tbuckley/cabot-search huggingface dataset:
Prophylactic Use of Oral Penicillin in Rheumatic Fever, Chorea, and Carditis
Authors: S. Cope, G. Sanderson, C. A. ST. Hill, E. N. Chamberlain
Journal: BMJ (1960)

MEDICA,L JOIJRNAL I1).At this time also the early morning urine was of low and fixed specific gravity.After potassium repletion both these findings disappeared.Denton, Wynn, McDonald, and Simon (1951) have reported two cases in which a similar amino-aciduria occurred during potassium depletion.Neither had glycosuria.In one of their two patients' treatment with potassium abolished the amino-aciduria; the other patient died while still depleted of potassium.ln his recent review Stanbury (1958) draws attention to the fact that amino-aciduria has resulted from severe and acquired renal tubular disturbances and that it has on occasion been reversible.We feel that the amino- aciduria in our patient was caused by a renal tubular disturbance for which the potassium deficiency was responsible.This interpretation is supported by the normal liver-function tests, by the low and fixed specific gravity of the urine at the time of amino-aciduria, and by the disappearance of the urinary abnormalities on correction of the potassium depletion.In the patient with nephrotic syndrome and both amino-aciduria and potassium depletion.reported by Stanbury and Macaulay (1957).treatment with potassium had no effect on the a mi ino-aciduria.In their patient potassium depletion had been present for much longer than in our patient or those reported by Denton et al. (13951).It is submitted that the possibility of potassium depletion and/or intracellular acidosis should be con- sidered in every case of amino-aciduria and also that ainino-aciduLria should be looked for when potassium depletion is suspected.Summary A case is presented in which potassium depletion was accompanied by significant amino-aciduria, which disappeared with potassium therapy.Attention is also drawn to the difficulties attendant upon a definitive diagnosis of potassium depletion, and it is again emphasized that normal serum potassium levels can be misleading.Possible implications of the findings are discussed.Thanks are due to Dr. J. D. Blainev (department of experimental pathology) for assessment of amino-aciduria, and to Drs.R. F. Crampton and D. Matthews (department of physiology) for help with the muscle biopsies
Multifunctional Skin‐Like Electronics for Quantitative, Clinical Monitoring of Cutaneous Wound Healing
Authors: Yoshiaki Hattori, Leo Falgout, Woosik Lee, Sung‐Young Jung, Emily Poon, Jung Woo Lee, Ilyoun Na, Amelia Geisler, Divya Sadhwani, Yihui Zhang, Yewang Su, Xiaoqi Wang, Zhuangjian Liu, Jing Xia, Huanyu Cheng, R. Chad Webb, Andrew P. Bonifas, Philip Won, Jae‐Woong Jeong, Kyung‐In Jang, Young Min Song, Beatrice Nardone, Michael Nodzenski, Jonathan A. Fan, Yonggang Huang, Dennis P. West, Amy S. Paller, Murad Alam, Woon‐Hong Yeo, John A. Rogers
Journal: Advanced Healthcare Materials (2014)

Non‐invasive, biomedical devices have the potential to provide important, quantitative data for the assessment of skin diseases and wound healing. Traditional methods either rely on qualitative visual and tactile judgments of a professional and/or data obtained using instrumentation with forms that do not readily allow intimate integration with sensitive skin near a wound site. Here, an electronic sensor platform that can softly and reversibly laminate perilesionally at wounds to provide highly accurate, quantitative data of relevance to the management of surgical wound healing is reported. Clinical studies on patients using thermal sensors and actuators in fractal layouts provide precise time‐dependent mapping of temperature and thermal conductivity of the skin near the wounds. Analytical and simulation results establish the fundamentals of the sensing modalities, the mechanics of the system, and strategies for optimized design. The use of this type of “epidermal” electronics system in a realistic clinical setting with human subjects establishes a set of practical procedures in disinfection, reuse, and protocols for quantitative measurement. The results have the potential to address important unmet needs in chronic wound management.
Abstract LB-190: RAF inhibitors transactivate RAF dimers and ERK signaling in a wild-type BRAF-dependent manner
Authors: Poulikos I. Poulikakos, Chao Zhang, Eric W. Joseph, Yogindra Persaud, Christine A. Pratilas, Gideon Bollag, David B. Solit, Kevan M. Shokat, Neal Rosen
Journal: Cancer Research (2010)

