tbuckley/cabot-search huggingface dataset:
THE VALUE OF DÉBRIDEMENT IN THE TREATMENT OF BURNS
Authors: A. MURAT WILLIS
Journal: JAMA (1925)

Owing largely to the investigations of Cannon<sup>1</sup>and his co-workers in this country, the belief has come to be widely established that secondary traumatic shock is due to an intoxication with protein cleavage products. Not only does it seem to have been conclusively proved that traumatized tissues may serve as a source of toxin formation, but the application of the principle of débridement, the removal of this traumatized tissue, has proved efficacious in the relief or prevention of shock. During the course of experiments<sup>2</sup>which appeared to indicate that diffuse peritonitis was a condition either very similar to or identical with traumatic shock, both in its genesis and in its manifestations, the question arose in my mind as to whether burned tissues might not serve as a source of toxin formation. It is a well known fact that patients suffering from severe burns may appear to be progressing
CARDIOVASCULAR DISEASES RISK SCORES: A COMPARISON OF THEIR PERFORMANCE IN A LOW AND MIDDLE INCOME COUNTRY
Authors: Juan Carlos Bazo-Alvarez, Julio Poterico, Frank Peralta-Alvarez, Renato Quispe, Giancarlo Valle, Robert H. Gilman, Juan F. Sánchez, Germán Málaga, Antonio Bernabé-Ortiz, Jaime Miranda
Journal: Journal of the American College of Cardiology (2014)
810-4 Remodeling of the Vascular Endothelium Following PTCA in Rabbit Iliac Arteries with Fibrin Adhesive/Endothelial Cell Matrix
Authors: John E. Baker, Victor Nikolaychik, Harry Sahota, Richard Komarowski, Sean D. Keane, Michael H. Keelan, Nicholas Kipshidze
Journal: Journal of the American College of Cardiology (1995)
The Effect of Exercise in Muscular Dystrophy
Authors: Paul J. Vignos
Journal: JAMA (1966)

Twenty-four patients with muscular dystrophy carried out a maximum resistance exercise program for one year. Improvement in muscle strength occurred in all patients throughout the first four months of exercise regardless of type of dystrophy. Subsequently, a plateau occurred which was maintained throughout the period of observation. The increased muscle function as documented by objective measurements was correlated with the initial level of muscle function. Improvement in functional abilities was less than increase in muscle strength. Patients with "limb-girdle" and facioscapulohumeral dystrophy derived the greatest physical and functional benefit from the program. A resistive exercise program in muscular dystrophy is most effective if instituted early in the course of disease.
Vulnerability of Pulmonary Capillaries in Heart Disease
Authors: John B. West, Odile Mathieu-Costello
Journal: Circulation (1995)

Abstract The pulmonary blood-gas barrier presents a dilemma. It must be extremely thin for efficient gas exchange. However, it also needs to be immensely strong because the stresses in the pulmonary capillary wall become extremely high when the capillary pressure rises. Stress failure of the capillaries occurs in several pathological conditions. It causes high-permeability edema as in neurogenic pulmonary edema or high-altitude pulmonary edema; alveolar hemorrhage, which occurs in all galloping racehorses; or a combination of the two as in severe congestive heart failure. The vulnerability of the capillary wall to increased mechanical stress has not previously been sufficiently appreciated.
Carriage of Reduced-Function <i>CYP2C19</i> Allele Among Patients Treated With Clopidogrel
Authors: Ruben L. J. Osnabrugge, A. Pieter Kappetein, A. Cecile J. W. Janssens
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract B40: PALB2-KEAP1 interaction links oxidative stress to cancer and Fanconi anemia
Authors: Jianglin Ma, Bing Xia
Journal: Clinical Cancer Research (2010)

