tbuckley/cabot-search huggingface dataset:
Primary care in the United States: problems and possibilities
Authors: Robert L Phillips
Journal: BMJ (2005)

The UK government is hoping to improve primary care through competition. But US experience shows the difficulties created by a system reliant on market forces 

The United States has never had a more robust primary care workforce, but dysfunctional financing schemes and inability to compete for the hearts and minds of the next generation of young doctors threaten its future. Many of the problems are a direct result of the market approach to health care. Innovation is needed in how primary care functions are financed, protected, organised, and taught in order to identify options for a stable and robust health system built on primary care.



The US undervalues family doctors



Primary medical care in the US is delivered by three specialties: family medicine, general internal medicine, and general paediatrics. The specialties have a combined workforce of 222 000 doctors, whose primary function is to direct patient care. There is at least one doctor for every 1321 people in the US (table).1 In addition, more than 100 000 nurse practitioners and physician assistants work in primary care.1 Together, their offices serve as the medical home for most Americans and receive more visits than any other setting.2 It is concerning then that many recent publications have concluded that these specialties and the way they currently care for people is untenable.3 4 These publications show that people in the US are confused about the primary care specialties, sceptical about their claim to deliver comprehensive care, and unable to associate primary care with science or technology. They also indicate that the generalist specialties suffer from a lack of respect in academic circles, administrative burdens, and inflexible appointment schedules and brief visits that satisfy neither patient nor provider.

View this table:

Distribution of doctors in United States, 2004



The hospitalist movement, which continues to …
Respiration and Phthisis.
Authors: Edward Playter
Journal: JAMA (1897)

Ottawa, Ont., March 6, 1897. <h3>To the Editor:</h3> —Will you kindly give space to the following in an early issue and thus aid in this important work? Without the coöperation of the leading medical journals nothing can be accomplished in that behalf. Trusting you will so favor, I may hereby thank you in advance, and am, sir, Very truly yours,Edward Playter, M.D. <h3>To Members of the Medical Profession, Individually—in the Interest of Medical Science:</h3> — As there is evidence tending to prove the theory that all persons predisposed by heredity to consumption have a respiratory capacity or action insufficient for good vigorous health, probably a proportionately small chest with insufficiency of lung membrane, that the predisposition is mainly or primarily due to this cause; in other words, that the insufficient respiratory function is the special primary feature of the predisposition (a condition which may be, practically, acquired by habit,
Surgical ablation of ventricular tachycardia with sequential map-guided subendocardial resection: electrophysiologic assessment and long-term follow-up.
Authors: D E Haines, B B Lerman, I L Kron, J P DiMarco
Journal: Circulation (1988)

A new operative technique of sequential map-guided subendocardial resection (SER) was used in 45 consecutive patients for the treatment of sustained ventricular tachycardia due to coronary artery disease. This technique is characterized by map-guided SER or cryothermic ablation during normothermic cardiopulmonary bypass, followed by repeated sequences of programmed stimulation to assess adequacy of resection. The patients' mean age was 59 +/- 10 years and the mean left ventricular ejection fraction was 34 +/- 12%. Twenty-five (56%) patients had a history of myocardial infarction within the previous 2 months. After ventriculotomy, 34 patients (76%) had inducible monomorphic ventricular tachycardia. These patients underwent repeated sequences of ventricular tachycardia induction and mapping during normothermic bypass followed by successive SER or cryothermic ablation until sustained monomorphic ventricular tachycardia was no longer inducible. Twenty-seven patients had a total of 60 discrete, mappable tachycardias induced and seven patients had 10 discrete tachycardias that were too fast to accurately map. In the remaining 11 patients, no ventricular tachycardia was inducible after ventriculotomy and SER, which included all visually identifiable scar, was performed. The mean cardiopulmonary bypass time was 102 +/- 27 min. Forty-one of 45 patients (91%) survived to hospital discharge, and 35 of 41 patients (85%) had no inducible ventricular tachycardia at postoperative electrophysiologic evaluation performed in the absence of all antiarrhythmic drugs. The remaining six patients had no inducible ventricular tachycardia with drug therapy. All four operative nonsurvivors had refractory cardiac collapse preoperatively. Over 19 +/- 12 months of follow-up, there were four sudden cardiac deaths and no nonfatal recurrences of ventricular tachycardia. There were seven additional cardiac deaths. Actuarial cardiac survival was 0.57, and freedom from arrhythmic events was 0.76 at 42 months. Thus, in the absence of cardiogenic shock, the technique of sequential map-guided SER achieves: (1) a high operative survival with acceptable perfusion times, (2) excellent long-term arrhythmia control, and (3) survival comparable to that in patients with similar left ventricular function and no history of ventricular tachyarrhythmia.
Laparoscopic diagnosis of ascites in Lesotho.
Authors: R I Menzies, J M Fitzgerald, K Mulpeter
Journal: BMJ (1985)