Abstract Discussion Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-190.
Flow-dependent epigenetic DNA methylation regulates endothelial gene expression and atherosclerosis
Authors: Jessilyn Dunn, Haiwei Qiu, Soyeon Kim, Daudi Jjingo, Ryan Hoffman, Chan Woo Kim, Inhwan Jang, Dong Ju Son, Daniel Kim, Chenyi Pan, Yuhong Fan, I. King Jordan, Hanjoong Jo
Journal: Journal of Clinical Investigation (2014)

In atherosclerosis, plaques preferentially develop in arterial regions of disturbed blood flow (d-flow), which alters endothelial gene expression and function. Here, we determined that d-flow regulates genome-wide DNA methylation patterns in a DNA methyltransferase-dependent (DNMT-dependent) manner. Induction of d-flow by partial carotid ligation surgery in a murine model induced DNMT1 in arterial endothelium. In cultured endothelial cells, DNMT1 was enhanced by oscillatory shear stress (OS), and reduction of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5Aza) or siRNA markedly reduced OS-induced endothelial inflammation. Moreover, administration of 5Aza reduced lesion formation in 2 mouse models of atherosclerosis. Using both reduced representation bisulfite sequencing (RRBS) and microarray, we determined that d-flow in the carotid artery resulted in hypermethylation within the promoters of 11 mechanosensitive genes and that 5Aza treatment restored normal methylation patterns. Of the identified genes, HoxA5 and Klf3 encode transcription factors that contain cAMP response elements, suggesting that the methylation status of these loci could serve as a mechanosensitive master switch in gene expression. Together, our results demonstrate that d-flow controls epigenomic DNA methylation patterns in a DNMT-dependent manner, which in turn alters endothelial gene expression and induces atherosclerosis.
Clinical diagnosis of pyloric stenosis: a declining art.
Authors: J Macdessi, R K Oates
Journal: BMJ (1993)

OBJECTIVE--To assess whether diagnostic imaging of pyloric stenosis has made a difference in rapidity of diagnosis, duration of pre-operative hydration, and length of stay in hospital. DESIGN--Chart review of infants with confirmed diagnosis of pyloric stenosis. SETTING--Paediatric teaching hospital. SUBJECTS--215 infants with a confirmed diagnosis of pyloric stenosis seen during 1974-7 and 187 infants with pyloric stenosis seen during 1988-91. MAIN OUTCOME MEASURES--State of hydration on admission, time between presentation to hospital and a definite diagnosis, techniques used to make the diagnosis, whether a pyloric mass was felt before or after an imaging procedure, time between presentation and surgery, and length of stay in hospital. RESULTS--The average age at presentation was 40 days in both groups. A pyloric mass was palpated either without or before an imaging study in 87% (187/215) of cases during 1974-7 but in only 49% (91/187) during 1988-91. The use of barium meal examination and ultrasonography increased from 20% (42/215) of cases during 1974-7 to 61% (114/187) during 1988-91. There were no significant differences between the two groups in the time taken to establish a diagnosis, the mean duration of preoperative treatment, or the length of stay in hospital (after allowance for the decline in average length of stay of all hospital patients between the two periods). CONCLUSIONS--An increased use of diagnostic imaging for pyloric stenosis did not lead to earlier diagnosis or better management. While imaging is important in identifying pyloric stenosis in difficult cases, increasing reliance on imaging has reduced doctors9 skills in diagnosing pyloric stenosis clinically.
Nitric oxide inhibition induces early activation of type I collagen gene in renal resistance vessels and glomeruli in transgenic mice. Role of endothelin.
Authors: C Chatziantoniou, J J Boffa, R Ardaillou, J C Dussaule
Journal: Journal of Clinical Investigation (1998)

