tbuckley/cabot-search huggingface dataset:
The Body in the Library: A Literary Anthology of Modern Medicine
Authors: H. Mathiasen
Journal: JAMA (2004)

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 Publications 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
The Relationship Between Cutaneous and Visceral Carcinomas
Authors: John C. Maize
Journal: JAMA (1975)

The relationship between cutaneous carcinoma and visceral malignant neoplasms has long been a subject of considerable interest as well as controversy. Moller et al<sup>1</sup>and Andersen and colleagues<sup>2</sup>at the Finsen Institute in Denmark have recently refocused attention on this problem. They have found no appreciable deviation from the expected incidence of visceral neoplasms in patients with either Bowen disease or multiple basal cell carcinomas. Their conclusion in the case of Bowen disease differs considerably from that of US authors. Bowen disease is a relatively uncommon type of in situ carcinoma. Graham and Helwig<sup>3</sup>studied 155 patients with Bowen disease; in more than one quarter of their patients, a primary extracutaneous malignant neoplasm developed on an average of five to six years after onset of the cutaneous tumor. Treatment of the Bowen disease had no effect on the subsequent development of systemic malignant neoplasm. Several other investigators
Overexpression of Muscarinic Receptor 3 Promotes Metastasis and Predicts Poor Prognosis in Non–Small-Cell Lung Cancer
Authors: Gengpeng Lin, Longhua Sun, Ran Wang, Yubiao Guo, Canmao Xie
Journal: Journal of Thoracic Oncology (2014)

Chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer development, but the mechanism is not fully understood. Muscarinic receptor 3 (M3R) has been found to be involved in the progression of small-cell lung cancer and the pathological process of COPD. We hypothesized that M3R may contribute to lung cancer development, especially in patients with COPD.The correlation between M3R expression and clinical features of non-small-cell lung cancer (NSCLC) was evaluated in 148 paraffin-embedded archived NSCLC specimens with the use of immunohistochemistry. M3R agonist and siRNA treatments were used to study the role of M3R in NSCLC cell lines. Western blotting and zymography were used to examine the impact of M3R on the PI3K/Akt/matrix metalloproteinase 9 signaling pathway.The expression of M3R in NSCLC was significantly increased and correlated with tumor metastasis and poor survival of NSCLC patients. NSCLC patients with COPD showed higher expression of M3R than those without COPD (p = 0.0014). Moreover, M3R expression was inversely related to percent forced expiratory volume in 1 second (r = 0.7017, p < 0.0001) and forced expiratory volume in 1 second /forced vital capacity (r = 0.5057, p < 0.0001), but positively related to smoking history. Down-regulation of M3R resulted in the inhibition of migration and invasion ability of NSCLC cell lines A549 and L78. Furthermore, M3R enhanced the expression and activity of matrix metalloproteinase 9 through PI3K/Akt, which promoted the migration and invasion of NSCLC cell lines.Our results suggest that overexpression of M3R in NSCLC promotes the progression of NSCLC, which could contribute to lung cancer development in COPD patients. M3R could be another pharmacological target in lung cancer, especially in COPD patients.
Effects of Acetylstrophanthidin on Coronary Vascular Resistance and Myocardial Oxygen Consumption
Authors: JOHN A. WALDHAUSEN, JAMES W. KILMAN, THOMAS L. HERENDEEN, FRANCIS L. ABEL
Journal: Circulation Research (1965)

The effects of acetylstrophanthidin on coronary circulation were studied in 31 dogs. Coronary blood flow was measured in empty beating hearts or in fibrillating hearts by collecting coronary venous return during perfusion of the systemic circulation (cardiopul-monary bypass). In 14 animals with ventricular fibrillation, acetylstrophanthidin caused an initial coronary constriction and fall in coronary blood flow. This was followed, after approximately 10 minutes, by a significant drop in resistance and a rise in coronary blood flow which persisted for the remainder of the experiment. Associated with the increase of blood flow was an increase of myocardial oxygen consumption. This effect was not abolished by ganglionic blockade, cardiac denervation or bilateral adrenalectomy. In nine dogs with beating but empty hearts, after the initial constriction of the coronary vessels, there was only a small change in coronary blood flow and resistance, although myocardial oxygen consumption was increased. The lack of coronary vasodilatation was attributed to increased mechanical resistance due to the augmented force of contraction produced by the drug.
Peers' rejection of statutory duty of candour is a missed opportunity, say campaigners
Authors: M. Limb
Journal: BMJ (2012)

The House of Lords has dashed campaigners’ hopes for a new law requiring the NHS to be open with patients about errors that cause harm after peers rejected a proposed amendment to the Health and Social Care Bill calling for a statutory duty of candour.