In a prospective study of 98 consecutive patients with undiagnosed ascites examined by laparoscopy a correct immediate diagnosis was made in 76 (78%) and a final diagnosis in 92 (94%) of those who underwent laparoscopy. Visual diagnosis was highly accurate in patients with tuberculous peritonitis but only moderately accurate in those with carcinomatosis and liver disease. When the laparoscopic findings were compared with histological and microbiological results visual diagnosis was found to be the most accurate diagnostic method. Laparoscopy may readily be used in rural hospitals for diagnosing ascites.
Gefitinib-induced acute generalized exanthematous pustulosis in two patients with advanced non-small-cell lung cancer
Authors: H-C. Shih, Y-P. Hsiao, M.F. Wu, J-H. Yang
Journal: British Journal of Dermatology (2006)

Conflicts of interest: none declared. H‐C.S. and Y‐P.H. contributed equally to this article. Sir, We report two patients with advanced non‐small‐cell lung cancer (NSCLC) with metastasis who received gefitinib (Iressa®; AstraZeneca, Macclesfield, Cheshire, U.K.) for approximately 1 week, and then developed acute generalized exanthematous pustulosis (AGEP). Gefitinib is a novel anticancer agent that acts by inhibiting epidermal growth factor receptor (EGFR) signal transduction and provides clinically significant symptom relief for patients with advanced NSCLC.1, 2 Although a variety of cutaneous adverse effects have been reported in patients treated with gefitinib, AGEP induced by gefitinib has not been reported before. Patient 1, a 66‐year‐old woman, was treated with gefitinib 250 mg daily as monotherapy for NSCLC with bone metastasis. One week later, widespread erythematous patches studded with painful pustules, and erosions and crusts over the scalp, trunk and both thighs were found (Fig. 1a,b). She denied history of drug allergy, and had not previously undergone combined therapy with gemcitabine or cisplatin. Her temperature was normal. The laboratory data including white blood count, neutrophil count, liver and renal function tests, and serum electrolytes were all within normal limits, except for C‐reactive protein, which was slightly elevated (0·798 mg dL−1, normal < 0·3 mg dL−1). Bacterial culture of the pus and skin was negative. The skin biopsy showed a subcorneal pustule, papillary dermal oedema and a perivascular infiltrate with lymphocytes, eosinophils and neutrophils (Fig. 1c,d). Based on the drug history and clinical manifestations, the patient was diagnosed with AGEP caused by gefitinib. We stopped using gefitinib and prescribed prednisolone 30 mg daily; the skin lesions resolved with desquamation and prednisolone was tapered off in 2 weeks. Thereafter, the patient continued to take gefitinib with only few pustules.
A Method for the Detection and Estimation of Aortic Regurgitant Flow in Man
Authors: EUGENE BRAUNWALD, ANDREW G. MORROW
Journal: Circulation (1958)

When a diastolic murmur is present at the base of the heart, it may be difficult on clinical grounds to determine whether or not aortic insufficiency is present. Further, in patients in whom this lesion definitely exists, the magnitude of aortic regurgitant flow has been the subject of considerable speculation among both clinicians and physiologists. A technic has been devised that not only makes possible the detection of aortic insufficiency but also permits an estimate of the regurgitant volume to be made.
The Effect of Stethoscope-Applied Pressure in Auscultation
Authors: WILLIAM L. HOWELL, C. FOSTER ALDRIDGE
Journal: Circulation (1965)

