tbuckley/cabot-search huggingface dataset:
Ozone dose and effect in humans and rats. A comparison using oxygen-18 labeling and bronchoalveolar lavage.
Authors: G E Hatch, R Slade, L P Harris, W F McDonnell, R B Devlin, H S Koren, D L Costa, J McKee
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

In an effort to improve risk assessments for ozone (O3) we compared the incorporation of inhaled oxygen-18-labeled O3 (18O3) into the lungs of humans and laboratory rats. Cells and fluids obtainable through bronchoalveolar lavage (BAL) were examined after exposure to 18O3 to determine whether excess 18O concentrations (presumed to be reaction products of 18O3) could be detected and equated to the O3 dose to the lung. Three O3 effect measurements (increased BAL protein and neutrophils and decreased BAL macrophages) were also made in subjects or animals exposed in parallel to determine whether there was a correspondence between dose and effect measurements. Eight human male volunteers 18 to 35 yr of age were exposed to 18O3 (0.4 ppm for 2 h) with 15-min alternating periods of heavy treadmill exercise and rest. Rats (F344) were exposed identically, except without exercise. 18O3 was generated directly from pure 18O2. BAL cells and centrifugally separable surfactant material were freeze-dried and analyzed by mass spectrometer for excess 18O. Results showed that the exercising humans had four- to fivefold higher 18O concentrations in all of their BAL constituents than did the rats. The humans also had significant increases in all of the effects markers after 0.4 ppm O3, whereas the rats did not. Rats that were exposed to higher concentrations of 18O3 (2.0 ppm) had levels of 18O in BAL that were more comparable to but still lower than those of exercising humans. Changes in all of the effects markers in these rats were comparable or higher than in exercising humans.(ABSTRACT TRUNCATED AT 250 WORDS)
RV1A and dsRNA highly induce a biphasic expression of MIP-3α/CCL20 in human bronchial epithelial cells (hBECs)
Authors: J.M. Bellak, K. Hanson, R.A. Brockman-Schneider, H. Dagher, J.E. Gern
Journal: Journal of Allergy and Clinical Immunology (2005)
The chemokine monokine induced by IFN-g (Mig, CXCL9) is potent inhibitor of eosinophils in vitro and in vivo
Authors: P.C. Fulkerson, N. Zimmermann, E.B. Brandt, E.E. Muntel, J. Kavanaugh, A. Mishra, Y. Ming, P.S. Foster, J.M. Farber, M.E. Rothenberg
Journal: Journal of Allergy and Clinical Immunology (2003)
Targeting the cell cycle inhibitor p57Kip2 promotes adult human β cell replication
Authors: Dana Avrahami, Changhong Li, Ming Yu, Yang Jiao, Jia Zhang, Ali Naji, Seyed Ziaie, Benjamin Glaser, Klaus H. Kaestner
Journal: Journal of Clinical Investigation (2014)

Children with focal hyperinsulinism of infancy display a dramatic, non-neoplastic clonal expansion of β cells that have undergone mitotic recombination, resulting in paternal disomy of part of chromosome 11. This disomic region contains imprinted genes, including the gene encoding the cell cycle inhibitor p57Kip2 (CDKN1C), which is silenced as a consequence of the recombination event. We hypothesized that targeting p57Kip2 could stimulate adult human β cell replication. Indeed, when we suppressed CDKN1C expression in human islets obtained from deceased adult organ donors and transplanted them into hyperglycemic, immunodeficient mice, β cell replication increased more than 3-fold. The newly replicated cells retained properties of mature β cells, including the expression of β cell markers such as insulin, PDX1, and NKX6.1. Importantly, these newly replicated cells demonstrated normal glucose-induced calcium influx, further indicating β cell functionality. These findings provide a molecular explanation for the massive β cell replication that occurs in children with focal hyperinsulinism. These data also provided evidence that β cells from older humans, in which baseline replication is negligible, can be coaxed to re-enter and complete the cell cycle while maintaining mature β cell properties. Thus, controlled manipulation of this pathway holds promise for the expansion of β cells in patients with type 2 diabetes.
Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure.
Authors: D M Mancini, E Coyle, A Coggan, J Beltz, N Ferraro, S Montain, J R Wilson
Journal: Circulation (1989)