Abstract PALB2/FANCN is mutated or silenced in breast, ovarian and pancreatic cancers and Fanconi anemia. It was initially discovered as a major binding protein for BRCA2 and controls the function of BRCA2 in homologous recombination, DNA double strand break repair and tumor suppression (Xia et al 2006). Nowadays, PALB2 itself has been also identified as a BRCA2-like breast cancer susceptibility protein and links BRCA1 and BRCA2 in the DNA damage response (Zhang and Ma et al 2009, Sy et al 2009). Therefore, PALB2 has been thought as an integral component of BRCA complex required for maintaining genomic stability via DNA recombinational repair. In order to explore what other functions PALB2 protein may have, we performed a comprehensive search of PALB2-binding partners using the tandem affinity purification (TAP) assay combined with tandem mass spectrometry (LC-MS/MS) analysis. We show that PALB2 directly interacts with KEAP1, an oxidative stress sensor that binds and represses the anti-oxidant transcription factor NRF2. NRF2-KEAP1 pathway has been characterized as an important endogenous mechanism for combating oxidative stress. Oxidative stress-induced damage can lead to a variety of pathologies such as cancer, Parkinson's diseases, diabetes, Alzheimer's diseases and the aging process (Valko et al 2007). We demonstrate that PALB2 shares a conserved “ETGE” motif with NRF2 and competes with NRF2 for KEAP1 binding, thereby relieving NRF2 from KEAP1-mediated repression. As such, PALB2 promotes NRF2 nuclear accumulation, protects cells against oxidative stress and reduces cellular level of reactive oxygen species (ROS). Our findings establish a new function for PALB2 and provide a direct link between oxidative stress and the predisposition of cancer and Fanconi anemia. References: 1. Xia B et al. Mol Cell. 2006;22:719. 2. Zhang F et al. Curr Biol. 2009;19:524. 3. Sy S et al. Proc Natl Acad Sci USA. 2009;106:7155. 4. Valko M et al. Int J Biochem Cell Biol. 2006;39:44. Citation Information: Clin Cancer Res 2010;16(14 Suppl):B40.
False-Positive 111ln-Labeled Leukocyte Scan in Cystic Fibrosis
Authors: JEFFREY R. CRASS, PHILIPPE L??HEUREUX, MERLE LOKEN
Journal: Clinical Nuclear Medicine (1979)

A false-positive 111In-labeled leukocyte scan was obtained in a girl with cystic fibrosis and infection. There was focal accumulation of 111In activity in the abdomen and marked pulmonary uptake. Surgical exploration and postmortem examination revealed no abdominal abnormality. The abdominal activity was apparently due to swallowed sputum which contained labeled leukocytes. Broader clinical implications are discussed.
Human Peyer's patches: an immunohistochemical study.
Authors: J Spencer, T Finn, P G Isaacson
Journal: Gut (1986)

We have used immunoperoxidase techniques to characterise the Peyer9s patches in human terminal ileum. The mantle zones of the B cell follicles in human Peyer9s patches were surrounded by B cells which did not express surface IgD but which mostly expressed surface immunoglobulin of the IgM and/or IgA1 isotype. Few cells expressing surface IgG or IgA2 were detected. Cells with cytoplasmic immunoglobulin of all isotypes except IgD were present in the dome regions of the Peyer9s patches as well as in the lamina propria. There was little evidence of traffic of immunoglobulin synthesising cells across the high endothelial venules. T cells were seen to surround the lymphoid follicles. They were most concentrated on the serosal aspect around the high endothelial venules. Cells with macrophage-like morphology were present in both the lamina propria and the dome region of the follicles; those in the lamina propria containing lysozyme and those in the dome region S100 protein. The results are discussed in relation to the generation and dissemination of antibody producing cells in human gut.
Limitations of Cyanoacrylate Injection for the Treatment of Gastric Fundic Varices: Reply to Matsumoto et al.
Authors: C.-Y. Chen, H.-C. Cheng
Journal: Endoscopy (2004)

We are grateful to Dr. Matsumoto and his colleagues for their comments on our case report regarding a complication of endoscopic injection sclerotherapy for bleeding gastric varices. As we mentioned in the case report [1], the extravasation of sclerosant was caused by variceal rupture due to an abrupt increase in intravariceal pressure. The increase in pressure was caused by the additional injection of 2 ml of sclerosant, rather than by residual blood flow from the afferent vein of the gastric varix, as the blood flow ceases after the increase in intravariceal pressure, while the manual injection of sclerosant does not. In addition, a follow-up panendoscopy examination 28 months after the development of the complication showed complete eradication of the gastric varix, indicating that there had been no residual blood flow after the sclerotherapy.
Re: Renzo Colombo, Lorenzo Rocchini, Nazareno Suardi, et al. Neoadjuvant Short-term Intensive Intravesical Mitomycin C Regimen Compared with Weekly Schedule for Low-grade Recurrent Non–muscle-invasive Bladder Cancer: Preliminary Results of a Randomised Phase 2 Study. Eur Urol 2012;62:797–802
Authors: Manish Garg, Apul Goel, Jai Prakash
Journal: European Urology (2012)
Developing organisational vision in general practice.
Authors: A al-Shehri, I Stanley, P Thomas
Journal: BMJ (1993)

