tbuckley/cabot-search huggingface dataset:
Epidemiology and demographics of aggressive periodontitis
Authors: Cristiano Susin, Alex N. Haas, Jasim M. Albandar
Journal: Periodontology 2000 (2014)

Abstract Epidemiologic studies of aggressive periodontitis have used different study designs and a range of examination methods and case definitions, and this greatly complicates the study of disease prevalence in populations. The wide range of disease case definitions, in particular, profoundly impacts the reported rate of disease, and the use of a standard disease definition is strongly recommended. Surveys of aggressive periodontitis that use only clinical examinations, without radiographic examination to confirm the presence of a distinctive pattern of tissue loss, may overestimate the prevalence of this disease, particularly when a low threshold of attachment loss is used. The prevalence of aggressive periodontitis varies significantly between populations, and differences in race/ethnicities seem to be a key factor. Studies consistently show that aggressive periodontitis is most prevalent in Africa and in populations of African descent and is least prevalent in Caucasians in Europe and North America. Among children and young adults the prevalence of this disease is higher in older than in younger age groups. Most studies show comparable disease prevalence in male and female subjects. These findings show that aggressive periodontitis is a significant health problem in certain populations. This review also highlights a lack of information on the epidemiology and demographics of this disease in many parts of the world, particularly in Asia and Africa. Epidemiologic studies of aggressive periodontitis in high‐risk populations are important and could provide vital data on the determinants of this disease, and this information is needed for the establishment of effective health‐promotion measures.
Variability of Infectious Aerosols Produced during Coughing by Patients with Pulmonary Tuberculosis
Authors: Kevin P. Fennelly, Edward C. Jones-López, Irene Ayakaka, Soyeon Kim, Harriet Menyha, Bruce Kirenga, Christopher Muchwa, Moses Joloba, Scott Dryden-Peterson, Nancy Reilly, Alphonse Okwera, Alison M. Elliott, Peter G. Smith, Roy D. Mugerwa, Kathleen D. Eisenach, Jerrold J. Ellner
Journal: American Journal of Respiratory and Critical Care Medicine (2012)

Mycobacterium tuberculosis is transmitted by infectious aerosols, but assessing infectiousness currently relies on sputum microscopy that does not accurately predict the variability in transmission.
Human Experimentation
Authors: Irving Ladimer
Journal: New England Journal of Medicine (1957)

BIOLOGIC and medical investigation is accepted as essential to progress in health. Recent advances in the prevention, cure and treatment of disease attest to the power and value of research. Today, the public and the professions alike agree that medical research must precede and then succeed practice to provide a basis for action and an evaluation of its worth. Such research, frequently in the most critical areas, takes the form of experimentation on human beings.Development of standard diagnosis and treatment calls first for trial of novel methods. Ultimately, every innovation intended to benefit mankind must be tried on a . . .
Remarks on Burns by Gunpowder and Scalds by Steam
Authors: W. R. E. Smart
Journal: BMJ (1876)

that probably would have been gastro-duodenal in a non-dysenteric climate, on the eighteenth day ; the third, by exhaustion of nerve- REMARKS ~~~fo r c e andl bl-ood-poisoning, ending in renal suppression, on the ON thirtieth day.
Consistent associations between hepatic lesions in English sole (Parophrys vetulus) and polycyclic aromatic hydrocarbons in bottom sediment.
Authors: J T Landahl, B B McCain, M S Myers, L D Rhodes, D W Brown
Journal: Environmental Health Perspectives (1990)

A consistent and statistically significant association between prevalence of hepatic neoplasms in free-living sole (Parophrys vetulus) and levels of anthropogenic polycyclic aromatic hydrocarbons in bottom sediment from sites of fish capture was documented in a series of studies conducted over a period of 7 years in Puget Sound, Washington. This result strengthens the evidence supporting a causal relationship between exposure to sediment-associated hydrocarbons and development of hepatic neoplasms in this bottom-dwelling marine fish species. Prevalences of two other distinct categories of idiopathic hepatic lesions-megalocytic hepatosis and steatosis/hemosiderosis-also showed consistent, statistically significant associations with polycylic aromatic hydrocarbon concentrations in bottom sediment, and association with prevalence of a third category (putatively preneoplastic foci of cellular alteration) approached statistical significance. On the basis of other studies, megalocytic hepatosis and foci of cellular alteration are both considered to be important precursor lesions in the stepwise histogenesis of hepatic neoplasms.
The Harvard Way
Authors: David C. Levin
Journal: JAMA (1985)

