tbuckley/cabot-search huggingface dataset:
Drug-Resistant Tuberculosis: Inconsistent Results of Pyrazinamide Susceptibility Testing-Reply
Authors: Max Salfinger
Journal: JAMA (1995)

<h3>In Reply.</h3> —Pyrazinamide is one of the most important drugs in modern chemotherapy of tuberculosis; its inclusion in treatment regimens has made possible the shortening of therapy to 6 months. The recent increase in tuberculosis with several nosocomial outbreaks of multidrug-resistant strains has challenged the public health system. New recommendations by the CDC and the American Thoracic Society<sup>1,2</sup>require in vitro drug susceptibility testing of<i>M tuberculosis</i>isolates for all five first-line drugs (pyrazinamide included) from all patients and reporting of these results to the local health department. Unfortunately, testing the susceptibility of tubercle bacilli to pyrazinamide is problematic since pyrazinamide is active only at an acid pH. After a series of reports regarding susceptibility testing (available from the author on request), 100 μg of pyrazinamide per milliliter at pH 6.0 is now the recommended test concentration.<sup>3</sup> The results of Dr Hewlett and coworkers are so unexpectedly divergent
Hearing loss and connexin 26
Authors: M. H Kemperman, L. H Hoefsloot, C. W R J Cremers
Journal: Journal of the Royal Society of Medicine (2002)

Hearing impairment is a sensory disability that affects millions of people all over the world. Though not life-threatening, it can become a major burden in social and professional life. In the industrialized world, deafness of infective and/or environmental origin has become less frequent, with a consequent rise in the proportion of hereditary hearing impairment. Deafness occurs in 1:1000 neonates1 and the cause is hereditary in about half. This type of hearing impairment is sometimes referred to as prelingual, as it affects the child before the age of speech development. A distinction can be made between syndromic deafness, in which the deafness is accompanied by other specific abnormalities, and non-syndromic deafness (about 75%), in which there are no additional abnormalities. Approximately three-quarters of the non-syndromic forms are caused by a recessive disorder1,2,3,4. Table 1 gives an overview of some epidemiological features.



Table 1

Epidemiological features of prelingual hearing loss



Between 1997 and today, many non-syndromic hereditary forms of deafness have been localized on the human genome by genetic linkage techniques. Depending on the pattern of inheritance of the deafness, these loci are designated DFNA (autosomal dominant), DFNB (autosomal recessive) or DFN (X-linked). They are numbered in chronological order of discovery. For the majority of these loci the underlying disease-causing genes have not been identified so far. On the Hereditary Hearing Loss Homepage5 all these currently known forms of hereditary deafness are summarized. Tables ​Tables22,​,33,​,44,​,5, 5, derived from this homepage, illustrate the achievements in this field of research. Certain research groups, having found preliminary evidence of a new locus, have claimed (‘reserved’) loci in advance. ‘Withdrawn’ indicates those which turned out not to be correct. Most of these genetic types of hearing impairment are quite rare, with the exception of DFNB1. This paper addresses DFNB1, which is caused by mutations in the connexin 26 gene.



Table 2

Loci and genes associated with autosomal dominant non-syndromic hearing impairment, with the year of publication





Table 3

Loci and genes associated with autosomal recessive non-syndromic hearing impairment, with the year of publication





Table 4

Loci and genes associated with X-linked non-syndromic hearing impairment, with the year of publication





Table 5

Mitochondrial mutations associated with non-syndromic hearing impairment, with the year of publication
Medullary Sponge Kidneys
Authors: John H. Felts, Robert N. Headley, Joseph E. Whitley, Ernest H. Yount
Journal: JAMA (1964)