Vision is a fashionable but ill defined term in management circles. Nevertheless, it embodies a significant concept related to guiding an organisation from present realities, through opportunities and hazards, to a viable future. Until recently a typical general practice could assume a stable external environment, but now it is caught up in the uncertainties stemming from the NHS reforms. For such a practice to undertake effective strategic planning it will have to develop a vision connecting the present with aspirations for the future. While vision is usually considered to be an individual talent, it is possible to develop a collective organisational vision within a general practice, and the small size of general practices makes this relatively easy. The vision needs to be broad; it needs to be continuous; and its capacity to predict the future needs to be monitored.
Blood Glucose Area Under the Curve: Methodological Aspects
Authors: Jean-Pierre Le Floch, Philippe Escuyer, Eric Baudin, Dominique Baudon, Léon Perlemuter
Journal: Diabetes Care (1990)

To specify the influence of methods used in estimating area under the curve (AUC) and the meaning of total and incremental AUC, 75 glycemic responses to a mixed meal were studied in 75 diabetic patients, 39 with insulin-dependent diabetes mellitus and 36 with non-insulin-dependent diabetes mellitus. AUC was integrated with five computerized methods: polynomial interpolation of third and fourth degree, trapezoidal rule, Simpson's integration, and cubic interpolatory splines. Although these methods gave significantly different results (P &amp;lt; 0.001), a strong correlation was found between estimations of AUC with different methods (r &amp;gt; 0.99, P &amp;lt; 0.001). In addition, variation between methods was ≤2%, whereas the coefficient of variation between subjects was 38%. Total AUC was strongly correlated with basal blood glucose value (r = 0.90, P &amp;lt; 0.001), whereas incremental and positive AUC were not (r = 0.12 and 0.07, respectively, NS). Incremental and positive AUC were strongly correlated with glycemic rise (r = 0.89 and 0.93, respectively, P &amp;lt; 0.001), whereas total AUC was only slightly so (r = 0.31, P &amp;lt; 0.01). Incremental and positive AUC gave slightly but significantly different information on glucose response. These results suggest that variations related to the method used in estimating AUC are not clinically relevant and that a simple method such as trapezoidal rule can be used. Total AUC is a descriptive factor related to basal blood glucose value, whereas incremental and positive AUC more accurately describe glycemic response to foods.
To feed or what to feed in cirrhosis?
Authors: Richard D. Johnston, Grace E. Dolman, Guruprasad Aithal
Journal: Hepatology (2011)

