tbuckley/cabot-search huggingface dataset:
A MODIFICATION OF ALBERT'S STAIN FOR THE DIPHTHERIA BACILLUS
Authors: R. L. Laybourn
Journal: JAMA (1924)

Albert<sup>1</sup>described a new stain for diphtheria bacilli in 1920 and 1921 which has been used extensively in these laboratories. The advantages claimed for this stain are that the metachromatic granules are stained black and display a marked contrast to the body of the organism and other organisms present, facilitating the detection of the diphtheria bacillus when only a few are present in the smear. While this stain has been found useful, its efficiency might be greatly increased by a modification that would deepen the staining of both the granules and the body of the cell, without destroying the marked contrast between these elements. This may be accomplished by the substitution of malachite green for the methyl green of Albert's formula. This modification has been used in these laboratories on about twenty thousand cultures, with highly gratifying results. The formulas for the modified stain are: The solution should stand
Monitoring Resuscitation of the Injured Patient
Authors: John M. Hartong
Journal: JAMA (1977)

Physicians are being called on with increasing frequency to initiate resuscitation of the severely injured patient. The medical literature is confusing regarding the best way that this can be done. A study was undertaken to evaluate simultaneously four common, easily measured indexes—blood pressure, pulse rate, central venous pressure, and pulmonary artery pressure. A shock-trauma model employing laboratory-bred beagle dogs was developed. Results indicate that the best single index is pulmonary artery pressure. Certain physiologic principles make central venous pressure an unreliable index. (<i>JAMA</i>237:242-244, 1977)
Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter.
Authors: Ralph J Delfino, Penelope J E Quintana, Josh Floro, Victor M Gastañaga, Behzad S Samimi, Michael T Kleinman, L-J Sally Liu, Charles Bufalino, Chang-Fu Wu, Christine E McLaren
Journal: Environmental Health Perspectives (2004)

Exposure to particulate matter (PM) air pollution has been shown to exacerbate children's asthma, but the exposure sources and temporal characteristics are still under study. Children's exposure to PM is likely to involve both combustion-related ambient PM and PM related to a child's activity in various indoor and outdoor microenvironments. Among 19 children with asthma, 9-17 years of age, we examined the relationship of temporal changes in percent predicted forced expiratory volume in 1 sec (FEV1) to personal continuous PM exposure and to 24-hr average gravimetric PM mass measured at home and central sites. Subjects were followed for 2 weeks during either the fall of 1999 or the spring of 2000, in a southern California region affected by transported air pollution. FEV(subscript)1(/subscript) was measured by subjects in the morning, afternoon, and evening. Exposure measurements included continuous PM using a passive nephelometer carried by subjects; indoor, outdoor home, and central-site 24-hr gravimetric PM2.5 (PM of aerodynamic diameter < 2.5 microm) and PM10; and central-site hourly PM10, nitrogen dioxide, and ozone. Data were analyzed with linear mixed models controlling for within-subject autocorrelation, FEV1 maneuver time, and exposure period. We found inverse associations of FEV1 with increasing PM exposure during the 24 hr before the FEV1 maneuver and with increasing multiday PM averages. Deficits in percent predicted FEV1 (95% confidence interval) for given PM interquartile ranges measured during the preceding 24-hr were as follows: 128 microg/m3 1-hr maximum personal PM, -6.0% (-10.5 to -1.4); 30 microg/m3 24-hr average personal PM, -5.9% (-10.8 to -1.0); 6.7 microg/m3 indoor home PM2.5, -1.6% (-2.8 to -0.4); 16 microg/m3 indoor home PM10, -2.1% (-3.7 to -0.4); 7.1 microg/m3 outdoor home PM2.5, -1.1% (-2.4 to 0.1); and 7.5 microg/m3 central-site PM2.5, -0.7% (-1.9 to 0.4). Stronger associations were found for multiday moving averages of PM for both personal and stationary-site PM. Stronger associations with personal PM were found in boys allergic to indoor allergens. FEV1 was weakly associated with NO2 but not with O3. Results suggest mixed respiratory effects of PM in asthmatic children from both ambient background exposures and personal exposures in various microenvironments.
Adenosine-to-inosine RNA editing and human disease
Authors: William Slotkin, Kazuko Nishikura
Journal: Genome Medicine (2013)

