tbuckley/cabot-search huggingface dataset:
Ampicillin/Sulbactam
Authors: Petros I Rafailidis, Eleni N Ioannidou, Matthew E Falagas
Journal: Drugs (2007)

Ampicillin/sulbactam is a β-lactam/β-lactamase inhibitor combination with a broad spectrum of antibacterial activity against Gram-positive, Gram-negative and anaerobic bacteria. Data from comparative studies justify the use of ampicillin/sulbactam in a 2: 1 ratio in various severe bacterial infections. In comparative clinical trials, ampicillin/sulbactam has proved to be a significant drug in the therapeutic armamentarium for lower respiratory tract infections and aspiration pneumonia, gynaecological/obstetrical infections, intra-abdominal infections, paediatric infections such as acute epiglottitis and periorbital cellulitis, diabetic foot infections, and skin and soft tissue infections. Of particular interest during this era of increasing antimicrobial resistance in various settings and populations is the effectiveness of sulbactam against a considerable proportion of infections due to Acinetobacter baumannii.
Avoiding delays in emergency admissions
Authors: R Madhok
Journal: BMJ (1994)

EDITOR, - Once a decision has been made to admit acutely ill patients it is absurd to keep them waiting on trolleys in busy accident and emergency departments while hard pressed junior doctors search for beds to accommodate them. Charging the hospitals with the responsibility to ensure a minimum wait1 may help to alleviate the sufferings of patients and the staff. Achieving the objective may, …
Basic fibroblast growth factor improves myocardial function in chronically ischemic porcine hearts.
Authors: K Harada, W Grossman, M Friedman, E R Edelman, P V Prasad, C S Keighley, W J Manning, F W Sellke, M Simons
Journal: Journal of Clinical Investigation (1994)

The effect of basic fibroblast growth factor (bFGF) administration on regional myocardial function and blood flow in chronically ischemic hearts was studied in 26 pigs instrumented with proximal circumflex coronary artery (LCX) ameroid constrictors. In 13 animals bFGF was administered extraluminally to the proximal left anterior descending (LAD) and LCX arteries with heparin-alginate beads and 13 other animal served as controls. bFGF-treated pigs showed a fourfold reduction in left ventricular infarct size compared to untreated controls (infarct size: 1.2 +/- 0.4% vs. 5.1 +/- 1.3% of LV mass, mean +/- SEM, P < 0.05). Percent fractional shortening (% FS) in the LCX area at rest was reduced compared with the LAD region in both bFGF and control pigs. However, there was better recovery in the LCX area after rapid pacing in bFGF-treated pigs (% FSLCX/% FSLAD, 22.9 +/- 7.3%-->30.5 +/- 8.5%, P < 0.05 vs. prepacing) than in controls (16.0 +/- 7.8%-->14.3 +/- 7.0%, P = NS). Furthermore, LV end-diastolic pressure rise with rapid pacing was less in bFGF-treated than control pigs (pre-pacing; pacing; post-pacing, 10 +/- 1; 17 +/- 3; 11 +/- 1* mmHg vs 10 +/- 1; 24 +/- 4; 15 +/- 1 mmHg, *P < 0.05 vs. control). Coronary blood flow in the LCX territory (normalized for LAD flow) was also better during pacing in bFGF-treated pigs than in controls. Thus, periadventitial administration of bFGF in a gradual coronary occlusion model in pigs results in improvement of coronary flow and reduction in infarct size in the compromised territory as well as in prevention of pacing-induced hemodynamic deterioration.
SUDDEN INFANT DEATH AND LONG-CHAIN 3-HYDROXYACYL-CoA DEHYDROGENASE
Authors: R.J.A. Wanders, M. Duran, L. Ijlst, J.P. De Jager, A.H. Van Gennip, C. Jakobs, L. Dorland, F.J. Van Sprang
Journal: The Lancet (1989)
THE PROBLEMS OF TUBERCULOSIS CONTROL
Authors: ESMOND R. LONG
Journal: Annals of Internal Medicine (1952)

