomas
Authors: Albert J. van Hell, Menno van Lummel, Gerben A. Koning, Wim J. van Blitterswijk, Marcel Verheij
Journal: Cancer Research (2010)

Abstract Background: Insufficient delivery of chemotherapeutic agents to their intended intracellular targets within the tumor remains a major obstacle in clinical oncology. Most of these drugs are amphiphilic and their diffusion through the plasma membrane is, therefore, slow and a major limitation for sufficient uptake within the tumor cell. We have found that certain short-chain sphingolipids enhance the intratumoral drug accumulation by modulation of inward translocation of cytostatics over the plasma membrane. Here, we examine this novel approach in an in vivo mouse model of aggressive invasive lobular breast carcinoma (ILC), designed to closely mimic its human counterpart. Results: In a panel of cell lines, short-chain sphingolipids, such as C8-glucosylceramide (GC) increase the intracellular accumulation of doxorubicin up to 4-fold. A clinically approved drug carrier (100 nm liposomes) was employed for co-delivery of both lipid and drug to the tumor tissue. The addition of 10 mol% GC markedly enhanced the cellular doxorubicin content in vivo, as was demonstrated with intravital fluorescence microscopy. In the metastatic and aggressive mouse ILC tumors, the efficacy of GC doxorubicin liposomes was significantly improved compared to the currently applied conventional doxorubicin liposomes. The enrichment with the GC membrane modulator resulted in a significant tumor growth delay (p = 0.0119) and an overall survival benefit (p = 0.0143) for mice treated with the GC enriched liposomal doxorubicin as compared to conventional liposomes. Conclusion: Short-chain sphingolipids improve the translocation of various cytostatics, including doxorubicin, over the plasma membrane of tumor cells. This membrane modulating strategy can be successfully applied in vivo, e.g. as a co-formulation with doxorubicin liposomes, thereby enhancing their anti-tumor efficacy. Furthermore, our data suggest that GC-enriched doxorubicin liposomes hold promise as anti-neoplastic therapy in human breast cancer. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 5527.
Abstract 1576: An oral therapeutic vaccine for colorectal cancer effectively eradicates intestinal tumors independently of target tumor-antigen specific immunities in APCMin/+ hCEA mice
Authors: Zhenyu Zhong, Yougang Zhai, Liang Qiao
Journal: Cancer Research (2012)

Abstract Colorectal cancer is among the leading cause of cancer-related death in patients worldwide, and the requirement of an effective vaccine is urgent. Here, we designed a pseudovirus-based therapeutic vaccine for colorectal cancer, which is comprised of a plasmid encoding a colorectal tumor-associated antigen (human CEA) packaged inside the bovine papillomavirus like particles (VLP-CEA vaccine). Oral immunization of APCMin/+ hCEA mice (a mouse model of human colorectal cancer) with VLP-CEA vaccine greatly reduced the tumor number compared with those received PBS. More importantly, the APCMin/+ hCEA mice that received pseudovirus vaccine had dramatically enhanced survival rates than those only received PBS. Surprisingly, CEA-specific adaptive immunities are dispensible for tumor elimination as similar tumor number reductions are seen in the APCMin/+ or APCMin/+ hCEA mice that are immunized with either VLP-CEA or VLP-GFP (VLPs packaging a GFP-containing plasmid). Consistently, we found that CTL responses are not required for tumor eradication since depleting CD8 T cells prior to vaccinations didn't impair the vaccine efficacy. Finally, we found that VLP-CEA and VLP-GFP are both able to activate the inflammasome which might directly induce tumor cell death. Thus, our data indicate that independent of the target tumor-antigen specific adaptive immunity, our pseudovirus-based therapeutic vaccine for colorectal cancer effectively eliminates already established intestinal tumors in an animal model, and the understanding of the immune mechanism by which pseudovirus vaccines eradicate colorectal tumorigenesis will further our knowledge for designing vaccines for other cancers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1576. doi:1538-7445.AM2012-1576
Beware of transfusions and hyperhaemolysis
Authors: A. Patel
Journal: BMJ (2008)

de Montalembert touches on important aspects of managing sickle cell disease, including the use of red blood cell transfusion as acute or regular top-ups and red cell exchanges.1

Hyperhaemolysis is a life threatening complication of red cell transfusions seen in 4% of paediatric and 1% of adult patients with sickle …
Abstract 1844: Reduced expression of miR-342-3p in prostate cancer.
Authors: Dominique Jones, Divine Anene, April Aloway, Praise Anene, Diana Avila, Leila Gobejishvili, Shirish Barve, Lacey McNally, LaCreis Kidd
Journal: Cancer Research (2013)