A congenital condition characterized by dilated renal collecting ducts and medullary cysts, medullary sponge kidneys are usually diagnosed incidentally by intravenous pyelography with the demonstration of radially oriented ducts and cysts ramifying from the calyces in a bristle pattern. Nephrocalcinosis, hypercalciuria, and pyelonephritis are common findings, but impaired glomerular filtration is uncommon and renal insufficiency unusual. Urine concentration power may be decreased and defective tubular capacity for elaboration of ammonia has been postulated. Two patients with this condition excreted hyperosmolal urine in response to 14-hour fluid deprivation and short-term oral ammonium chloride loading indicated no impairment of urine acidification, of titratable acid excretion, or of ammonium production. Presumably disturbances in discrete renal functions are determined by the extent and sites of cystic tubular dilatation and of associated epithelial alterations.
High-definition vs. standard-definition colonoscopy in the characterization of small colonic polyps: results from a randomized trial
Authors: G. Longcroft-Wheaton, J. Brown, D. Cowlishaw, B. Higgins, P. Bhandari
Journal: Endoscopy (2012)

<b>Background and study aims:</b> The resolution of endoscopes has increased in recent years. Modern Fujinon colonoscopes have a charge-coupled device (CCD) pixel density of 650000 pixels compared with the 410000 pixel CCD in standard-definition scopes. Acquiring high-definition scopes represents a significant capital investment and their clinical value remains uncertain. The aim of the current study was to investigate the impact of high-definition endoscopes on the in vivo histology prediction of colonic polyps. <b>Patients and methods:</b> Colonoscopy procedures were performed using Fujinon colonoscopes and EPX-4400 processor. Procedures were randomized to be performed using either a standard-definition EC-530 colonoscope or high-definition EC-530 and EC-590 colonoscopes. Polyps of < 10 mm were assessed using both white light imaging (WLI) and flexible spectral imaging color enhancement (FICE), and the predicted diagnosis was recorded. Polyps were removed and sent for histological analysis by a pathologist who was blinded to the endoscopic diagnosis. The predicted diagnosis was compared with the histology to calculate the accuracy, sensitivity, and specificity of in vivo assessment using either standard- or high-definition scopes. <b>Results:</b> A total of 293 polyps of < 10 mm were examined – 150 polyps using the standard-definition colonoscope and 143 polyps using high-definition colonoscopes. There was no difference in sensitivity, specificity or accuracy between the two scopes when WLI was used (standard vs. high: accuracy 70 % [95 %CI 62 – 77] vs. 73 % [95 %CI 65 – 80]; <i>P</i> = 0.61). When FICE was used, high-definition colonoscopes showed a sensitivity of 93 % compared with 83 % for standard-definition colonoscopes (<i>P</i> = 0.048); specificity was 81 % and 82 %, respectively. <b>Conclusions: </b>There was no difference between high- and standard-definition colonoscopes when white light was used, but FICE significantly improved the in vivo diagnosis of small polyps when high-definition scopes were used compared with standard definition.
Endothelial Progenitor Cells Are Related to Glycemic Control in Children With Type 1 Diabetes Over Time
Authors: Thomas Hörtenhuber, Birgit Rami-Mehar, Miriam Satler, Katrin Nagl, Clemens Höbaus, Florian Höllerl, Renate Koppensteiner, Guntram Schernthaner, Edith Schober, Gerit-Holger Schernthaner
Journal: Diabetes Care (2013)

The risk of cardiovascular death before the age of 40 is 20-fold higher in patients with type 1 diabetes mellitus (T1DM). Endothelial progenitor cells (EPCs) predict cardiovascular morbidity and mortality in patients without diabetes. We hypothesized that EPCs are modified in children with T1DM and are related to characteristics of T1DM such as glycemic control.
Evidence of an oxidative mechanism for the hemolytic activity of silica particles.
Authors: B L Razzaboni, P Bolsaitis
Journal: Environmental Health Perspectives (1990)

The formation of reactive oxygen species resulting from the interaction of silica dust particles with red blood cell membranes was investigated; particularly, the effect of surface hydroxyl (silanol) group concentration on the rate of formation of such reactive oxygen species was investigated. The rate of formation was measured indirectly through the effect of catalase, a hemoprotein peroxidase, on silica-induced hemolysis. It was found that the addition of exogenous catalase to erythrocytes markedly reduces the hemolysis caused by silica particles. Furthermore, the amount of catalase required for deactivation of silica per unit area of particle surface is lower for fumed silica particles and calcined crystalline particles than for uncalcined, crystalline silica, suggesting a correlation between the concentration of OH groups at the silica particle surface and its potential for generation of H2O2. The addition of albumin, a copper chelator, also decreases hemolysis. These results suggest that the hemolysis caused by silica particles is at least partly related to the formation of H2O2 at the particle surface and its subsequent reaction with Cu+ ions. The relationship between the concentration of surface silanol groups on the silica surface and the amount of catalase required to decrease hemolysis may also provide a method for testing potential fibrogenicity of respirable dusts.
Severe vaccine complications are rare, review finds
Authors: M. McCarthy
Journal: BMJ (2014)