Editorial1 November 1952THE PROBLEMS OF TUBERCULOSIS CONTROLESMOND R. LONG, F.A.C.P.ESMOND R. LONG, F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-37-5-1095 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptRecent advances in the treatment of tuberculosis have raised for new consideration the much debated question of proper balance among the various procedures employed in control of this disease. A review of past achievements, with an analysis of the current program, and a reévaluation of immediate objectives seem to be warranted at this time.ACHIEVEMENTS OF THE LAST HALF CENTURYFor historical perspective in the problem it will be useful to review the accomplishments of the last fifty years in tuberculosis control by quarter centuries. The period from 1900 to 1925 was characterized by rapid advance in diagnosis through the...1 AndersonBlomquist RJET: Tuberculosis control: a total program, Public Health Reports 66 (Tuberculosis Control Issue No. 59): 132, 1951. CrossrefMedlineGoogle Scholar2 Case Finding, Tuberculosis Morbidity, and other Data, 1951. A Computation and Preliminary Analysis of Data Submitted by States on the Semi-Annual and Annual Tuberculosis Reports for the Calendar Year 1951. Circulated in mimeographed form by the Public Health Service, Federal Security Agency, Washington, D. C., 1952. Google Scholar3 Dempsey M: Current status of the tuberculosis problem. Circulated in mimeographed form by the National Tuberculosis Association, New York, N. Y., 1952. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byEarly Ambulatory Treatment of Pulmonary Tuberculosis with IsoniazidDiscussion 1 November 1952Volume 37, Issue 5Page: 1095-1099 Issue Published: 1 November 1952 PDF downloadLoading ...
Polymorphisms in xenobiotic transporters ABCB1, ABCG2, ABCC2, ABCC1, ABCC3 and multiple myeloma risk: a case–control study in the context of the International Multiple Myeloma rESEarch (IMMEnSE) consortium
Authors: A Martino, D Campa, G Buda, J Sainz, R García-Sanz, K Jamroziak, R M Reis, N Weinhold, M Jurado, R Ríos, Z Szemraj-Rogucka, H Marques, J Szemraj, A Stein, R Kumar, E Orciuolo, F Gemignani, S Landi, H Goldschmidt, M Petrini, C Dumontet, F Canzian, A M Rossi
Journal: Leukemia (2011)
Overexpression of far upstream element binding proteins: A mechanism regulating proliferation and migration in liver cancer cells
Authors: Mona Malz, Achim Weber, Stephan Singer, Vera Riehmer, Michaela Bissinger, Marc-Oliver Riener, Thomas Longerich, Christopher Soll, Arndt Vogel, Peter Angel, Peter Schirmacher, Kai Breuhahn
Journal: Hepatology (2009)

Microtubule-dependent effects are partly regulated by factors that coordinate polymer dynamics such as the microtubule-destabilizing protein stathmin (oncoprotein 18). In cancer cells, increased microtubule turnover affects cell morphology and cellular processes that rely on microtubule dynamics such as mitosis and migration. However, the molecular mechanisms deregulating modifiers of microtubule activity in human hepatocarcinogenesis are poorly understood. Based on profiling data of human hepatocellular carcinoma (HCC), we identified far upstream element binding proteins (FBPs) as significantly coregulated with stathmin. Coordinated overexpression of two FBP family members (FBP-1 and FBP-2) in >70% of all analyzed human HCCs significantly correlated with poor patient survival. In vitro, FBP-1 predominantly induced tumor cell proliferation, while FBP-2 primarily supported migration in different HCC cell lines. Surprisingly, reduction of FBP-2 levels was associated with elevated FBP-1 expression, suggesting a regulatory interplay of FBP family members that functionally discriminate between cell division and mobility. Expression of FBP-1 correlated with stathmin expression in HCC tissues and inhibition of FBP-1 but not of FBP-2 drastically reduced stathmin at the transcript and protein levels. In contrast, further overexpression of FBP-1 did not affect stathmin bioavailability. Accordingly, analyzing nuclear and cytoplasmic areas of HCC cells revealed that reduced FBP-1 levels affected cell morphology and were associated with a less malignant phenotype.The coordinated activation of FBP-1 and FBP-2 represents a novel and frequent pro-tumorigenic mechanism promoting proliferation (tumor growth) and motility (dissemination) of human liver cancer cells. FBPs promote tumor-relevant functions by at least partly employing the microtubule-destabilizing factor stathmin and represent a new potential target structure for HCC treatment.
What Does Brain Thyrotropin-Releasing Hormone Do?
Authors: Arthur J. Prange, Robert D. Utiger
Journal: New England Journal of Medicine (1981)

IN this issue of the Journal,1 Faden and his colleagues report that thyrotropin-releasing hormone (TRH) dramatically ameliorates the neurologic consequences of spinal-cord injury in cats. This finding has both specific and general implications. Specifically, it holds promise for the treatment of cord trauma in human beings. Generally, it adds to the already imposing list of properties of TRH.TRH and several other hypothalamic peptides that regulate the secretion of several pituitary hormones have been isolated and characterized within the past 10 to 12 years. It soon became evident that these peptides were present not only in hypothalamic tissue but . . .
Fibroblast growth factor 2 isoforms and cardiac hypertrophy
Authors: E KARDAMI
Journal: Cardiovascular Research (2004)