Patients with heart failure frequently exhibit abnormal skeletal muscle metabolic responses to exercise, as assessed with 31P NMR. To investigate whether these metabolic abnormalities are due to intrinsic skeletal muscle changes, we performed gastrocnemius muscle biopsies on 22 patients with heart failure (peak VO2, 15.4 +/- 4.7 ml/kg/min; ejection fraction, 20 +/- 7%) and on eight normal subjects. Biopsies were analyzed for fiber type and area, capillarity, citrate synthase, phosphofructokinase, lactate dehydrogenase, and beta-hydroxyacyl CoA dehydrogenase activity. All patients with heart failure also underwent 31P NMR studies of their calf muscle during plantarflexion at three workloads. Muscle pH responses and the relation of the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) to systemic VO2 were then evaluated. Compared with normal subjects, patients with heart failure exhibited a shift in fiber distribution with increased percentage of the fast twitch, glycolytic, easily fatigable type IIb fibers (normal subjects, 22.7 +/- 10.1; heart failure, 33.1 +/- 11.1%; p less than 0.05), atrophy of type IIa (normal subjects, 5,477 +/- 1,109; heart failure, 4,239 +/- 1,247 microns 2; p less than 0.05) and type IIb fibers (normal subjects, 5,957 +/- 1,388; heart failure, 4,144 +/- 945 microns 2; p less than 0.01), and decreased activity of beta-hydroxyacyl CoA dehydrogenase (normal subjects, 5.17 +/- 1.44; heart failure, 3.67 +/- 1.68 mol/kg protein/hr; p less than 0.05). No significant linear correlation could be identified between the slope of the Pi/PCr to VO2 relation and muscle histochemistry or enzyme activities. Similarly, no linear relation was found between intracellular pH at peak exercise and any muscle variable.(ABSTRACT TRUNCATED AT 250 WORDS)
Strong Promoters Are the Key to Highly Efficient, Noninflammatory and Noncytotoxic Adenoviral-Mediated Transgene Delivery into the Brain in Vivo
Authors: Christian A. Gerdes, Maria G. Castro, Pedro R. Löwenstein
Journal: Molecular Therapy (2000)

Using the major immediate early murine cytomegalovirus (MIEmCMV) promoter to drive expression of β-galactosidase, we have demonstrated that, following adenoviral-mediated transduction of brain cells in vivo, a single viral infectious unit is capable of producing detectable levels of transgene expression and that gene transfer into the brain is close to 100% efficient. By reducing 100-fold the amount of virus needed to detect large numbers of transduced brain cells, we were able to completely eliminate the cellular inflammation and viral cytotoxicity associated with the delivery of adenoviral vectors into the brain compared to saline-injected controls. These results demonstrate that a strong promoter is necessary to allow the use of low concentrations of adenoviral vectors for gene transfer into the brain, thereby eliminating deleterious side effects and increasing the potential efficacy of gene therapy. Using the major immediate early murine cytomegalovirus (MIEmCMV) promoter to drive expression of β-galactosidase, we have demonstrated that, following adenoviral-mediated transduction of brain cells in vivo, a single viral infectious unit is capable of producing detectable levels of transgene expression and that gene transfer into the brain is close to 100% efficient. By reducing 100-fold the amount of virus needed to detect large numbers of transduced brain cells, we were able to completely eliminate the cellular inflammation and viral cytotoxicity associated with the delivery of adenoviral vectors into the brain compared to saline-injected controls. These results demonstrate that a strong promoter is necessary to allow the use of low concentrations of adenoviral vectors for gene transfer into the brain, thereby eliminating deleterious side effects and increasing the potential efficacy of gene therapy.
Commentary: Why we didn't ask patients for their consent
Authors: M. Dennis
Journal: BMJ (1997)

In our trial we asked patients to consent to follow up but not to consent to randomisation itself. There were several reasons for adopting this approach, which was approved by our local ethics committee. Firstly, we did not expect our intervention to be harmful, though whether this expectation was fulfilled must be judged from our results. Secondly, patients and their carers could refuse to see our stroke family care worker or follow up psychologist whenever they wished. Thus half the patients and their carers were asked to consent to the intervention and all were asked to …
The way I don't see it--living with a visual impairment
Authors: J D Wright
Journal: BMJ (1996)

“I am a visually handicapped doctor and wish to visit the medical section, can you help me?” The man at the door of the Science Museum in London guided me to an official and said, “This is a mentally handicapped doctor who wants to visit the medical section.” This experience poignantly illustrates some people's attitude to disability.