The effect of pressure against the chest wall in the use of the stethoscope for both the bell and the diaphragm chest piece is discussed. A modified diaphragm chest piece in a single head designed to increase the auscultatory discrimination is discussed. Comparison of the modified and conventional diaphragm chest pieces on an artificial precordium and with the employment of accepted engineering principles in the study of sound revealed the superiority of the modified diaphragm.
Adiponectin is associated with abnormal lipid profile and coronary microvascular dysfunction in patients with dilated cardiomyopathy without overt heart failure
Authors: Daniela Giannessi, Chiara Caselli, Silvia Del Ry, Maristella Maltinti, Silvia Pardini, Stefano Turchi, Manuela Cabiati, Tiziana Sampietro, Nader Abraham, Antonio L'Abbate, Danilo Neglia
Journal: Metabolism (2010)
Aspirin Cuts Cancer Risk
Authors: M. J. Friedrich
Journal: JAMA (2011)

Daily use of low-dose aspirin reduces the risk of death from several common cancers, report investigators at the University of Oxford and other UK centers (Rothwell PM et al. Lancet. doi:10.1016/S0140-6736(10)62110-1 [published online ahead of print December 6, 2010]).
THE SIMULTANEOUS OCCURRENCE OF TUMORS IN THE THYROID, UTERUS AND BREAST
Authors: MAX BALLIN
Journal: JAMA (1922)

Every surgeon who operates upon goiters must have noticed the frequent occurrence of tumors in the thyroid, uterus and breast. Apparently there has been very little written on the subject, however, for we could find only two references in the literature. Falta's<sup>1</sup>"Ductless Glandular Diseases" contains this note: There seems to exist a certain relationship between goiter and myomata of the uterus. At least it has been observed that in strumous women who also suffer from myomata the struma also decreases in size with the retrogression of the myoma at the menopause. Falta's note is quoted from an article by Ullman<sup>2</sup>of Vienna. This article reads: It has been known for a long time that a relationship exists between the uterus and the normal thyroid gland. The nature of this relationship is, of course, enshrouded in darkness; we only know that in a not infrequent number of women
ASSOCIATION BETWEEN CORONARY CALCIFICATION AND BLEEDING AFTER PCI IN ACS: POOLED ANALYSIS FROM HORIZONS-AMI AND ACUITY TRIALS
Authors: Philippe Genereux, Akiko Maehara, Ajay Kirtane, Sorin Brener, Tullio Palmerini, Laura Lasalle, Elias Sanidas, Madhusudhan Tarigopula, Mayank Yadav, Tom McAndrew, Martin Fahy, Alexandra Lansky, Roxana Mehran, Gary Mintz, Gregg Stone
Journal: Journal of the American College of Cardiology (2013)
Cardiac autophagy is a maladaptive response to hemodynamic stress
Authors: Hongxin Zhu, Paul Tannous, Janet L. Johnstone, Yongli Kong, John M. Shelton, James A. Richardson, Vien Le, Beth Levine, Beverly A. Rothermel, Joseph A. Hill
Journal: Journal of Clinical Investigation (2007)

Cardiac hypertrophy is a major predictor of heart failure and a prevalent disorder with high mortality. Little is known, however, regarding mechanisms governing the transition from stable cardiac hypertrophy to decompensated heart failure. Here, we tested the role of autophagy, a conserved pathway mediating bulk degradation of long-lived proteins and cellular organelles that can lead to cell death. To quantify autophagic activity, we engineered a line of "autophagy reporter" mice and confirmed that cardiomyocyte autophagy can be induced by short-term nutrient deprivation in vivo. Pressure overload induced by aortic banding induced heart failure and greatly increased cardiac autophagy. Load-induced autophagic activity peaked at 48 hours and remained significantly elevated for at least 3 weeks. In addition, autophagic activity was not spatially homogeneous but rather was seen at particularly high levels in basal septum. Heterozygous disruption of the gene coding for Beclin 1, a protein required for early autophagosome formation, decreased cardiomyocyte autophagy and diminished pathological remodeling induced by severe pressure stress. Conversely, Beclin 1 overexpression heightened autophagic activity and accentuated pathological remodeling. Taken together, these findings implicate autophagy in the pathogenesis of load-induced heart failure and suggest it may be a target for novel therapeutic intervention.
Molecular detection of minimal residual disease is a strong predictive factor of relapse in childhood B-lineage acute lymphoblastic leukemia with medium risk features. A case control study of the International BFM study group
Authors: A Biondi, MG Valsecchi, T Seriu, E D'Aniello, MJ Willemse, K Fasching, A Pannunzio, H Gadner, M Schrappe, WA Kamps, CR Bartram, JJM van Dongen, ER Panzer-Grümayer
Journal: Leukemia (2000)
Unemployment and Health: A Disaster and Challenge
Authors: Steven D. Helgerson
Journal: JAMA (1988)