Hypertension is often associated with the development of nephroangio- and glomerulo-sclerosis. This pathophysiological process is due to increased extracellular matrix protein, particularly type I collagen, accumulation. This study investigated whether nitric oxide (NO) synthesis is involved in the mechanism(s) regulating activation of the collagen I gene in afferent arterioles and glomeruli. Experiments were performed on transgenic mice harboring the luciferase gene under the control of the collagen I-alpha2 chain promoter [procolalpha2(I)]. Measurements of luciferase activity provide highly sensitive estimates of collagen I gene activation. NO synthesis was inhibited by NG-nitro-L-arginine methyl ester (L-NAME) (20 mg/kg per day) for a period of up to 14 wk. Systolic blood pressure was increased after 6 wk of treatment (117+/-2 versus 129+/-2 mmHg, P < 0.01) and reached a plateau after 10 wk (around 160 mmHg). Luciferase activity was increased in freshly isolated afferent arterioles and glomeruli as early as week 4 of L-NAME treatment (150 and 200% of baseline, P < 0.01, respectively). The activation of procolalpha2(I) became more pronounced with time, and at 14 wk increased four- and tenfold compared with controls in afferent arterioles and glomeruli, respectively (P < 0.001). In contrast, luciferase activity remained unchanged in aorta and heart up to 8 wk and was increased thereafter. Increased histochemical staining for extracellular matrix deposition, and particularly of collagen I, was detected in afferent arterioles and glomeruli after 10 wk of L-NAME treatment. This fibrogenic process was accompanied by an increased urinary excretion rate of endothelin. In separate experiments, the stimulatory effect of L-NAME on collagen I gene activation was abolished when animals were treated with bosentan, an endothelin receptor antagonist. Similarly, bosentan reduced the increased extracellular matrix deposition in afferent arterioles and glomeruli during NO inhibition. Interestingly, bosentan had no effect on the L-NAME- induced increase of systolic pressure. These data indicate that NO inhibition induces an early activation of the collagen I gene in afferent arterioles and glomeruli. This activation in the kidney precedes the increase in blood pressure and the procolalpha2(I) activation in heart and aorta, suggesting a specific renal effect of NO blockade on collagen I gene expression that is independent of increased blood pressure and, at least partly, mediated through stimulation of the endothelin receptor. Use of procolalpha2(I) transgenic mice provides a novel and efficient model to study the pathophysiological mechanism(s) regulating renal fibrosis.
Detection of anti-ADAM 10 antibody in serum of a patient with pulmonary fibrosis associated with dermatomyositis
Authors: J. Fujita, T. Takeuchi, N. Dobashi, Y. Ohtsuki, M. Tokuda, J. Takahara
Journal: Annals of the Rheumatic Diseases (1999)

<h3>OBJECTIVES</h3> It has been suggested that the humoral immune system plays a part in the pathogenesis of pulmonary fibrosis. Although circulating autoantibodies to lung protein(s) have been suggested, few lung proteins have been characterised. The purpose of this study is to determine the antigen recognised by serum of a patient with pulmonary fibrosis associated with dermatomyositis. <h3>METHODS</h3> To accomplish this, anti-small airway epithelial cell (SAEC) antibody in a patient9s serum was evaluated using a western immunoblot. <h3>RESULTS</h3> An autoantibody against SAEC was found, and the antigen had a molecular weight of 62 kDa. Using the patient9s serum, clones from the normal lung cDNA library were screened and demonstrated that anti-SAEC antibody in the patient9s serum was against ADAM (A disintegrin and metalloprotease) 10. <h3>CONCLUSION</h3> This is the first report that demonstrates the existence of anti-ADAM 10 antibody in a patient with pulmonary fibrosis associated with dermatomyositis.
Blindness in Childhood in Developing Countries: Time for a Reassessment?
Authors: Parikshit Gogate, Khumbo Kalua, Paul Courtright
Journal: PLoS Medicine (2009)

Magnitude of Childhood BlindnessN Globally, vitamin A deficiency-and measles-related blindness in children has declined substantially although it persists in some focal settings.N With reductions in nutritional and infectious causes of blindness, intra-uterine and genetic causes of blindness (e.g., cataract and congenital anomalies) have assumed increased importance and need tertiary care-level interventions and long-term follow-up to achieve good visual rehabilitation.N Further research is needed to identify the underlying causes of congenital and developmental cataract and to determine the best strategies for recognition, referral, treatment, and rehabilitation.N Changing patterns of global childhood blindness suggest a reassessment of research, training, and programmatic needs.
A Case of Simultaneous Uterine and Extrauterine Gestation
Authors: T. E. Mitchell
Journal: BMJ (1896)

THE following case of primary malignant disease of the pan- creas presents some striking resemblances to the two de- scribecd by Dr. Guthrie Rankin in the BRITlSH MEDICAL JOURNAL of May iith, I895, and, like them, it differs from the classical descriptions of the condition.
US cancer patients often forgo follow-up treatments because of cost
Authors: J. H. Tanne
Journal: BMJ (2010)

One in six patients in the United States with cancer skips some of their continuing health care because of cost, concludes a new study. The authors conclude that more than two million of about 12 million Americans with a history of cancer “did not get needed medical services because of financial concerns.”

In one year in the study period, 2005, 7.8% of people who had had cancer went without some medical treatment because of the cost, reports the study, which was published in Cancer , the journal of the American Cancer Society (doi:10.1002/cncr.25209). The percentage of the general population who skipped treatment they needed that year because of cost was 5.2%.