A-to-I RNA editing is a post-transcriptional modification that converts adenosines to inosines in both coding and noncoding RNA transcripts. It is catalyzed by ADAR (adenosine deaminase acting on RNA) enzymes, which exist throughout the body but are most prevalent in the central nervous system. Inosines exhibit properties that are most similar to those of guanosines. As a result, ADAR-mediated editing can post-transcriptionally alter codons, introduce or remove splice sites, or affect the base pairing of the RNA molecule with itself or with other RNAs. A-to-I editing is a mechanism that regulates and diversifies the transcriptome, but the full biological significance of ADARs is not understood. ADARs are highly conserved across vertebrates and are essential for normal development in mammals. Aberrant ADAR activity has been associated with a wide range of human diseases, including cancer, neurological disorders, metabolic diseases, viral infections and autoimmune disorders. ADARs have been shown to contribute to disease pathologies by editing of glutamate receptors, editing of serotonin receptors, mutations in ADAR genes, and by other mechanisms, including recently identified regulatory roles in microRNA processing. Advances in research into many of these diseases may depend on an improved understanding of the biological functions of ADARs. Here, we review recent studies investigating connections between ADAR-mediated RNA editing and human diseases.
Heparan sulfate: growth control with a restricted sequence menu
Authors: John T. Gallagher
Journal: Journal of Clinical Investigation (2001)

The growth and differentiation of cells and their organization into organs and tissues are complex processes, largely determined by the concerted actions of the ECM and small, soluble “effector” proteins in the pericellular milieu. Cells respond to the instructive potential of their microenvironment by means of specialized plasma membrane receptors, which elicit intracellular signals when activated by cognate ECM or soluble peptide ligands. In many receptor systems, ligand binds first to an abundant, low-affinity receptor, which draws the ligand onto the cell surface and then transfers it to a second, high-affinity receptor that transduces the appropriate signal into the cell. The most common and widely acting low-affinity receptors are the heparan sulfate proteoglycans (HSPGs), which play central roles in the reception and modulation of a wide range of growth factors, morphogens, and chemokines (1–3). They also act in combination with membrane integrins to control cell adhesion and migration in the ECM (4).

The question arises as to how the structure and properties of the HSPGs enable them to fulfill such diverse and fundamental roles. These issues are the subject of intense experimental study, and a growing body of data has been published on the protein recognition properties of HSPGs and their association with signaling receptor complexes. However, more questions are being raised than problems solved by these analyses, perhaps as a result of the unusual properties of the HS chains that determine the majority of the interactions of PGs with external proteins. HS polysaccharides display a versatility in conformation and orientation of functional groups that permits them to employ different modes of binding with any individual protein or protein complex. Here, I argue that this versatility could offset the need for the controlled synthesis of a vast repertoire of defined sequences for exclusive binding of individual proteins.
Staphylococcal colonization in atopic dermatitis and the effect of topical mupirocin therapy
Authors: ROSEMARY LEVER, KAY HADLEY, D. DOWNEY, RONA MACKIE
Journal: British Journal of Dermatology (1988)

Forty-nine patients with atopic dermatitis entered a double blind placebo controlled cross-over study of mupirocin, a new topical antistaphylococcal antibiotic. Forty-five patients were evaluable. Quantitative bacteriological assessment before treatment showed that heavy colonization of the skin with Staphylococcus aureus was present in nearly all patients even in the absence of overt infection. However, the bacterial count was significantly reduced by 2 weeks' treatment with topical mupirocin, but not by the placebo. Moreover, a significant reduction of clinical severity was also observed after treatment with mupirocin, which was maintained over the following 4 weeks, although recolonization occurred during this period, with bacterial counts rising to pre-treatment levels. Despite recolonization, clinical deterioration was not observed during the trial period. No serious side-effects were observed. Phage typing showed that 50% of patients carried more than one bacterial phage type. Recolonization in eight patients (17%) was with a 'new' strain that had not previously been isolated.
Influence of Multidrug Resistance on Tuberculosis Treatment Outcomes with Standardized Regimens
Authors: Anton Mak, Adam Thomas, Mirtha del Granado, Richard Zaleskis, Nigor Mouzafarova, Dick Menzies
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Rationale: Multidrug-resistant tuberculosis (TB) poses a major challenge to global TB control. We analyzed the association between estimated prevalence of initial or acquired MDR-TB, and treatment outcomes reported nationally.Objectives: We analyzed the estimated prevalence of initial or acquired MDR-TB and treatment outcomes reported nationally.Methods: Countries were analyzed if multidrug resistance prevalence estimates were available, and if they reported outcomes for more than 250 cases treated using standardized regimens in 2003 and/or 2004. Data sources were the World Health Organization for treatment regimens, prevalence of initial multidrug resistance, and reported cases and treatment outcomes in 2003 and 2004; the Joint United Nations Programme on HIV/AIDS for HIV seroprevalence; and the World Bank for income per capita. The adjusted impact of initial multidrug resistance on initial and retreatment outcomes was estimated with weighted multivariate linear regression.Measurements and Main Results: Among countries using one of two standardized initial regimens, failure rates averaged 5.0%, and relapse rates averaged 12.8% in the 20 countries where prevalence of initial multidrug resistance exceeded 3%, compared with an average of 1.6% (P < 0.0001) and 8.1% (P = 0.0002), respectively, in 83 countries where initial multidrug resistance prevalence was less than 3%. In 92 countries using one standardized retreatment regimen, failure rates were 2.7%, 3.8%, 6.2%, and 8.1% in quartiles of increasing prevalence of acquired multidrug resistance (P < 0.0001). When stratified by initial multidrug resistance prevalence, initial and retreatment outcomes in the 79 countries using the 6-month rifampin initial regimen were not significantly different from the 24 countries using the 2-month rifampin initial regimen.Conclusions: Currently recommended standardized TB initial and retreatment regimens should be reevaluated in countries where prevalence of initial multidrug resistance exceeds 3%, in view of poor treatment outcomes.
Effects of incremental doses of procainamide on ventricular refractoriness, intraventricular conduction, and induction of ventricular tachycardia.
Authors: F Morady, L A DiCarlo, M de Buitleir, R B Krol, J M Baerman, W H Kou
Journal: Circulation (1986)