Unemployment, like smoking, is a health hazard not only for the unemployed person but also for his or her family members. In this short book Dr Smith, who is an assistant editor for the<i>British Medical Journal</i>, provides a thorough, easy-to-read review of what is known about the relationship between unemployment and health. The book consists of a revised and expanded series of articles that appeared in the<i>British Medical Journal</i>; the contents are heavily oriented toward Britain, and this will probably limit the book's appeal to an American audience. To document that unemployment harms health, the author has drawn on material from psychology, sociology, economics, history, literature, and journalism, as well as medicine. Throughout the book he draws parallels between unemployment and its effects in the 1930s, on the one hand, and unemployment's effects in the 1980s, on the other. To the extent that the author's aim was to
Society and Health — Doctors Less Anonymous — Harmonious Postscript
Authors: John Lister
Journal: New England Journal of Medicine (1960)

A WIDE range of medicosocial problems was surveyed at the annual congress of the Royal Society of Health. In his presidential address Lord Morrison of Lamberth spoke of the problem of the administration of the nationalized hospital service. The present method of centralized governmental administration, with regional boards exercising remote control over a large number of hospitals, was not satisfactory. Local conditions could not be fully appreciated, and the necessary control of expenditure was often inevitably somewhat arbitrary. Lord Morrison believed that there was a good case for returning the control of many hospitals to the local authorities since this . . .
The Role of the Carotid Body in Erythropoiesis in Man
Authors: Robert Lugliani, Brian J. Whipp, Benjamin Winter, Kouichi R. Tanaka, Karlman Wasserman
Journal: New England Journal of Medicine (1971)

To test the relevance to man of the hypothesis that the carotid bodies are the source of erythropoietin in cats, we studied 57 patients who had had both carotid bodies removed. Our data on these patients gave no evidence of anemia after bilateral carotid-body resection. When five of these subjects were challenged by acute phlebotomy of 1 liter of blood, reticulocytosis developed that was as marked as in the control, nonresected group, and the rate at which the red-cell count and hematocrit returned to control levels was also similar in both groups. Measurements of reticulocyte count and hematocrit were not affected by bilateral carotid-body resection in five additional subjects who had daily measurements before and every day for 12 days after operation. From these studies, we conclude that the carotid bodies are not an important source of erythropoietin in man.
Some Observations on Peak Expiratory Flow
Authors: R. J. Shephard
Journal: Thorax (1962)

The peak flow meter (Wright and McKerrow, 1959) was originally conceived as a simple port- able method of estimating forced expiratory volume (F.E.V.).However, the correlation with F.E.V. and with maximum voluntary ventilation (M.V.V.) was not always very close, and the peak flow meter reading was therefore advocated as a measure of "ventilatory capacity" in its own right.The present paper reports some normal peak flow readings obtained with the Wright meter: such values are influenced not only by airway resistance but also by the pressure developed by the thoracic musculature, and the results obtained depend largely on co-operation from the patient.I have used peak flow read- ings, obtained before and after introduction of an external resistance, to calculate a value for airway resistance that is less dependent on subjective co-operation and muscular power.The frequency response characteristics of the Wright peak flow meter do not permit measurements with an external resistance; however, if peak flow readings are obtained by high frequency equip- ment, such as a screen pneumotachograph, and a small external resistance is used, the calculated airway resistance does not differ systematically from interrupter valve values.
Oncostatin M Induces Bone Loss and Sensitizes Rat Osteosarcoma to the Antitumor Effect of Midostaurin<i>In vivo</i>
Authors: Bénédicte Brounais, Céline Chipoy, Kanji Mori, Céline Charrier, Séverine Battaglia, Paul Pilet, Carl D. Richards, Dominique Heymann, Françoise Rédini, Frédéric Blanchard
Journal: Clinical Cancer Research (2008)