We congratulate Berzigotti et al.1 for performing an excellent study that raises more questions, just as many post hoc analyses of observational studies do. It is intriguing that obesity may predict future decompensation in patients with compensated cirrhosis and portal hypertension. The potential mechanism is unexplained. The presence of a proinflammatory and proangiogenic state driven by extrahepatic adipose tissue may accelerate existing liver disease. Furthermore, hemodynamic changes linked to metabolic syndrome may affect the development of portal hypertension. Age is another well-recognized determinant of outcomes for patients with liver disease. Obesity and smoking have been shown to accelerate the biological aging process.2 Therefore, it would be interesting to determine whether smoking was also associated with accelerated decompensation in this cohort. Finally, the presence of a dual hepatic pathology must be considered as an explanation for the reported association. Hence, a review of biopsy findings for cirrhosis and earlier stages of fibrosis (where available) could further clarify the current findings. The translation of the findings of this study into an effective intervention could be challenging. The prognosis of patients with cirrhosis is influenced by different macronutrient intake patterns3 and is worsened by protein-energy malnutrition.4 In addition, weight-loss targets have been difficult to achieve in the setting of nonalcoholic fatty liver disease without cirrhosis, even with motivated patients and intensive community support.5 In comparison with calorie-matched daytime supplementation, nocturnal nutritional supplements improve total body protein,6 and this suggests that prolonged fasting is probably detrimental for patients with cirrhosis. Very low-calorie diets and carbohydrate restriction may pose risks to patients with cirrhosis by inducing hepatic stressors (i.e., an increased demand for endogenous gluconeogenesis and an increased requirement for catabolizing ketone bodies). We have limited data about a cirrhotic liver's ability to cope with such insults. Increased exercise is ordinarily an attractive weight-loss strategy, but impaired endogenous gluconeogenesis in patients with cirrhosis results in the potential risk of exercise-induced hypoglycemia during aerobic exercise.7 Therefore, caution needs to be applied when weight loss is being recommended as an intervention for these patients. We reinforce the authors' comment that dedicated studies on the effects of obesity and weight loss on the prognosis of patients with compensated cirrhosis are needed. These studies should be performed in parallel with studies evaluating the methods, safety, and efficacy of lifestyle interventions. Richard D. Johnston M.D.*, Grace E. Dolman M.D.*, Guruprasad Aithal M.D., Ph.D.*, * Nottingham Digestive Diseases Centre, National Institute for Health Research Biomedical Research Unit,Nottingham, United Kingdom.
Experimental Acute Lead Encephalopathy in the Juvenile Rhesus Monkey
Authors: Raymond A. Clasen, J. Francis Hartmann, Philip S. Coogan, Sylvia Pandolfi, Iris Laing, Ruth A. Becker
Journal: Environmental Health Perspectives (1974)

Lead subacetate (0.5g) and 1000 units of vitamin D were given three times a week to four newly-weaned rhesus monkeys. In addition, two animals received only the vitamin D. The poisoned animals had an increase in the urinary excretion of delta-aminolevulinic acid, an elevated content of lead in the blood, and a fall in hemoglobin concentration. Between 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, generalized weakness, and convulsions. At this time the animals were killed by perfusion of fixative and the brain prepared for light and electron microscopic studies. Definite morphological evidence of disease was confined to the central nervous system, except for one animal which showed the characteristic renal inclusions of lead poisoning. All animals showed PAS-positive globules associated with blood vessels and an exudative edema involving the white matter of the cerebral hemispheres and cerebellum. Ultra-structurally, this appeared as a granular precipitate within an expanded extracellular space. Alterations of nerve fibers were not seen in the white matter but axonal swelling was observed in the cerebral cortex. The perikaryon and neuropil appeared normal. The control animals showed no significant cerebral changes.
Two cases of monocular visual loss during oral arsenic trioxide therapy of acute promyelocytic leukemia
Authors: Wing‐Yan Au, Charmaine Hon, Kin Yau, Wico W. Lai, Bonnie M. Fong, Sidney Tam, Yok‐Lam Kwong
Journal: American Journal of Hematology (2009)