Although some childhood vaccines are associated with severe adverse events, these complications are “extremely” rare, according to a new systematic review.1

The review, which updates and adds to the 2011 Institute of Medicine (IOM) report entitled Adverse Effects of Vaccines: Evidence and Causality , was commissioned by the US Agency for Healthcare Research and Quality to identify gaps in evidence on the safety of vaccines.2

The review focused on vaccines recommended for routine use in the US for children aged 6 years and younger: DTaP (diphtheria, tetanus, and acellular pertussis); hepatitis A; hepatitis B, haemophilus influenza type b (Hib); influenza (live attenuated and inactivated); …
Insurance medical reports
Authors: C P Newcombe
Journal: BMJ (1989)

wheelchairs, and wheelchairs required for short term loan.It includes maintenance and cleaning procedures and guidance on providing cushions and establishes who is responsible for each group of wheelchairs.The hospital is about to replace its antiquated stock of ward based and portering wheelchairs with new ones, chosen to meet speci- fications written by the wheelchair committee.Unfortunately, not many hospitals will find themselves in such a privileged position with regard to their trust funds.This financial provision should, however, be weighed up against any possible claim against the hospital due to the inadequacy of its wheelchairs.All hospital wheelchairs should be distinctive in colour, colour coded according to their use and geographical area, and clearly marked with a hospital identification number.It is important to remember that hospital wheelchairs are used not only for transporting patients; some patients are required to sit in them for up to eight hours continuously.This not only causes considerable discomfort but may also lead to ischial pressure sores.5
Antibiotics for Animals
Authors: Mike Mitka
Journal: JAMA (2012)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
TCTAP A-077 Two-year Imaging Results of the Absorb Bioresorbable Everolimus Eluting Vascular Scaffold with Planned Overlapping from the ABSORB EXTEND Optical Coherence Tomography Subgroup
Authors: Chiung-Jen Wu, Paul Hsien-Li Kao, Yoshinobu Onuma
Journal: Journal of the American College of Cardiology (2015)
S128 Highly invasive capsular serotypes of Streptococcus pneumoniae bind high levels of Factor H and are resistant to complement and phagocytosis
Authors: C. Hyams, K. Trzcinski, D. M. Weinberger, M. Lipsitch, J. S. Brown
Journal: Thorax (2011)

The <i>Streptococcus pneumoniae</i> polysaccharide capsule is an essential virulence factor that varies in structure between serotypes. While certain serotypes are highly invasive, it is unknown why these serotypes frequently cause infection yet others generally cause nasopharyngeal colonisation. Complement is vital in immunity to pneumococcus, and the capsule is known to affect complement deposition. Activation of the alternative complement pathway is promoted by factor B (Bf) binding, but inhibited by factor H (FH) activation. We hypothesised that capsule effects on FH and Bf interactions could alter <i>S pneumoniae</i> complement sensitivity, partially explaining serotype-dependent differences in invasiveness. C3b/iC3b deposition, FH and Bf binding to <i>S pneumoniae</i> were measured using flow cytometry assays on 20 distinct capsule-switch variants constructed on TIGR4 genetic background. These strains were therefore identical in protein structure, differing only in capsular serotype. Phagocytosis was investigated using an established flow cytometry assay, fresh human neutrophils and FAMSE labelled <i>S pneumoniae</i>. FH binding showed wide variations between TIGR4-capsular switched strains, with a 7.5-fold difference between the highest (serotype2) and lowest (serotype11A) results. Differences in FH binding between strains did not correlate with capsular thickness, or with capsule structural motifs such as numbers of carbon atoms per repeating unit. FH binding negatively correlated with Bf binding and C3b/iC3b deposition, demonstrating that increased FH binding was associated with reduced alternative pathway activity and increased resistance to complement. IgG binding did not correlate with C3b/iC3b results, suggesting C3b deposition was independent of antibody-mediated complement activity. Neutrophil association correlated with C3b/iC3b deposition (R<sup>2</sup>=0.47, p=0.0008) but negatively with FH binding (R<sup>2</sup>=0.74, p&lt;0.0001), confirming that high FH binding by pneumococcus was associated with reduced neutrophil phagocytosis. Weakly- and highly-invasive serotypes showed large significant differences between median C3b deposition (p=0.007), neutrophil association (p=0.0002) and FH binding (p=0.0005). Weakly-invasive serotypes had reduced FH binding, increased C3b/iC3b deposition and increased neutrophil association. Our novel finding that the degree of FH binding to <i>S pneumoniae</i> capsular serotypes is associated with large variations in virulence offers a mechanistic explanation as to why certain serotypes are more invasive than others. It also provides a potential in vitro method for identifying highly invasive strains.
Leprosy Case—Where it should be Reported.
Authors: Albert S. Ashmead
Journal: JAMA (1895)