Abstract Patients with bone metastasis of the prostate have a 5-year survival rate of less than 30%. Due to inconsistencies in the presentation, prognosis, and treatment options of metastatic prostate cancer (PCa), biomarkers are urgently needed for personalized treatment of this disease. MicroRNAs (miRNAs) are small, non-coding, single-stranded endogenous RNAs that regulate the expression of multiple messenger RNA targets. Studies have demonstrated that these non-coding RNAs are significantly expressed in lung, breast and prostate cancer tumors. We hypothesize that miRNAs are differentially expressed between non-cancerous and aggressive tumor phenotypes in PCa, e.g. bone-specific metastasis. To test this hypothesis, we evaluated 384 miRNAs in the serum of stage-matched patients with stage I (n = 5), stage III (n = 5), stage IV (n = 5) PCa compared to non-cancerous age and stage-matched controls (n = 5). Total RNA was isolated from 500 μl of serum (Bioserve Biotechnologies, Ltd). The expression profiles of miRNAs were measured using TLDA cards and statistical analyses were performed using Expression Suite Software version 1.0. MiRNAs (miR-106b/17, -302b, -342-3p) were differentially expressed in the serum of PCa patients with (stage I, III, IV) when compared to controls. Mir-342-3p was significantly reduced in expression (P = 0.018-0.028) in all PCa patients relative to non-cancerous controls, after adjusting multiple hypothesis testing. However, other serum miRNAs were differentially expressed for only stage III PCa (P=0.001-0.018). Validation of these differentially expressed miRNAs in large sample sizes will lead to the identification of pre- and metastatic biomarkers. Ultimately, the investigation of these biomarkers will improve personalized treatment of PCa patients. Citation Format: Dominique Jones, Divine Anene, April Aloway, Praise Anene, Diana Avila, Leila Gobejishvili, Shirish Barve, Lacey McNally, LaCreis Kidd. Reduced expression of miR-342-3p in prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1844. doi:10.1158/1538-7445.AM2013-1844
Executive summary of the national “Sun Safety: Protecting Our Future” Conference: American Academy of Dermatology and Centers for Disease Control and Prevention New York, New York, May 1 and 2, 1997
Authors: June K. Robinson, Rex Amonette, Stephen W. Wyatt, Barbara A. Bewerse, Wilma F. Bergfeld, Patricia K. Farris
Journal: Journal of the American Academy of Dermatology (1998)
STUDIES OF L FORMS AND PROTOPLASTS OF GROUP A STREPTOCOCCI
Authors: Earl H. Freimer, Richard M. Krause, Maclyn McCarty
Journal: The Journal of Experimental Medicine (1959)

L forms of Group A streptococci have been isolated by the use of penicillin gradient agar plates. Osmotically fragile protoplasts of Group A streptococci have been obtained by the use of Group C phage-associated lysin which lyses Group A streptococci and their isolated cell walls. Membranes surrounding these enzymatically derived protoplasts have been isolated, and chemical and immunological studies indicate that they are free of cell wall carbohydrate and M protein. The streptococcal protoplasts reproduce as colonies which are morphologically indistinguishable from streptococcal L forms. Evidence is presented to show that these two streptococcal derivatives are serologically and physiologically related to each other as well as to the parent streptococcal strain from which they were isolated.
Expanding the Phenotype Associated With the<i>NEFL</i>Mutation
Authors: Pankaj B. Agrawal, Mugdha Joshi, Nicholas S. Marinakis, Klaus Schmitz-Abe, Pedro D. S. C. Ciarlini, Jane C. Sargent, Kyriacos Markianos, Umberto De Girolami, David A. Chad, Alan H. Beggs
Journal: JAMA Neurology (2014)

Newer sequencing technologies in combination with traditional gene mapping techniques, such as linkage analysis, can help identify the genetic basis of disease for patients with rare disorders of uncertain etiology. This approach may expand the phenotypic spectrum of disease associated with those genetic mutations.To elucidate the molecular cause of a neuromuscular disease among a family in which 4 members, a mother and her 3 sons, were affected.Two of 4 affected members manifested nemaline myopathy, a common subtype of congenital myopathy, while the other 2 had a nonspecific myopathy. Single-nucleotide polymorphism-based linkage analysis was performed on DNA samples from the 4 affected family members, and whole-genome sequencing was performed in the proband. Real-time quantitative reverse transcription-polymerase chain reaction, immunofluorescence, and Western blot analysis were performed on muscle biopsy specimens.Whole-genome sequencing and linkage analysis identified a variant in a gene that explains the phenotype.We identified a novel neurofilament light polypeptide (NEFL) nonsense mutation in all affected members. NEFL mutations have been previously linked to Charcot-Marie-Tooth disease in humans. This led us to reevaluate the diagnosis, and we recognized that several of the findings, especially those related to the muscle biopsy specimens and electromyography, were consistent with a neurogenic disease.NEFL mutations are known to cause Charcot-Marie-Tooth disease in humans and motor neuron disease in mice. We report the identification of an NEFL mutation in a family clinically manifesting congenital myopathy. We also describe potential overlap between myopathic and neurogenic findings in this family. These findings expand the phenotypic spectrum of diseases associated with NEFL mutations. This study is an example of the power of genomic approaches to identify potentially pathogenic mutations in unsuspected genes responsible for heterogeneous neuromuscular diseases.
Binge Drinking and Mortality After Acute Myocardial Infarction
Authors: Kenneth J. Mukamal, Malcolm Maclure, James E. Muller, Murray A. Mittleman
Journal: Circulation (2005)