The study, …
Next-generation sequencing of the TET2 gene in 355 MDS and CMML patients reveals low-abundance mutant clones with early origins, but indicates no definite prognostic value
Authors: Alexander E. Smith, Azim M. Mohamedali, Austin Kulasekararaj, ZiYi Lim, Joop Gäken, Nicholas C. Lea, Bartlomiej Przychodzen, Syed A. Mian, Erick E. Nasser, Claire Shooter, Nigel B. Westwood, Corinna Strupp, Norbert Gattermann, Jaroslaw P. Maciejewski, Ulrich Germing, Ghulam J. Mufti
Journal: Blood (2010)
Electrocardiogram and Pulmonary Infarction
Authors: Travis Winsor
Journal: JAMA (1968)

The electrocardiogram assists in the diagnosis of infarction when tracings are taken within 24 hours of the pulmonary arterial occlusion, when tracings are repeated at least daily, and when the infarcts are large. Electrocardiographic changes are detected in 70% to 80% of these patients, but if tracings are taken late or infrequently or if infarcts are small, changes are detected in only 10% to 20% of the patients. Electrocardiographic changes occur when at least 65% of the total cross-sectional area of the pulmonary arterial system is occluded (organically or by spasm) and hemodynamic abnormalities are present. Certain ECG changes indicate right atrial enlargement, while others indicate rotation of the right ventricle into the field of the left precordial (V<sub>4</sub>and V<sub>5</sub>) electrode position (clockwise rotation about the long axis as viewed from the apex). The enlargement is brought about by right atrial and right ventricular strain, and pulmonary
Reduction in Carotid Arterial Wall Thickness Using Lovastatin and Dietary Therapy
Authors: Howard N. Hodis
Journal: Annals of Internal Medicine (1996)

Objective: To assess the effects of lipid-lowering therapy on the progression of early, preintrusive carotid arterial atherosclerosis. Design: Randomized, double-blind, placebo-controlled, serial carotid arterial imaging trial. Setting: University Atherosclerosis Research Unit. Patients: 188 patients from the Monitored Atherosclerosis Regression Study who were 37 to 67 years of age and had angiographically defined coronary artery disease. Intervention: Cholesterol-lowering diet plus placebo or lovastatin, 80 mg/d. Measurements: High-resolution B-mode ultrasonographic quantification of the combined thickness of the distal common carotid arterial far wall intima-media complex (carotid arterial intima-media thickness) at baseline and every 6 months for as long as 4 years. Results: The annual rate of change in carotid arterial intima-media thickness differed significantly between the lovastatin group and the placebo group at 2 and 4 years (P < 0.001). Patients receiving lovastatin had consistent reduction of the intima-media thickness (P < 0.001 as early as 1 year), whereas patients receiving placebo had consistent increase of the intima-media thickness at 2 and 4 years (P < 0.02). On-trial levels of low-density lipoprotein cholesterol, triglycerides, and apolipoproteins B, C-III, and E correlated significantly with the annual rate of change in carotid arterial intima-media thickness (P < 0.001). Conclusion: Lipid-lowering therapy reverses the progression of early, preintrusive atherosclerosis of the carotid artery. Both cholesterol-rich and triglyceride-rich lipoproteins correlate with the progression of early, preintrusive atherosclerosis of the carotid artery. These findings, together with earlier reports of the effects of lovastatin therapy on the progression of atherosclerosis of the coronary arteries, indicate that carotid arterial far wall intima-media thickness is a useful end point for anti-atherosclerosis trials.
Skin exfoliation after renal failure.
Authors: C Giordano, N G De Santo, D Cirillo, N Perna
Journal: BMJ (1972)

<h3>Abstract</h3> Development of single cell sequencing allows detailing the transcriptome of individual oocytes. Here, we compare different RNA-seq datasets from single and pooled mouse oocytes and show higher reproducibility using single oocyte RNA-seq. We further demonstrate that UMI (unique molecular identifiers) based and other deduplication methods are limited in their ability to improve the precision of these datasets. Finally, for normalization of sample differences in cross-stage comparisons, we propose that external spike-in molecules are comparable to using the endogenous genes stably expressed during oocyte maturation. The ability to normalize data among single cells provides insight into the heterogeneity of mouse oocytes.
Intralymphatic immunotherapy for cat allergy induces tolerance after only 3 injections
Authors: Gabriela Senti, Reto Crameri, Daniela Kuster, Pål Johansen, Julia M. Martinez-Gomez, Nicole Graf, Martin Steiner, Ludwig A. Hothorn, Hans Grönlund, Christine Tivig, Anna Zaleska, Ozge Soyer, Marianne van Hage, Cezmi A. Akdis, Mübeccel Akdis, Horst Rose, Thomas M. Kündig
Journal: Journal of Allergy and Clinical Immunology (2012)
Honeycomb Lungs and Malignant Pulmonary Adenomatosis in Scleroderma
Authors: H. Caplan
Journal: Thorax (1959)