New York,March 31,1895. <h3>To the Editor:</h3> —I beg to state, with reference to one of your remarks in the Public Health columns, of theJournal of the American Medical Association, March 30, as to my not reporting a certain case of leprosy directly to the local Board of Health that I take, in such affairs, a higher ground. According to my opinion, such cases should be reported to a United States Health Officer, and the State or City Board of Health should have nothing to do with them. The State Board of Health would think only of the protection of its own citizens, and would most probably do everything possible to shift the responsibility, that is the expense of the maintenance of the leprous family on some relations or friends of the leper, living perhaps in another State. If the danger was averted from their own vicinity, their particularistic
Echocardiographic study of the morphology and growth of the aortic arch in the human fetus. Observations related to the prenatal diagnosis of coarctation.
Authors: L K Hornberger, R G Weintraub, E Pesonen, A Murillo-Olivas, I A Simpson, C Sahn, S Hagen-Ansert, D J Sahn
Journal: Circulation (1992)

In a study of normal and abnormal growth of the aorta before birth, high-resolution echocardiographic imaging of the aortic arch in 92 normal fetuses aged 16-38 weeks was used to establish normal values for aortic arch dimensions at varying gestational ages.From long-axis views of the aortic arch, the internal diameter of the aortic root, ascending aorta, transverse aortic arch, aortic isthmus, proximal descending thoracic aorta, and left common carotid artery were measured. Correlation coefficients for the diameter of each aortic arch segment when related to gestational age varied from r = 0.87 to r = 0.94 (p less than 0.001 for each), and growth curves were derived from the third and 97th percentiles around each linear regression analysis. In most of the fetuses, there was progressive tapering of the aortic arch, with the smallest diameter being at the isthmus. The ratio of the transverse aorta, isthmus, descending aorta, and aortic root to the ascending aorta remained relatively constant with gestational age, with mean values of 0.94, 0.81, 0.96, and 1.13, respectively. In five fetuses in whom a prenatal diagnosis of aortic coarctation was confirmed postnatally, transverse aortic and isthmic measurements fell on or below the third percentile for gestational age from the above data. In each case, the ratio of left common carotid artery to transverse aorta was greater than or equal to 0.73 compared with less than or equal to 0.62 for the 92 normal fetuses (mean ratios, 0.77 +/- 0.05 [SD] for coarctation versus 0.48 +/- 0.08 for normal fetuses; p less than or equal to 0.001).Use of normal growth curves for the developing aortic arch should facilitate the prenatal diagnosis of left heart and aortic arch abnormalities, particularly aortic coarctation, which until recently has been a difficult prenatal diagnosis to make with certainty.
The glucose paradox. Is glucose a substrate for liver metabolism?
Authors: J Katz, J D McGarry
Journal: Journal of Clinical Investigation (1984)