The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.
Cohypermethylation of <i>p16</i> and <i>FHIT</i> Promoters as a Prognostic Factor of Recurrence in Surgically Resected Stage I Non–Small Cell Lung Cancer
Authors: Jin Seuk Kim, Jin Wook Kim, Joungho Han, Young Mog Shim, Joobae Park, Duk-Hwan Kim
Journal: Cancer Research (2006)

Abstract Despite advances in the detection and treatment of lung cancer, the prognosis for patients with lung cancer is poor, partly as a result of recurrences. We retrospectively analyzed the relationship between recurrence and survival in patients with non–small cell lung cancers (NSCLC), and the promoter methylation of p16, GSTP1, FHIT, H-cadherin, and RARβ2 genes to identify a prognostic molecular marker associated with the recurrence of NSCLC. Methylation status from 335 paraffin blocks was determined by methylation-specific PCR. Of the 335 NSCLC samples, promoter methylation was detected in 35% for p16, 39% for RARβ2, 42% for H-cadherin, 7% for GSTP1, and 21% for FHIT. Recurrence was observed in 39% (132 of 335) of the patients. Recurrence was significantly associated with histology (P = 0.001) and pathologic stage (P = 0.009). Hypermethylation of any single gene was not associated with recurrence in patients. However, cohypermethylation of p16 and FHIT genes in stage I NSCLCs was associated with an increased risk of recurrence [odds ratio, 6.43; 95% confidence interval (CI), 1.04-20.19; P = 0.02] and poor recurrence-free survival after surgery (hazard ratio, 2.03; 95% CI, 1.09-6.23; P = 0.02). In addition, their survival after recurrence was also 4.62 times poorer (95% CI, 1.27-16.48; P = 0.005) than for those without cohypermethylation of both genes. In conclusion, the present study suggests that cohypermethylation of p16 and FHIT genes in patients with stage I NSCLC may be a valuable biomarker for predicting the recurrence-associated prognosis of the disease. (Cancer Res 2006; 66(8): 4049-54)
The Carpal Tunnel Syndrome in Cardiologists
Authors: Kenneth Stevens
Journal: Annals of Internal Medicine (1990)

Letters and Corrections15 May 1990The Carpal Tunnel Syndrome in CardiologistsKenneth Stevens, MDKenneth Stevens, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-112-10-796_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:I noticed that the recent article (1) and accompanying editorial (2) on work-related carpal tunnel syndrome did not mention an under-reported group of people: those involved with invasive cardiology. In our large multispecialty group, a number of cardiologists as well as cardiovascular technicians have the condition. Some of them have required constant splinting or a change in job whereas others have needed carpal tunnel release. This aspect of the syndrome appears related to the the performance of intra-aortic balloon pump and sheath removal for cardiac catheterization and percutaneous transluminal coronary angioplasty. At Marshfield, we are currently pursuing...References1. KatzLarsonSabra JMA. The carpal tunnel syndrome: diagnostic utility of the history and physical examination findings. Ann Intern Med. 1990;112:321-7. LinkGoogle Scholar2. BakerEhrenberg ER. Preventing the work-related carpal tunnel syndrome: physician reporting and diagnostic criteria [Editorial]. Ann Intern Med. 1990;112:317-9. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Marshfield Clinic Marshfield, WI 54449 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByInvited Epidemiologic Comment 15 May 1990Volume 112, Issue 10Page: 796-796KeywordsCatheterizationPercutaneous transluminal coronary angioplastyTechnicians Issue Published: 15 May 1990 PDF DownloadLoading ...
Adenosine triphosphate-dependent transport of estradiol-17?(?-d-glucuronide) in membrane vesicles by MDR1 expressed in insect cells
Authors: Liyue Huang, Tim Hoffman, Mary Vore
Journal: Hepatology (1998)