As a result of my predisposing myopia, the retina of my right eye became detached when I was 16 and I was admitted to Moorfields Hospital. Limited surgical techniques were available and I was sentenced to several weeks immobile on my back. I lost the sight of that eye and during my training it was enucleated after concern about sympathetic ophthalmia. While I was a student the retina of the left eye first detached and I well remember a supportive consultant who said, “If you go blind you could always be a physiotherapist.” I insisted that I was training to be a doctor.

I eventually qualified in 1962. I enjoyed two years in hospital medicine and then moved into community child health. My acuity deteriorated further and I was told to give up driving. I loved driving and the loss of independence, which I still feel, was devastating. So what next if clinical medicine was not possible? I advertised in the …
Physician as Supergod
Authors: Alfred B. Mason
Journal: JAMA (1971)

To the Editor.—  In Playing Supergod, S.V. pointed out that no mortal has received a divine estimate of his remaining days on earth. To be sure divine revelations are hard to come by in any subject, in these agnostic times. But aside from the element of divinity, few of us receive dependable estimates of our remaining days.  A notable exception to this rule in the condemned criminal, in such localities as still practice capital punishment. It might be said that this is the essence of such punishment—not to die, for all of us must; not to have our life shortened, a fate visited upon innocent as well as guilty; but to know a precise day, hour, and minute beyond which our life may not extend. And so our unlucky patient with the fatal disease—in proportion to the precision of the estimate we give him—shares with the criminal a punishment otherwise
The molecular basis of hereditary 1,25-dihydroxyvitamin D3 resistant rickets in seven related families.
Authors: P J Malloy, Z Hochberg, D Tiosano, J W Pike, M R Hughes, D Feldman
Journal: Journal of Clinical Investigation (1990)

Hereditary 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] resistant rickets (HVDRR) is an autosomal recessive disease caused by target organ resistance to the action of 1,25(OH)2D3, the active form of the hormone. The defect in target cells is heterogenous and commonly appears to be a mutation in the gene encoding the vitamin D receptor (VDR). We have studied cultured skin fibroblasts and Epstein-Barr virus transformed lymphoblasts of seven family branches of an extended kindred having eight children affected with HVDRR. We have previously shown that cells from three affected children in this group contain an "ochre" nonsense mutation coding for a premature stop codon in exon 7 within the steroid-binding domain of the VDR gene. In the current studies, we found that cells from affected children failed to bind [3H]1,25(OH)2D3 and had undetectable levels of VDR as determined by immunoblots using an anti-VDR monoclonal antibody. Measurement of VDR mRNA by hybridization to a human VDR cDNA probe showed undetectable or decreased abundance of steady-state VDR mRNA. Parents, expected to be obligate heterozygotes, showed approximately half the normal levels of [3H]1,25(OH)2D3 binding, VDR protein, and mRNA. The mutation at nucleotide 970 (counting from the mRNA CAP site) results in the conversion of GTAC to GTAA, which eliminates an Rsa I restriction enzyme site and facilitates identification of the mutation. We found that polymerase chain reaction (PCR) amplification of exons 7 and 8 from family members and subsequent Rsa I digestion allows detection of the specific genotype of the individuals. When Rsa I digests of PCR-amplified DNA are subjected to polyacrylamide gel electrophoresis, children with HVDRR exhibit a homozygous banding pattern with loss of an Rsa I site. Parents exhibit a heterozygotic DNA pattern with detection of both normal and mutant alleles. In summary, our data show that the genetic abnormality is a point mutation within the steroid-binding domain of the VDR in all seven related families with HVDRR. Analysis of restriction fragment length polymorphism at the 970 locus of PCR-amplified DNA fragments can be used to diagnose this mutation in both affected children and parents carrying the disease.
Sydenham's chorea. A model for childhood autoimmune neuropsychiatric disorders
Authors: S. E. Swedo
Journal: JAMA (1994)