Fibroblast growth factor 2 (FGF-2), a multifunctional polypeptide that affects cell growth and differentiation and becomes upregulated by stress, is expressed as AUG-initiated 18 kDa FGF-2 or CUG-initiated 21–34 kDa (hi-FGF-2) isoforms. Animal models have provided strong evidence that FGF-2 is essential for the manifestation of overload- and angiotensin-induced cardiac hypertrophy. Nevertheless, studies to-date have not discriminated between the activities of 18 kDa FGF-2 and hi-FGF-2. Our recent work has pointed to a potent pro-hypertrophic effect of added hi-FGF-2, and a pro-apoptotic effect of sustained intracrine hi-FGF-2 signaling. In the future, it will be important to differentiate between the activities of the different FGF-2 isoforms in the context of adaptive and maladaptive myocardial hypertrophy and heart failure. Based on all available evidence, we propose that while the 18-kDa FGF-2 is a component of an adaptive trophic response, a switch to hi-FGF-2 accumulation would exacerbate hypertrophy and contribute to cell death, thus driving the myocardium towards a maladaptive phenotype.
Anti‐eosinophil activity and clinical efficacy of the <scp>CRTH</scp>2 antagonist <scp>OC</scp>000459 in eosinophilic esophagitis
Authors: A. Straumann, S. Hoesli, Ch. Bussmann, M. Stuck, M. Perkins, L. P. Collins, M. Payton, R. Pettipher, M. Hunter, J. Steiner, H.‐U. Simon
Journal: Allergy (2013)

Abstract Background Eosinophilic esophagitis ( E o E ) is a chronic, T h2‐type inflammatory disease. Chemoattractant receptor‐homologous molecule on Th2 cells ( CRTH 2) is a prostaglandin D 2 ( PGD 2 ) receptor, expressed by Th2 cells and other inflammatory cells, including eosinophils and basophils, that mediates chemotaxis and activation. OC 000459 is a selective CRTH 2 antagonist and would be expected to suppress eosinophilic tissue inflammation. The purpose of this study was to evaluate the efficacy and safety of an OC 000459 monotherapy in adult patients with active, corticosteroid‐dependent or corticosteroid‐refractory E o E . Methods In this randomized, double‐blind, placebo‐controlled trial, 26 adult patients (m/f = 22/4; mean age 41 years, range 22–69 years) with active E o E , dependent or resistant to corticosteroids, were treated either with 100 mg OC 000459 ( n = 14) or placebo ( n = 12) twice daily. Pre‐ and post‐treatment disease activity was assessed clinically, endoscopically, histologically, and via biomarkers. The primary end point was the reduction in esophageal eosinophil infiltration. Results After an 8‐week OC 000459 treatment, the esophageal eosinophil load decreased significantly, from 114.83 to 73.26 eosinophils per high‐power field [(eos/hpf), P = 0.0256], whereas no reduction was observed with placebo (102.80–99.47 eos/hpf, P = 0.870). With OC 000459, the physician's global assessment of disease activity improved from 7.13 to 5.18 ( P = 0.035). OC 000459 likewise reduced extracellular deposits of eosinophil peroxidase and tenascin C , the effects not seen with placebo. No serious adverse events were observed. Conclusions An 8‐week treatment with the CRTH 2‐antagonist, OC 000459, exerts modest, but significant, anti‐eosinophil and beneficial clinical effects in adult patients with active, corticosteroid‐dependent or corticosteroid‐refractory EoE and is well tolerated.
Assessment of transesophageal doppler echography in dissecting aortic aneurysm
Authors: Satoshi Hashimoto, Toshiaki Kumada, Genta Osakada, Shigeru Kubo, Shingo Tokunaga, Shunichi Tamaki, Arid Yamazato, Kazunobu Nishimura, Toshihiko Ban, Chuichi Kawai
Journal: Journal of the American College of Cardiology (1989)
Abstract 5261: Transfection of nerve growth factor cDNA into SK-N-BE(2)C neuroblastoma modulates TrkA and p75 receptor expression and activation
Authors: Janette L. Holub, Timothy B. Lautz, Fei Chu, Sandra H. Clark, Mary Beth Madonna
Journal: Cancer Research (2010)