<h3>To the Editor.—</h3> I strenuously object to the unwarranted slur upon the Harvard Medical School and the many physicians associated with it in the essay entitled "The Harvard Way."<sup>1</sup>It's hard to believe a responsible journal would publish material of this sort, specifically identifying and castigating a single medical school, without any attempt to actually ascertain the facts of the case. Although I don't know Dr Walker and am not in the department in which he took a part of his residency, I have been a member of the faculty at Harvard Medical School for ten years. The institution is full of dedicated physicians who are busy providing patient care, running teaching programs, and carrying out medical research—often "working like slaves and getting very little sleep," just like Dr Walker. Hundreds of residents complete training at Harvard teaching hospitals each year and go on to pursue their medical careers,
Does long-term oxygen therapy reduce hospitalisation in hypoxaemic chronic obstructive pulmonary disease?
Authors: T.J. Ringbaek, K. Viskum, P. Lange
Journal: European Respiratory Journal (2002)

The aim of this study was to determine whether long-term oxygen therapy (LTOT) reduces hospitalisation in hypoxaemic patients with chronic obstructive pulmonary disease (COPD). The circumstances of initiation of LTOT (start during hospitalisation <i>versus</i> start as an outpatient) and compliance with oxygen were also investigated (continuous oxygen therapy (COT) ≥15 h daily <i>versus</i> noncontinuous oxygen therapy (NCOT) &lt;15 h daily). A total 246 COPD patients were studied, with each patient acting as their own control. Patients were divided into four groups: 125 patients on COT who started LTOT in conjunction with hospitalisation, 37 patients on COT who started LTOT as outpatients, 58 patients on NCOT who started LTOT in conjunction with hospitalisation and 26 patients on NCOT who started LTOT as outpatients. Admission rates, days spent in hospital and number of patients with at least one hospitalisation (ever hospitalised) were compared in two periods of 10 months before and after initiation of LTOT. Overall during the LTOT period, in comparison with the preoxygen period, the admission rates, hospital days and "ever hospitalised" were reduced by 23.8%, 43.5% and 31.2%, respectively. Among patients who started LTOT as outpatients, a tendency towards a higher effect in the compliant group was observed. This study shows that in hypoxaemic chronic obstructive pulmonary disease patients, long-term oxygen therapy is associated with a reduction in hospitalisation.
Platelet spherocytosis: A new bleeding disorder
Authors: James G. White, Pedro A. de Alarcon
Journal: American Journal of Hematology (2002)

Abstract The present study evaluated a child with thrombocytopenia and a rare congenital bleeding disorder associated with platelet spherocytosis. Differential interference phase contrast microscopy (DIC) revealed that his platelets were spherical in form. Examination of thin sections in the electron microscope showed that his platelets were nearly devoid of microtubules (MT) and microtubule coils (MTC) that support the discoid shape in 100% of normal platelets. Immunofluorescence with a monoclonal antibody to tubulin, the precursor protein of MT, revealed bright rings in normal cells and diffuse fluorescence of patient platelets. The brightness of the fluorescence emitted by patient platelets was comparable to the diffuse fluorescence of normal platelets after chilling to dissolve intact MT, suggesting normal and patient cells contained comparable amounts of tubulin. Exposure of patient platelets to Taxol, an agent that stabilizes and induces MT, caused MT formation in 82% of patient platelets and MTC development in 11%, resulting in their conversion to discs. Glycoproteins GPIIb/IIIa and GPIb were present on patient platelets, and the cells contained normal numbers of dense bodies, ruling out storage pool disease. The patient's platelets adhered to and spread normally on glass but failed to undergo rapid, irreversible aggregation when stirred with agents that produced a complete response in normal discoid platelets, even when the patient's platelets were concentrated. The poor response of spherical platelets was associated with failure to become irregular and extend long filopodia. Thus, the spherical shape of patient platelets may contribute to the thrombocytopenia and to the clinical bleeding symptoms. Am. J. Hematol. 70:158–166, 2002. © 2002 Wiley‐Liss, Inc.
Inhibitors of Factor VIII in Black Patients with Hemophilia
Authors: Kevin R. Viel, Afshin Ameri, Thomas C. Abshire, Rathi V. Iyer, Raymond G. Watts, Charles Lutcher, Cynthia Channell, Shelley A. Cole, Karl M. Fernstrom, Shelley Nakaya, Carol K. Kasper, Arthur R. Thompson, Laura Almasy, Tom E. Howard
Journal: New England Journal of Medicine (2009)