Background— Moderate drinkers have a lower risk of mortality after myocardial infarction (MI). Although binge drinking has been associated with a higher risk of MI in some studies, its relation to prognosis after MI is uncertain. Methods and Results— In a prospective, inception cohort study conducted at 45 US hospitals, 1935 patients hospitalized with a confirmed MI between 1989 and 1994 underwent detailed personal interviews. Patients reported their usual frequency of binge drinking of beer, wine, and liquor, defined as intake of 3 or more drinks within 1 to 2 hours, and were followed up for mortality for a median of 3.8 years. Of 1919 eligible patients, 250 (94% men) reported binge drinking during the prior year, and a total of 318 patients died during follow-up. Binge drinkers had a 2-fold higher risk of mortality than drinkers who did not binge (hazard ratio, 2.0; 95% confidence interval, 1.3 to 3.0). A comparison of 192 binge drinkers and 192 other patients matched on propensity scores yielded a similar result. The association between binge drinking and total mortality tended to be similar among patients whose usual alcohol intake was light or heavier and for binge drinkers who consumed beer, wine, or liquor. Usual alcohol intake was inversely associated with mortality, but binge drinking completely attenuated this relation. Conclusions— Our results suggest that alcohol consumption may be linked to potential hazards among patients who survive acute MI. Although moderate intake has been associated with lower mortality, binge drinking, even among light drinkers, appears to be associated with 2-fold higher mortality.
The Scal atrial natriuretic peptide gene wariants are associated with the extent of coronary artery disease
Authors: Dariusz Ciecwierz, Marcin Gruchala, Bartosz Wasag, Radoslaw Targonski, Karolina Ochman, Witold Dubaniewicz, Wojciech Sobiczewski, Jerzy Bellwon, Adam Grzybowski, Bartosz Curyllo, Andrzej Rynkiewicz
Journal: Journal of the American College of Cardiology (2002)
Monoclonal immunoglobulin with antitransferrin activity: a rare cause of hypersideremia with increased transferrin saturation
Authors: Marie-Alexandra Alyanakian, Youri Taes, Mimouna Bensaïd, Berta Segovia, Pierre Aucouturier, Jean-Didier Rain, Joris Delanghe, Bruno Varet, Carole Beaumont
Journal: Blood (2006)
Coffee Intake and Serum Lipids in Men-Reply
Authors: Paul T. Williams
Journal: JAMA (1985)

In Reply.—  The letters of Drs Weyrauch, Hershberg, Zeller, and Kirkland raise several issues we now address.  Diet Records.—  In response to Dr Weyrauch, we emphasize that the nutrient and cholesterol content of creamers added to coffee was included in the adjustment of the coffee-lipoprotein relationship for dietary factors.  The NASA Study.—  Dr Hershberg is not correct in his statement that the mere selection of a larger sample eliminates the potential for confounding variables to influence the results. Case-control studies such as the National Aeronautics and Space Administration (NASA) study are particularly sensitive to confounding variables and depend entirely on the adequacy of the matching of patients with controls; the NASA study as described was controlled (matched) for age and sex only. The status of coffee as a risk factor is similar to that of other nutrients; reduced intakes of dietary saturated fat, cholesterol, and salt and increased intakes of
Near patient testing for respiratory syncytial virus in paediatric accident and emergency: prospective pilot study
Authors: A. Mackenzie, N. Hallam, E. Mitchell, T. Beattie
Journal: BMJ (1999)

Time was the most critical criterion; only 14% of the patients were admitted in due time.However, this percentage would probably increase if alteplase were approved, so we also estimated treatment effect assuming the ideal-all patients admitted in due time.In this case 539 patients (45%) would have been eligible (figure).Of these patients, 119 died and 150 had full recovery, leaving 270 patients who survived but did not achieve full recovery who could have benefited from treatment.An estimated 48 patients (150 × 0.32 = 48 (1 to 105)), or 4% (0.1% to 8%) of the stroke population, would have benefited from treatment.