Langerhans cell histiocytosis following acute leukemia in an adultTo the editor: A 69-year-old man presents with cough and SOB approximately 3.5 years following diagnosis of a poorly differentiated acute lymphocytic leukemia (progenitor cell phenotype).By flow cytometry, the initial leukemia in 1998 was positive for HLA-DR, CD34, and CD45 and negative for lymphoid and myeloid markers including: CD3, CD5, CD7, CD19, CD10, CD20, CD13, CD33, CD11b, and CD14; CD1a and S-100 protein staining were not available on this sample.A pathologic diagnosis of a progenitor cell leukemia most suggestive of acute lymphocytic leukemia was made.The patient received induction therapy in November 1998 and achieved a complete remission.Consolidation therapy was discontinued after one cycle due to severe cytopenias.Maintenance therapy was discontinued after 6 months secondary to methotrexate-induced hepatoxicity.Approximately 3.5 years after the initial diagnosis, the patient presented with back pain and leg weakness and found to have a paraspinal mass with cord compression.He underwent surgical resection followed by consolidative radiation.The lesion (see Fig. 1) was composed of sheets of medium to large sized mitotically active cells with relatively abundant cytoplasm.Occasional multinucleated tumor giant cells were also identified.The cell nuclei were vesicular with irregular contour and occasional grooves.Considering the remote history of a lymphocytic leukemia and the morphologic features which raised the possibility of an epithelioid/dendritic cell neoplasm, a panel of immunohistochemical stains was used to characterize the lesion.The tumor cells were positive for vimentin, CD1a, S-100 protein, CD43 and focally for keratins, CD45, CD68, and lysozyme.Negative immunostains included EMA, Melan-A, CD3, CD20, CD21, CD35, Kappa and Lambda light chains, and MPO.Leder's histochemical stain was negative.Based on the morphology and the immunohistochemical profile, a diagnosis of a dendritic cell neoplasm most consistent with Langerhans cell sarcoma was rendered.Electron microscopic studies were not performed.Bone marrow biopsy revealed trilineage hematopoiesis with no evidence of leukemic involvement.Approximately 2 months later, he developed a similar soft tissue mass in the right upper chest extending into the right supraclavicular area.Radiation treatment resulted in a complete clinical response in the chest mass and he had no evidence of progression for 1 year.The patient then developed shortness of breath and fevers.A CXR showed a right
Objective assessment of photoageing effects using high-frequency ultrasound in PUVA-treated psoriasis patients
Authors: P-G. Sator, J.B. Schmidt, H. Honigsmann
Journal: British Journal of Dermatology (2002)

Summary Background Skin ageing can be differentiated into intrinsic (chronological) ageing, and photoageing due to chronic sun exposure. Photoageing is the superimposition of photodamage on the ageing process. Objectives The aim of the study was to investigate possible differences between the skin of photochemotherapy (PUVA)‐treated psoriasis patients and of untreated normal subjects using a high‐frequency ultrasound system. Methods A total of 124 volunteers (aged 21–88 years, median 52 years, 62 female, 62 male), 62 psoriasis patients who had received PUVA therapy and 62 healthy controls, were investigated. Skin thickness and a subepidermal low‐echogenic band (SLEB), a parameter for photodamage, were measured in 12 different areas. Results Female skin is thinner than male skin. The skin thickness values of PUVA patients were more markedly decreased than those of the controls for the older patients. There was a clear dependence of the occurrence of SLEB on PUVA therapy in psoriasis patients. Conclusions Long‐term PUVA treatment in psoriasis patients accelerates thinning of the skin in comparison to age‐matched controls. The results show that ultrasonography is a sensitive method to investigate the effects of PUVA‐induced skin ageing.
Superoxide is involved in the pathogenesis of paraquat-induced injury in cultured rat liver slices*1
Authors: H TOGASHI
Journal: Hepatology (1991)

We examined whether superoxide is a factor responsible for paraquat-induced liver injury in terms of superoxide dismutase using cultured rat liver slices exposed to various concentrations of paraquat. The degree of liver injury was assessed by measurement of percentage of lactate dehydrogenase leakage into the medium and lipid hydroperoxides in the liver slices and by direct histopathological observation. Paraquat produced concentration- and time-related liver injury in the cultured rat liver slices. Notably, after exposure to 5 mmol/L paraquat, a significant increase of the percentage of lactate dehydrogenase leakage occurred from 4 hr (p less than 0.05 vs. control group), and this gradually increased up to 8 hr (p less than 0.01 and p less than 0.001 vs. control group at 6 and 8 hr, respectively). Changes in lipid hydroperoxides in the liver slices were similar to those in percentage of lactate dehydrogenase leakage (p less than 0.05 and p less than 0.01 vs. control group at 6 and 8 hr, respectively). Liver injury was located around the central vein at 6 hr and gradually spread at 8 hr. Paraquat-induced liver injury was aggravated both biochemically and histopathologically by pretreatment with 5 mmol/L diethyldithiocarbamate, an inhibitor of copper- and zinc-containing superoxide dismutase activity (percentage of lactate dehydrogenase leakage: p less than 0.01 and p less than 0.001 vs. paraquat group at 6 and 8 hr, respectively; lipid hydroperoxides: p less than 0.01 vs. paraquat group at 8 hr). Incubation of liver slices with liposome-encapsulated superoxide dismutase increased the augmentation of superoxide dismutase in the liver slices.(ABSTRACT TRUNCATED AT 250 WORDS)