<h3>SELECTED CASE</h3> Faith (not her real name), a 9-year-old girl, presented to the local hospital's emergency department with a chief complaint of "St Vitus' dance." Her grandfather had noticed her clumsy gait and frequent jerky movements and had concluded that "she must have St Vitus' dance, just like her Aunt Cecilia did when she was 7." In retrospect, Faith had at least a 2-week history of increasing fidgetiness, clumsiness, and subtle choreiform movements. During the week prior to presentation, she had noticed a deterioration in her handwriting skills and had been having increasing difficulties with speaking, walking, and such daily activities as brushing her teeth, manipulating a fork, and drinking from a glass. About a month prior to presentation, Faith had experienced the abrupt onset of nightmares and of anxiety about being separated from her mother. At about the same time, she began to wash her hands excessively (up to
Parents object to watering down of recommendations in infant death case
Authors: D. Spurgeon
Journal: BMJ (2001)

Three families whose children died seven years ago in Winnipeg's paediatric cardiac surgery unit, in a situation reminiscent of that at the cardiac surgery department of the Bristol Royal Infirmary in England, fear that recommendations from the inquest have been watered down

The findings of the inquest were not published until last December, six years after the deaths of the children ( BMJ 2000;321:1433). Paul Thomas, professor of political science at the University of Manitoba, was then given four months to devise a plan to implement the inquest's 36 recommendations. He produced a report last spring.

Saul Simmonds, lawyer for the three families who …
Dereliction of duty in an ageist society
Authors: I. Heath
Journal: BMJ (2000)

The Royal Commission on Long Term Care submitted its report to parliament over a year ago.1 The recommendations have been widely supported, perhaps most notably by the parliamentary health select committee, which declared that “failure to act would be dereliction of duty” and again recently by the presidents of three royal colleges and of the British Geriatrics Society.2 Yet the government has still to respond to the principal majority recommendation that “the costs of care for those individuals who need it should be split between living costs, housing costs, and personal care. Personal care should be available after an assessment, according to need and paid for from general taxation: the rest should be subject to a co-payment according to means.”

The royal commission was set up to examine the options for a sustainable system of funding long term care in the face of a widespread perception, particularly among older people, that the current system is unjust. With the apparently laudable aim of combining improved cost effectiveness with less care in institutions …
Management of Health Care Workers after Inadvertent Exposure to Tuberculosis: A Guide for the Use of Preventive Therapy
Authors: William W. Stead
Journal: Annals of Internal Medicine (1995)

To quantify the protection of previously infected persons from developing tuberculosis after intense exposure.6 hospitals and 22 nursing homes in which heavy tuberculosis exposure had occurred.Results of tuberculin skin tests before and after exposure and the development of tuberculosis among known reactors, both converters and nonconverters.All converters were given preventive therapy with isoniazid as soon as they could be identified. Nonconverters and previously known reactors were not treated.In 6 hospital outbreaks, largely aborted by prompt preventive therapy, 98 of 336 nonreactors (29%) showed skin test conversion, and, before therapy could be started, 19 (19% [95% CI, 12% to 29%]) had developed tuberculosis. No tuberculosis developed among the 238 nonconverters (0% [CI, 0% to 1.5%]) or the 76 known reactors who were not treated (0% [CI, 0.5% to 2%]). Tuberculosis developed in 5 of 209 known reactors (2.4% [CI, 0.8% to 5.5%]) in 22 nursing homes with heavy exposure, little more than 10 of 921 known reactors (1.1% [CI, 0.5% to 2%]) in 76 homes where there was no exposure (P = 0.17).Healthy persons who remain nonreactive to tuberculin after heavy exposure have escaped infection and require no chemotherapy. However, if exposure is discovered immediately, it is wise to start preventive therapy in particularly heavily exposed non-reactors and discontinue it if the skin test result is still negative at 3 months. Persons who react after exposure fall into three groups: 1) converters, in whom the risk for tuberculosis warrants preventive chemotherapy, regardless of age; 2) reactors with no preexposure test results, who should be treated as converters; and 3) previously known reactors, in whom the risk for tuberculosis generally is too slight to warrant therapy. However, those who are younger than age 35 years, have human immunodeficiency virus infection, are receiving cancer chemotherapy or long-term corticosteroid therapy, or are otherwise immunocompromised should be considered for preventive therapy, regardless of the exposure.
Efficacy of Influenza Vaccine in Nursing Homes
Authors: Peter A. Patriarca
Journal: JAMA (1985)