Black patients with hemophilia A (factor VIII deficiency) are twice as likely as white patients to produce inhibitors against factor VIII proteins given as replacement therapy. There are six wild-type factor VIII proteins, designated H1 through H6, but only two (H1 and H2) match the recombinant factor VIII products used clinically. H1 and H2 are found in all racial groups and are the only factor VIII proteins found in the white population to date. H3, H4, and H5 have been found only in blacks. We hypothesized that mismatched factor VIII transfusions contribute to the high incidence of inhibitors among black patients.We sequenced the factor VIII gene (F8) in black patients with hemophilia A to identify causative mutations and the background haplotypes on which they reside. Results from previous Bethesda assays and information on the baseline severity of hemophilia, age at enrollment, and biologic relationships among study patients were obtained from review of the patients' medical charts. We used multivariable logistic regression to control for these potential confounders while testing for associations between F8 haplotype and the development of inhibitors.Of the 78 black patients with hemophilia enrolled, 24% had an H3 or H4 background haplotype. The prevalence of inhibitors was higher among patients with either of these haplotypes than among patients with haplotype H1 or H2 (odds ratio, 3.6; 95% confidence interval, 1.1 to 12.3; P=0.04), despite a similar spectrum of hemophilic mutations and degree of severity of illness in these two subgroups.These preliminary results suggest that mismatched factor VIII replacement therapy may be a risk factor for the development of anti-factor VIII alloantibodies.
Worldwide Experience With the MicroMed DeBakey Ventricular Assist Device® as a Bridge to Transplantation
Authors: Daniel J. Goldstein
Journal: Circulation (2003)

Background— Ventricular assist device (VAD) support with pulsatile first generation pumps is a well-established therapy for bridging to transplantation. Shortcomings of this technology include limited applicability to small patients, noise, and high incidence of infection and pump malfunction. A second generation of pumps, spearheaded by the axial flow MicroMed DeBakey VAD®, is in clinical trials and potentially will address these shortcomings. Methods and Results— Between November 13, 1998 and May 7, 2002, 150 patients worldwide underwent placement of the Micromed DeBakey VAD® as a bridge to transplantation. Prospectively acquired data including demographics, adverse events and outcomes was collected. Follow up is 100% with 30.4 patient-years of cumulative support time. Mean age was 48±4 years and 18% were female. Twenty-three percent had prior sternotomy. Preoperatively, 25% were on balloon pump support, 20% had renal insufficiency, and 40% were on at least two inotropes with a mean cardiac index of 1.8 L/min/m 2 . Mean support time was 75±81 days. Linearized rates (events/patient-year) were: reoperation for bleeding 2.03, hemolysis 0.61, device infection 0.16, thromboembolic event 0.61, pump thrombus 0.61, and pump failure 0.13. Eight-two patients (55%) were either bridged to transplantation, recovery or are ongoing and 68 (45%) have died. Several patients have been supported as outpatients. Conclusions— This initial experience suggests that bridging to transplantation can be successfully approached with a small and quiet axial flow pump that provides low incidence of device infection and pump failure. The incidence of pump thrombus and thromboembolism is being addressed by incorporation of heparin coating to all device surfaces.
Outcome value of Clara cell protein in serum of patients with acute respiratory distress syndrome
Authors: Olivier Lesur, Stephan Langevin, Yves Berthiaume, Martin Légaré, Yoanna Skrobik, Jean-François Bellemare, Bruno Lévy, Yvan Fortier, Francois Lauzier, Gina Bravo, Marc Nickmilder, Eric Rousseau, Alfred Bernard
Journal: Intensive Care Medicine (2006)
Factors related to first dose hypotensive effect of captopril: prediction and treatment.
Authors: G P Hodsman, C G Isles, G D Murray, T P Usherwood, D J Webb, J I Robertson
Journal: BMJ (1983)