MDR1, an ABC transporter that confers multidrug resistance in tumor cells, is constitutively expressed in normal liver canalicular membrane. Human MDR1-expressing multidrug-resistant cells display increased resistance to estradiol-17beta(beta-D-glucuronide) (E217G). MDR1 substrates/modulators inhibit adenosine triphosphate (ATP)-dependent transport of E217G in the rat canalicular membrane and protect against E217G-mediated cholestasis in isolated perfused rat liver. The present studies were designed to determine if E217G is a substrate for MDR1 using a baculovirus expression system and if other estrogen glucuronides interact with MDR1. ATP-dependent transport of E217G (10 micromol/L) was linear for up to 2 minutes and yielded a rate of 45.6 pmol/min/mg protein in membrane vesicles from Sf9 cells infected with MDR1-baculovirus. This transport was saturable (Km = 62 micromol/L) and occurred into an osmotically sensitive space. ATP-dependent transport of E217G (10 micromol/L) was inhibited 63% by 10 micromol/L daunomycin, but not by 100 micromol/L S-(2,4-dinitrophenyl)glutathione (GS-DNP) (a substrate for canalicular multispecific organic anion transporter [cMOAT]). Glucuronide conjugates of the estrogen D-ring (100 micromol/L), estriol-17beta(beta-D-glucuronide) (E317G) and estriol-16(beta-D-glucuronide) (E316G), inhibited MDR1-mediated E217G transport by 58% and 35%, respectively. In contrast, noncholestatic glucuronides, estradiol-3-(beta-D-glucuronide) (E23G) or estradiol-3-sulfate-17beta(beta-D-glucuronide) (E23SO417G), had no effect. E217G neither stimulated MDR1 ATPase activity nor inhibited verapamil-stimulated ATPase activity. Infusion of 1.5 micromol/L doxorubicin or 1 micromol/L taxol protected against cholestasis induced by E316G and E317G in isolated perfused rat liver. These studies identify E217G, and probably E316G and E317G, as endogenous substrates for MDR1.
Wheezing with Rhinovirus but not Respiratory Syncytial Virus Infections in the First Three Years of Life Predicts Decreased Lung Function at Age Five
Authors: T.E. Pappas, M.D. Evans, K.T. Sullivan Dillie, K.A. Roberg, D.F. DaSilva, C.J. Tisler, E.L. Anderson, L.E. Pleiss, R. Gangnon, J.E. Gern, R.F. Lemanske
Journal: Journal of Allergy and Clinical Immunology (2006)
A7.7 Different Genetic Background of Dermatomyositis and Polymyositis in a Single Centre Cohort
Authors: M Remakova, M Skoda, T Svitalkova, M Faustova, L Plestilova, Z Betteridge, H Mann, J Vencovsky, O Krystukova, P Novota
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> The idiopathic inflammatory myopathies (IIM) are systemic connective tissue diseases in which autoimmune pathology is responsible for promotion of chronic muscle inflammation and weakness. As in many other autoimmune diseases, the development of IIM is also associated with genes of HLA complex. The aim of this study was to determine the basic relation between alleles of HLA genes and IIM. <h3>Materials and Methods</h3> We have performed low to high resolution genotyping to characterise the allelic profiles of HLA-DRB1, -DQB1 and -DQA1 loci in a large group of single centre cohort of patients suffering from IIM (n = 269). The genomic DNA was prepared by standard DNA extraction methods and the HLA typing was done using the commercial LABType® SSO kit (One Lambda, USA). Statistical evaluation of results was done with chi-2 test and Fisher exact test. Autoantibody profiles were analysed with radioactive immunoprecipitation. <h3>Results</h3> The frequencies of HLA-DRB1*03:01 and -DRB1*16:01 alleles were increased in IIM patients and the difference reached statistical significance when compared to healthy controls (P &lt; 0.01 for DRB1*03:01; P &lt; 0.05 for DRB1*16:01). Different alleles were associated with dermatomyositis (DM) or polymyositis (PM). The frequency of DRB1*16:01 was significantly higher in DM patients (P &lt; 0.01), whereas the frequency of DRB1*03:01 was higher in patients suffering from PM (P &lt; 0.01), when compared to controls. Presence of HLA-DRB1*03:01 allele was associated with anti-Jo-1, anti-Ro52, or anti-Pm-Scl positivity in all IIM patients (P &lt; 0.05). Interestingly, the DRB1*03:01 allele was also associated with the negativity for anti-p155/140 in our patients (P &lt; 0.01). The DRB1*16:01 allele was associated with negativity of all studied autoantibodies, particularly in subgroup of DM patients (P &lt; 0.05). <h3>Conclusions</h3> This study identifies different genetic background between patients with dermatomyositis and polymyositis in a homogenous population of patients from a single centre. <h3>Acknowledgement</h3> This work is supported by Internal Grant Agency of Ministry of Health of the Czech Republic NT/12438–4 and NT/13699.