From December 10, 1982, to March 4, 1983, when influenza A (H3N2) viruses circulated in Michigan, outbreaks of influenza-like illness were identified in seven nursing homes in Genesee County; 272 (27%) of 1,018 residents were affected. Unvaccinated residents were more likely than vaccinated residents to become ill (risk ratio [RR], 2.6; 95% confidence interval [Cl], 1.8-3.6) and were subsequently more likely to be hospitalized (RR, 2.4; 95% Cl, 1.2-4.8), develop roentgenographically proven pneumonia (RR, 2.9; 95% Cl, 1.6-5.3), or die (RR, 5.6; 95% Cl, 1.2-9.1). Similar observations were made during investigations in six of the eight remaining nursing homes in Genesee County, in which 57 (12%) of 458 residents became ill sporadically. These findings suggest that influenza vaccine can reduce the incidence and severity of influenza virus infections among the elderly and chronically ill and underscore the importance of vaccination programs for those in nursing homes and in the general community.
Tobacco Control in VA Hospitals—Reply
Authors: Jonathan Samet
Journal: JAMA (2009)

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Biochemistry of Neural Disease
Authors: Nicholas A. Vick
Journal: JAMA (1975)

This book comprises a series of review articles that encompass, with brevity, much of the field of neurochemistry. Those in the field may carp about what has not been included, but the book admirably fulfills its purpose, as stated by Dr Cohen in the preface, "to furnish the clinician with the biochemical information needed to understand the genesis of neurological symptoms, the pathology produced, and the rationale for therapy...." The contributors, as a group, are well-known and accomplished neurological scientists. In general, they present their topics with clarity. There are 11 chapters. Those dealing with convulsive disorders (P. D. Swanson), disorders of amino acid metabolism (J. H. Menkes), and lipid storage disease (F. M. Yatsu) are perhaps the best. Others deal with anoxia, disorders of carbohydrate and mucopolysaccharide metabolism, nutritional and toxic disorders, biochemical aspects of extrapyramidal disease and the psychoses, and central nervous system neoplasia. Biochemistry of Neural Disease
Reconsideration of Age as a Contraindication for Curative Therapy of Sickle Cell Disease
Authors: Allison A. King, John F. DiPersio
Journal: JAMA (2014)

Approximately 100 000 Americans, primarily African Americans, have sickle cell disease.1 Worldwide, the burden of this disease is much greater with an estimated 300 000 affected infants born.2 A single nucleotide substitution causes the autosomal recessive disease: valine replaces glutamic acid in the sixth position of the β-globin protein. Despite the discovery of the etiology of sickle cell disease more than 60 years ago,3 little progress has been achieved in the treatment or cure of this chronic disease.
Cozening the People with Ambiguous Claims
Authors: F. J. Ingelfinger
Journal: New England Journal of Medicine (1977)

AN organization called the "Tay-Sachs Prevention Program" displays publicly the following brightly colored sign:A SIMPLE BLOOD TEST CAN PREVENT TAY-SACHS DISEASEDETECTION AND COUNSELING ENABLE CARRIER COUPLESTO HAVE CHILDREN FREE OF THIS DISEASEHardly had I returned to my office after having seen this sign when I found in the mail a blurb from the National Foundation for Cancer Research, 7315 Wisconsin Avenue, Bethesda, Maryland. It was addressed to "Dear Concerned Fellow Citizen." Here are some of its paragraphs.We are actively developing a cure for cancer. If you will contribute towards this goal, I promise that your . . .