The blood pressure response to the first dose of captopril (6.25 mg, 12.5 mg, or 25 mg) was measured in 65 treated, severely hypertensive patients. Mean supine blood pressure was 187/108 mm Hg immediately before captopril was given. Twenty one patients experienced a fall in supine systolic pressure greater than 50 mm Hg, including five whose pressure fell more than 100 mm Hg and two whose pressure fell more than 150 mm Hg. Six patients developed symptoms of acute hypotension, including dizziness, stupor, dysphasia, and hemiparesis. Percentage reductions in blood pressure were greatest in those with secondary hypertension (p less than 0.05), high pretreatment blood pressure (p less than 0.05), and high concentrations of plasma renin and angiotensin II (p less than 0.01). No significant correlation was found between fall in blood pressure and serum sodium concentration, age, renal function, and the dose of captopril given. A severe first dose effect cannot be consistently predicted in individual patients who have received other antihypertensive drugs for severe hypertension. Such patients should have close medical supervision for at least three hours after the first dose of captopril.
Disseminated Intravascular Coagulation in Heat Stroke
Authors: James P. Knochel
Journal: JAMA (1975)

<h3>Response to Heparin Therapy</h3> Victims of heat stroke who die on the first day of their illness may demonstrate no more than alterations of cellular elements in the brain, cerebral edema, and widespread punctate hemorrhage. In contrast, those who survive several days commonly show frank evidence of cellular destruction including edema and congestion of the lungs, and necrotic lesions in the brain, liver, kidney, and skeletal muscle. Extensive hemorrhage may be the intermediate cause of death. Evidence that severe heat stroke may be associated with disseminated intravascular coagulation (DIC) is supported by findings of thrombocytopenia, hypofibrinogenemia, the appearance of fibrinsplit products in serum and urine, and in some patients, evidence of clinically significant bleeding. The initiating factor of DIC in patients with heat stroke is not entirely clear. Experimentally, modest fever induced by a high environmental temperature might be accompanied by subtle changes, suggesting activation of the clotting mechanism. On
Aitolia English (nee Georgiadis)
Authors: G. Haggie
Journal: BMJ (2010)

Aitolia English (nee Georgiadis) (“Tolia”) was born on the Greek island of Syros, but after her father died in the flu pandemic in 1918 her mother, who valued the emancipation of women, moved to London for a better education for her daughters.

Tolia was in her final year at UCH when war was declared. …
PD-1 tempers Tregs in chronic HCV infection
Authors: Henry Radziewicz, Richard M. Dunham, Arash Grakoui
Journal: Journal of Clinical Investigation (2009)

Adaptive T cell responses are critical for controlling infections with viruses such as HIV, HBV, and HCV. However, these responses must be carefully regulated because overly vigorous T cell activation can lead to excessive host tissue damage. T cell expression of the inhibitory receptor programmed death-1 (PD-1) and inhibition of effector T cells (Teffs) by CD4+Foxp3+Tregs are among the many described mechanisms for achieving a balanced immune response. Although the signals that contribute to Teff function are well understood, less is known about the signals controlling Tregs. In this issue of the JCI, Franceschini et al. extend our understanding of how Tregs are modulated during chronic HCV infection by demonstrating that Treg proliferation is inhibited by PD-1 and that this inhibition is mediated by a potentially novel mechanism involving the prevention of IL-2-driven STAT-5phosphorylation.
Macula densa arginine delivery and uptake in the rat regulates glomerular capillary pressure. Effects of salt intake.
Authors: W J Welch, C S Wilcox
Journal: Journal of Clinical Investigation (1997)

These studies tested the hypothesis that delivery and/or cellular uptake of L-arginine limits macula densa nitric oxide generation and actions on tubuloglomerular feedback (TGF) during salt restriction. Maximal TGF responses were assessed from reductions in proximal stop flow pressure during loop of Henle (LH) perfusion at 40 nl/min with artificial tubular fluid containing vehicles or drugs. Orthograde LH perfusion of L-arginine (10[-3] M) reduced maximal TGF significantly in rats adapted to low salt (LS: 7.9+/-0.4-6.3+/-0.4 mmHg; P < 0.05), but not high salt (HS: 5.8+/-0.3-5.9+/-0.3; NS). The effects were stereospecific and prevented by coperfusion with NG-methyl-L-arginine. Microperfusion of L-arginine (10[-3] M) into the peritubular capillaries reduced the maximum TGF response more in nephrons of LS than HS rats (deltaTGF: LS, 32+/-6 vs. HS, 13+/-4%; P < 0.05) and restored a TGF response to luminal perfusion of NG-methyl-L-arginine in LS rats. Coperfusion of nephrons with excess L-lysine or L-homoarginine, which compete with L-arginine for system y+ transport, blocked the fall in proximal stopflow pressure produced by orthograde LH perfusion of L-arginine in LS rats. Reabsorption of [3H]arginine by the perfused loop segment was similar in LS (93+/-2%) and HS (94+/-1%) rats. Coperfusion with excess L-arginine, L-lysine, or L-homoarginine, however, reduced [3H]arginine reabsorption significantly (P < 0.05) more in HS rats than in LS rats. In conclusion, blunting of maximal TGF responses in salt-restricted rats by nephron-derived NO is limited by L-arginine availability and cellular uptake via system y+.
Anthracycline-Induced Cardiotoxicity
Authors: Kesavan Shan, A. Michael Lincoff, James B. Young
Journal: Annals of Internal Medicine (1996)