Abstract The diverse biological role of nerve growth factor (NGF) as a necessary modulator of neuroectodermal cell survival, proliferation and differentiation has been previously well described in both normal and neoplastic cell lines. However, recent studies demonstrate that neuroectodermal tumors, such as neuroblastoma, contain genetic alterations that result in limited secretion of active NGF, as well as expression abnormalities of its receptors TrkA and p75. To better define the differential effects of exogenous and endogenously synthesized NGF, the in vitro response of wild-type and genetically engineered neuroblastoma cells was investigated. Replication-defective NGF-expressing retroviral vectors were prepared using the calcium phosphate co-precipitation method and used to transfect SK-N-BE(2)C cells. Presence of the NGF cDNA was confirmed by RT-PCR, and secretion of NGF into the conditioned media by western immunoblotting. NGF transfection resulted in decreased cell proliferation as determined by nonradioactive cell proliferation assay. Wild type and NGF transfected (BE(2)C-NGF) cells were then incubated with exogenous NGF at 200ng/mL for varying time periods up to 24 hours. The expression of TrkA and p75, as well as proteins of their associated survival and apoptosis cascades were determined by Western immunoblotting of whole cell lysates. p75 expression in the NGF transfected cell line was equivalent to the parental wild type cell, but TrkA expression was significantly lower in BE(2)C-NGF. At baseline, BE(2)C-NGF cells demonstrate significant down-regulation of phospho-cRAF and its downstream effector phospho-p42/44 in comparison to the wild type cell line. Additionally, NGF stimulation further down-regulated phospho-c-RAF expression in the NGF transfected cell line, with maximal down-regulation occurring at 24 hours. BE(2)C-NGF cells also demonstrate significant baseline activation of phospho-p38 in comparison to the wild type cell line, with expression further up-regulated with NGF stimulation at 5 minutes and 1 hour. In conclusion, nerve growth factor cDNA gene transfer into wild type SK-N-BE(2)C neuroblastoma results in decreased activation of the p-42/44 survival pathway and concomitant up-regulation of the p-38 apoptotic pathway, leading to a overall decreased rate of proliferation. This effect is likely the result of a decreased TrkA to p75 receptor ratio, and further understanding of these pathways may facilitate the discovery of novel therapeutic targets for neuroblastoma treatment. 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 5261.
“Anecdotal Evidence”: Why Narratives Matter to Medical Practice
Authors: Rafael Campo
Journal: PLoS Medicine (2006)

I want to tell you a story.

After a lecture I gave recently at a well-known medical school on the possible utility of narrative to clinical practice, from the back of the auditorium came the first question of the traditional question and answer portion of the program: “Don't you feel, Dr. Campo, that what you seem to regard as the arrogant biomedical science model of medicine is already sufficiently under attack these days?”

As the lights came up, I could make out a tall, bearded man in a long white coat, standing as if at attention near the end of one of the aisles. “We have creationists trying to teach ‘intelligent design’ in our children's science classes, and even closer to home, nurses and optometrists being given the right to prescribe medications.” Their applause having ceased, my audience now grew hushed as he went on, his voice steadily rising.

“Do you really expect physicians to accept the notion that what any ignorant patient tells us about his disease should carry a weight equal to what our years of training and expertise reveals to us about complex pathophysiology?” Then came what was clearly meant to be his coup de grace, delivered in an almost derisive tone. “Really, sir, do you have anything more than the anecdotal evidence you shared to support your thesis?”
Identification of three mutant alleles of the gene for mitochondrial acetoacetyl-coenzyme A thiolase. A complete analysis of two generations of a family with 3-ketothiolase deficiency.
Authors: T Fukao, S Yamaguchi, T Orii, R B Schutgens, T Osumi, T Hashimoto
Journal: Journal of Clinical Investigation (1992)

3-Ketothiolase deficiency (3KTD) stems from a deficiency of mitochondrial acetoacetyl-coenzyme A thiolase (T2). We analyzed the molecular basis of 3KTD in two generations of a family. A boy (patient 2, GK04), his father (patient 1, GK05), his mother, and his brother were studied; three mutant alleles of T2 gene were identified. Patient 1 is a compound heterozygote: one allele has a point mutation of G to A at position 547 on his T2 cDNA, causing Gly150 to Arg substitution of the mature T2 subunit, and the other allele has GT to TT transition at the 5' splice site of intron 8, causing exon 8's skipping of the T2 cDNA. Patient 2 is also a compound heterozygote: one allele inherited from his mother has AG to CG transition at the 3' splice site of intron 10, causing exon 11's skipping of the T2 cDNA, and the other allele derived from patient 1 has the G to A mutation (Gly to Arg). The brother of patient 2 is an obligatory carrier with the mutant allele causing the exon 8 skipping. This report seems to be the first complete molecular definition of 3KTD at the gene level.
Raised number of jejunal IgG2-producing cells in untreated adult coeliac disease compared with food allergy.
Authors: T O Rognum, K Kett, O Fausa, U Bengtsson, A Kilander, H Scott, P I Gaarder, P Brandtzaeg
Journal: Gut (1989)