Scleroderma was once thought to be a disease limited to the skin, but recent reports have demonstrated visceral involvement in many cases, and Goetz (1945) has suggested that a more appropriate name for the disease would be progressive systemic sclerosis.In early descriptions of generalized scleroderma (Finlay, 1891) dyspnoea and a tendency to pulmonary infections were attributed to restriction of respiratory movements produced by sclerotic changes in the skin and muscles of the chest wall.However, it seems more likely that the pulmonary symptoms are due to fibrotic changes in the lungs, and in some cases to cystic changes therein.The clinical and radiological features have been reviewed by several authors, including Hayman and Hunt (1952), who collected from the literature 27 cases of pulmonary fibrosis due to scleroderma, by Shuford, Seaman, and Goldman (1953), and by Harper (1953).Morbid anatomical studies are less complete, and it is the purpose of this paper to report on the histology of the lungs in two further cases, with special reference to the cystic changes.In these cases the epithelium lining the cysts is hyperplastic and, in one, appears to have under- gone multifocal malignant change.CASE REPORTS CASE 1.--A housewife, aged 42 years, was admitted to Whittington Hospital (under the care of Dr. H. E. S. Pearson) on August 7, 1953.About 16 years previously she had developed severe pain in the fingers, with much colour change and ulceration, and then some of the distal phalanges began to drop off.After a few years her feet became affected.In 1942 four sympathectomies were performed with no benefit; if anything, her condition deteriorated.More ulcers developed on the arms and legs, and the knees, feet, and hands became stiff and drawn up.In 1948 she began to have difficulty in swallowing and could only tolerate semi-solid food.Her general health deteriorated and she became bed-ridden.
MEF2A sequence variants and coronary artery disease: a change of heart?
Authors: David Altshuler, Joel N. Hirschhorn
Journal: Journal of Clinical Investigation (2005)

Rare mutations in MEF2A have been proposed as a cause of coronary artery disease (CAD) and myocardial infarction (MI). In this issue of the JCI, Pennacchio and colleagues report sequencing MEF2A in 300 patients with premature CAD and in controls. Only 1 CAD patient was found to carry a missense mutation not found in controls. The specific 21-bp deletion in MEF2A previously proposed as causal for CAD and/or MI was observed in unaffected individuals and did not segregate with CAD in families. These results do not support the hypothesis that mutations in MEF2A are a cause of CAD and/or MI but do illustrate general principles regarding the difficulty of connecting genetic variation to common diseases.
The hidden delight of psoriasis
Authors: F. Meulenberg
Journal: BMJ (1997)

In John Updike's novel The Centaur young Peter Caldwell has psoriasis.1 He is not sure whether to tell his girlfriend, but he is also aware of the power that the disease can involve, when he wonders: “Should he tell her? Would it, by making her share the shame, wed them inextricably; make her, by bondage of pity, his slave? Can he, so young, afford a slave?” And he does not conceal the fact that the disease also gives him pleasure. “The delight of feeling a large flake yield and part from the body under the insistence of a fingernail must be experienced to be forgiven.”

The visibility of psoriasis appeals to the imagination, perhaps because of the chronic, variable, and unpredictable nature of the disease, and has even led to literary language in the medical literature.2 For example, Ingram describes the plaques and colourful configurations as patterns that “may rival the heavens for beauty and design,” to which he adds with a sense of drama: “To leave a trail of silver scale about the house and blood-stains on the sheets and to fear the public gaze—this is a cruel fate.”3

The psychosocial dimensions of skin disorders like psoriasis have been described in the medical literature.4 5 6 7 But psoriasis has also been a theme in non-medical literature—autobiographies as well as fiction. Novelist Connie Palmen pointed out in The Laws that psoriasis seems to be “a perfectly visible, exterior, unhidden disease, but it is precisely the disease of the one who hides.”8 Autobiographical prose

John Updike devoted the chapter “At war with my skin” to psoriasis in Self-consciousness .9 He argues that psoriasis keeps you thinking: “Strategies of concealment ramify, and self-examination is endless.” The patient constantly invents new ways of hiding the symptoms. …