Purpose: To review the current understanding of the clinical significance, detection, pathogenesis, and prevention of anthracycline-induced cardiotoxicity. Data Sources: A MEDLINE search of the English-language medical literature and a manual search of the bibliographies of relevant articles, including abstracts from national cardiology meetings. Study Selection: Pertinent clinical and experimental studies addressing the clinical relevance, pathogenesis, detection, and prevention of anthracycline cardiotoxicity were selected from peer-reviewed journals without judgments about study design. A total of 137 original studies and 9 other articles were chosen. Data Extraction: Data quality and validity were assessed by each author independently. Statistical analysis of combined data was inappropriate given the differences in patient selection, testing, and follow-up in the available studies. Data Synthesis: Anthracycline-induced cardiotoxicity limits effective cancer chemotherapy by causing early cardiomyopathy, and it can produce late-onset ventricular dysfunction years after treatment has ceased. Detection of subclinical anthracycline-induced cardiomyopathy through resting left ventricular ejection fraction or echocardiographic fractional shortening is suboptimal. Conventional doses of anthracycline often lead to permanent myocardial damage and reduced functional reserve. Underlying pathogenetic mechanisms may include free-radical-mediated myocyte damage, adrenergic dysfunction, intracellular calcium overload, and the release of cardiotoxic cytokines. Dexrazoxane is the only cardioprotectant clinically approved for use against anthracyclines, and it was only recently introduced for selected patients with breast cancer who are receiving anthracycline therapy. Conclusions: A rapidly growing number of persons, including an alarming fraction of the 150 000 or more adults in the United States who have survived childhood cancer, will have substantial morbidity and mortality because of anthracycline-related cardiac disease. The development of effective protection against anthracycline-induced cardiotoxicity will probably have a significant effect on the overall survival of these patients.
Effects of Antihypertensive Treatment on Insulin Sensitivity With Special Reference to ACE Inhibitors
Authors: Christian Berne, Thomas Pollare, Hans Lithell
Journal: Diabetes Care (1991)

In 1984, the suspicion that pharmacological treatment may worsen the insulin resistance and associated metabolic abnormalities in lipid and carbohydrate metabolism and contribute to the relative failure of antihypertensive treatment to produce more than marginal reductions in cardiovascular morbidity and mortality led us to start a series of trials aimed at elucidating how antihypertensive drugs affect insulin sensitivity. These trials, which included assessment of insulin sensitivity by the euglycemic insulin clamp, showed that β-adrenergic blockade and thiazide diuretic treatment (hydrochlorothiazide) increase insulin resistance and basal plasma insulin, whereas Ca2+ - channel antagonists (verapamil and diltiazem), with the exception of the negative effect of nifedipine, are metabolically neutral. α-Adrenergic blockade with prazosin and angiotensin-converting enzyme (ACE) inhibition with captopril enhance insulin sensitivity. The mechanisms underlying the positive effects of ACE inhibition and β-adrenergic blockade are largely unknown, but hemodynamic factors (vasodilation) may contribute by improving the access of glucose and insulin to skeletal muscle. The drugs, which were favorable or neutral with respect to insulin sensitivity, caused no changes in lipids or glucose homeostasis. In contrast, β-blockers, except pindolol, had negative effects on triglycerides and high-density lipoprotein cholesterol, and thiazide diuretics caused adverse effects on total serum cholesterol, low-density lipoprotein cholesterol, and total and very-low-density lipoprotein triglyceride. The metabolic action of antihypertensive drugs is an important factor to consider in the choice of a proper treatment strategy in both diabetic and nondiabetic patients with hypertension.