The subclass distribution of IgG-producing immunocytes was studied by two colour immunohistochemistry with monoclonal antibodies in jejunal biopsy specimens from 10 adults with untreated coeliac disease, 11 coeliac disease patients on a gluten free diet, and seven patients with established food allergy. Paired immunofluorescence staining was performed with subclass specific murine monoclonal antibodies in combination with polyclonal rabbit antibody reagent to total IgG; the proportion of cells belonging to each subclass could thereby be determined. The ratio of IgG2 immunocytes was significantly higher (p less than 0.05) in untreated coeliac disease patients (median, 35.2%; range, 26.7-65.2%) than in those on a gluten free diet (median, 7.3%; range, 0-31.9%) or those having food allergy (median, 12.5%; range, 0-36.5%). The disparity in the local IgG2 response between patients with untreated coeliac disease and those with food allergy might be due to differences in the nature of the antigenic stimuli, dissimilar genetic 9make-up9 of the subjects, or both.
Surgery of the Ureter
Authors: Victor A. Politano
Journal: JAMA (1977)

The book on surgery of the ureter by Kuss is an excellent reference book. It covers the surgery of the ureter in considerable detail without being lengthy and repetitious. Surgical techniques to eliminate or minimize complications are stressed. Almost every conceivable condition and its method for resolution are presented. It is well illustrated in simple, easily understandable sketches. If there is any criticism of this book, it is that many of the anatomical sketches lack labeled structures, so the novice or anyone who is unfamiliar with pelvic or ureteral surgery may not immediately recognize all the structures illustrated. The section on ureteroneocystostomies, especially in reference to the management of vesicoureteral reflux, is perhaps the weakest section in the book. It is limited in surgical techniques and illustrations.
Differential response of early erythropoietic and granulopoietic progenitors to dexamethasone and cortisone.
Authors: F Zalman, M A Maloney, H M Patt
Journal: The Journal of Experimental Medicine (1979)

The sensitivity of erythropoietic (BFU-E) and granulopoietic (CFU-C) progenitor cells to dexamethasone and cortisone was studied in cultures of mouse bone marrow. Although the log dose-response relationships had a similar form, the BFU-E were much more sensitive than the CFU-C to either glucocorticoid. The dexamethasone concentration for 50% inhibition was 3 X 10)-9) M for BFU-E and 60 X 10(-9) M for CFU-C. The differential sensitivity to cortisone was even greater, with 60% inhibition of BFU-E and 18% inhibition of CFU-C at 0.1 microgram/ml. These findings suggest a specific rather than a general response to glucocorticoids and indicate that granulocyte-macrophage progenitors are less affected than early erythroid progenitors by physiologic concentrations of these hormones.
Case 20-1961
Authors: Richard C. Cabot, Benjamin Castleman, Betty U. Kibbee
Journal: New England Journal of Medicine (1961)

Presentation of Case A seventy-eight-year-old retired bartender was admitted to the hospital because of rectal bleeding. Six years previously there was an episode of bleeding by rectum, with the passage of bright-red blood. Subsequently, gradually increasing constipation occurred. The patient passed a bright-red stool on the day before entry. On the next day, after an enema and a cathartic, he passed four large, bloody stools. During the week before entry he was slightly anorectic, but there was no nausea, vomiting or loss of weight. There was a history of hypertension, orthopnea, nocturnal dyspnea and intermittent slight ankle edema. His physician . . .
Relation of boron to the composition and mechanical properties of bone.
Authors: H McCoy, M A Kenney, C Montgomery, A Irwin, L Williams, R Orrell
Journal: Environmental Health Perspectives (1994)

A review of the experimental studies relating boron to biological effects on appendicular and axial bones in animal models suggests that numerous influences, known and unknown, affect the responsiveness of bone to dietary boron. Degrees of skeletal response to boron are modified by other nutritional variables that include calcium, magnesium, vitamin D, and fluoride. Evidence suggests that appendicular and axial bones may differ in their responses. Tests of the mechanical properties of bones may provide useful criteria for assessing the impacts of boron status on bone. These tests might resolve questions about optimal intakes of boron because mechanical properties sometimes respond to boron when composition of bones does not. Difficulty in interpreting some of the existing research arises because of the incipient state of knowledge regarding boron nutriture, to analytical problems associated with determining accurately the small quantities of boron in feed and tissues, and to technological difficulties in controlling extraneous exposure of experimental animals to boron. Yet there is considerable evidence that both compositional and functional properties of bone are affected by boron status.