Abstract Purpose: In cultures, the cytokine oncostatin M (OSM) reduces the growth and induces differentiation of osteoblasts and osteosarcoma cells into glial/osteocytic cells. Moreover, OSM sensitizes these cells to apoptosis driven by various death inducers such as the kinase inhibitor staurosporine. Here, we asked whether OSM would have similar effects in vivo. Experimental Design: Adenoviral gene transfer of OSM (AdOSM) was done in naive and osteosarcoma-bearing rats, alone or in combination with Midostaurin (PKC412), a derivative of staurosporine currently used in cancer clinical trials. Bone variables were analyzed by micro-computed tomography scanner, by histology, and by the levels of various serum bone markers. Osteosarcoma progression was analyzed by the development of the primary bone tumor, evolution of pulmonary metastasis, histology (necrosis and fibrosis), and animal survival. Results: In naive rats, AdOSM reduced serum osteoblastic and osteoclastic markers in correlation with a reduced trabecular bone volume. In an osteosarcoma rat model, the combination of AdOSM with PKC412 reduced the progression of the primary bone tumor, pulmonary metastatic dissemination, and increased overall survival, whereas these agents alone had no antitumor effect. Increased tumor necrosis and tissue repair (fibrosis) were observed with this combination. Conclusion: These in vivo experiments confirm that systemic OSM overexpression alters osteoblast/osteosarcoma activity. Because OSM sensitizes rat osteosarcoma to apoptosis/necrosis, the use of kinase inhibitors such as Midostaurin in association with OSM could represent new adjuvant treatments for this aggressive malignancy.
Gastro-oesophageal cancer: death at the junction
Authors: J. A. Jankowski
Journal: BMJ (2000)

Neurons and oligodendrocytes are highly vulnerable to various insults, and their spontaneous replacement occurs to only a limited extent after damage in the adult spinal cord. The environment of injured tissue is thus thought to restrict the regenerative capacity of endogenous neural stem/progenitor cells; strategies for overcoming such restrictions remain to be developed. Here, we combined growth factor treatment and genetic manipulation to stimulate neurogenesis and oligodendrogenesis by endogenous progenitors <i>in vivo</i>. The recombinant retrovirus pMXIG, which was designed to coexpress green fluorescent proteins (GFPs) and a neurogenic/gliogenic transcription factor, was directly injected into the injured spinal cord parenchyma to manipulate proliferative cells <i>in situ</i>. We found that cells expressing Olig2, Nkx2.2, and NG2 were enriched among virus-infected, GFP-positive (GFP<sup>+</sup>) cells. Moreover, a fraction of GFP<sup>+</sup> cells formed neurospheres and differentiated into neurons, astrocytes, and oligodendrocytes <i>in vitro</i>, demonstrating that GFP retroviruses indeed infected endogenous neural progenitors <i>in vivo</i>. Neuronal differentiation of control virus-infected cells did not occur at a detectable level in the injured spinal cord. We found, however, that direct administration of fibroblast growth factor 2 and epidermal growth factor into lesioned tissue could induce a significant fraction of GFP-labeled cells to express immature neuronal markers. Moreover, retrovirus-mediated overexpression of the basic helix-loop-helix transcription factors Neurogenin2 and Mash1, together with growth factor treatment, enhanced the production and maturation of new neurons and oligodendrocytes, respectively. These results demonstrate that endogenous neural progenitors can be manipulated to replace neurons and oligodendrocytes lost to insults in the injured spinal cord.
Abstract 5337: Molecular dynamics study on keap1 point mutations in lung cancer
Authors: Chia-Ning Yang
Journal: Cancer Research (2014)

Abstract Keap1 is a BTB-Kelch substrate adaptor protein that regulates steady-state levels of Nrf2, a bZIP transcription factor, in response to oxidative stress. In basal condition, Nrf2 is negatively regulated through ubiquitination by Keap1. However, upon exposure to oxidative stress, ubiquitination of Nrf2 is inhibited, resulting increased steady-state level of Nrf2 and increased transcription of cytoprotective ARE (antioxidant response elements)-dependent genes. Reported in 2006, the structure of Keap1 Kelch domain in complex with a 16-mer peptide derived from Nrf2 has been solved by X-ray crystallography to a resolution of 1.85Å. Accordingly, it grants us a chance to evaluate the interaction between Keap1 and Nrf2 and further interpret numerous experimental findings on unbinding due to modifications on Keap1. Herein we apply molecular dynamics simulations to study the binding behaviors of Keap1 and Nrf2 based on the solved structure to investigate how single point mutations G364C and G430C on Keap1 affect Keap1-Nrf2 binding and further cause lung cancer. Note: This abstract was not presented at the meeting. Citation Format: Chia-Ning Yang. Molecular dynamics study on keap1 point mutations in lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5337. doi:10.1158/1538-7445.AM2014-5337