The Glucose Paradox Is Glucose a Substrate for Liver Metabolism? iver contains the full complement of enzymes for the synthesis as well as the catabolism of glucose, glycogen, and fat, and in many species, including the pig, chicken, and man, it is the predominant if not the sole site of triglyceride synthesis.Because the ingestion of a carbohydrate diet after a fast is followed promptly by replenishment of liver glycogen and activation of hepatic lipogenesis, it has become commonly accepted that glucose is a major hepatic substrate and serves as a direct' precursor for glycogen and fat.However, over the last decade, evidence has mounted that under physiological conditions glucose utilization by liver is rather limited and that it is in fact a poor precursor for glycogen and fatty acids (much inferior to gluconeogenic substrates such as fructose,2 glycerol, or lactate).This finding, at first sight at variance with common sense and established views, has been designated the "glucose paradox" (Riesenfeld et al. [1]; Boyd et al. [2]).Our purpose here is to call attention to the problem and to present the case that longstanding concepts in this area are in need of reevaluation.An exhaustive quotation of the voluminous literature in the field will not be attempted since much of this has already been covered in the excellent reviews of Stalmans (3) and Hers (4, 5).Rather, we have adopted a selective but, we believe, representative approach to the published work, both pro and con of our interpretations. Hepatic utilization ofglucoseThe central role of the liver in glucose homeostasis has been recognized since the time of Claude Bernard, over 100 years ago.In the 1930's, Soskin and co-workers showed that when
132 NLRP3-INFLAMMASOME ACTIVATION IS ESSENTIAL FOR PROGRESSION TO STEATOHEPATITIS AND FIBROSIS
Authors: A. Wree, M.D. McGeough, A. Eguchi, C.D. Johnson, C.A. Pena, A. Canbay, H.M. Hoffman, A.E. Feldstein
Journal: Journal of Hepatology (2013)
The Thorax in Ankylosing Spondylitis
Authors: F. D. Hart, A. Bogdanovitch, W. D. Nichol
Journal: Annals of the Rheumatic Diseases (1950)

One of the most interesting and characteristic findings in the condition known in Great Britain as Ankylosing Spondylitis, and in the U.S.A. as Rheumatoid Spondylitis, is the diminution in thoracic, i.e. intercostal, expansion due to involve- ment of the costo-transverse and costo-vertebral joints.This finding is not seen as a common or characteristic feature in any of the other rheumatic diseases; it is one of the characteristic and pathognomonic physical signs in ankylosing spondylitis.While the vital capacity in any febrile active locomotor disease may be reduced, figures in uncomplicated cases do not descend to the low level seen on occasion in ankylosing spondylitis, nor is the reduction in thoracic expansion as marked.For this reason, although some attention has been devoted to thoracic changes in ankylosing spondylitis (Hamilton, 1949; Hart, 1950), we have paid particular attention to this finding.It is a useful diagnostic pointer; in our series of cases the majority of patients had reduced thoracic expansion on their first attendance at the clinic.This particular finding is prominent and frequent enough to be taken as a cardinal early diagnostic sign.Under treatment by various methods the vital capacity and chest expansion may improve and even return to normal.This has been observed by us by the use of deep x-ray therapy and general body and breathing exercises, and by Swaim (1939) by the use of light jacket supports for the prevention and correction of kyphotic thoracic deformity.Restriction of intercostal respiration is therefore an early sign as well as a late one.It may disappear or lessen in the intermediate phase on therapy, though in many instances vital capacity and chest expansion remain subnormal throughout the course of the disease. SymptomatologyThe presence of joint changes in spine and/or hips may prevent the patient from taking sufficient exercise, but on occasion exertional dyspnoea is a complaint made spontaneously by patients with ankylosing spondylitis.This symptom is usually part of a more complex symptomatology.The dyspnoea complained of is quite unlike that noted in cardiac or pulmonary disease.Difficulty is experienced in moving the chest wall; tightness is noted in the ribs and muscles of the thoracic cage, more particularly anteriorly, but also in the flanks; the chest aches and feels stiff and immobile and the patient cannot fill his chest satisfactorily on deep inspiration.There is no bronchial spasm and the picture is quite unlike that seen in asthma or chronic bronchitis.On forced inspiration the chest wall aches, particularly after sharp inspiratory efforts as after coughing or sneezing, but the ache is not due to repeated coughing as it is in chronic bronchitis, for cough 116 copyright.