The amendment, which was tabled by the crossbencher Baroness Masham and had cross party support, was defeated by 234 to 194 votes after a two hour debate on Monday 13 February.

A coalition of patients’ charities and health organisations, led by Action against Medical Accidents (AvMA), had lobbied for the amendment and hoped that there would be enough support to defeat the government.

Peter Walsh, chief executive of AvMA, said afterwards, “This is a bad day for anyone who values …
The Suicidal Risk
Authors: John F. Oliven
Journal: New England Journal of Medicine (1951)

IN this country about 16,000 suicides are reported each year.1 In addition, about 100,000 suicidal attempts are believed to occur annually.2 , 3 Thus every physician may find himself in a position in which he must decide on the degree of suicidal risk that a given patient represents.Varieties of Suicidal Risk Encountered in Medical PracticeSuicide is a reaction common to the mentally disordered of many types. The mistaken belief that manic-depressive psychosis is the principal suicidiferous disorder may lull the physician into a false sense of security at times.Case 1. A man removed his mother, a patient with senile . . .
Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury.
Authors: J E Muller, P R Maroko, E Braunwald
Journal: Circulation (1975)

Precordial electrocardiographic mapping has been proposed as a method for evaluating the extent of myocardial injury in patients with acute myocardial infarction. To assess the relationship between direct measures of myocardial cell damage and findings obtained by precordial mapping, the left anterior descending coronary artery (LAD) was occluded in dogs instrumented for simultaneous recording of epicardial and precordial electrocardiograms. The sum in millivolts of ST-segment elevation recorded from 30 electrodes placed in a Silastic grid sutured to the epicardium (EPIsigmaST) was compared to that recorded from 30 precordial electrodes (PresigmaST). While ischemic injury was: 1) maintained constant with a fixed occlusion; 2) reduced by partial reperfusion; 3) increased by addition of a second occlusion; or 4) increased repeatedly by intermittent infusions of isoproterenol, EPIsigmaST and PresigmaST were always closely correlated in each of the 16 dogs studied: r equal 0.92 plus or minus 0.01 (SEM). In seven control dogs, 30 minutes after coronary occlusion, PresigmaST had fallen to 77.4 plus or minus 6.6% of its value 15 minutes postocclusion. In seven experimental dogs, two branches of the LAD were occluded. Fifteen minutes after double occlusion, one occlusion was released; 30 min after the initial occlusion PresigmaST had fallen significantly more than control, to 43.1 plus or minus 13.1% of its value 15 minutes postocclusion. Simultaneously, epicardial sites in the reperfused area also showed normalization of ST segments and 24 hours later exhibited normal myocardial creatine phosphokinase activity and normal histologic appearance. During the same experiment, the mean precordial R wave voltage of sites with ST-segment elevations exceeding 0.15 mV 15 minutes following occlusion fell significantly (P less than 0.05) more in the control group (from 1.14 plus or minus 0.15 to 0.75 plus or minus 0.06 mV) than in the reperfused group (from 1.06 plus or minus 0.09 to 0.96 plus or minus 0.17 mV) during the ensuing 45 minutes. Thus, more rapid normalization of PresigmaST or preservation of precordial R wave voltage reflected the actual prevention of myocardial necrosis by reperfusion. These findings demonstrate the usefulness of precordial electrocardiographic mapping for evaluation changes in myocardial ischemic injury. Sites at which appearance of epicardial ST segment is not a reliable index of ischemic injury were associated with the development of intraventricular conduction blocks with Q to intrinsic deflection intervals exceeding 40 mesc or QRS durations exceeding 65 msec; these changes were associated with precordial RSR' configurations. Such sites, whether recorded from precordial or epicardial leads, should be excluded from ST-segment measurements used in the assessment of myocardial ischemia.
Stimulation of CD5 enhances signal transduction by the T cell antigen receptor.
Authors: J B Imboden, C H June, M A McCutcheon, J A Ledbetter
Journal: Journal of Clinical Investigation (1990)

After the addition of a CD3 monoclonal antibody to peripheral T cells that have been previously stimulated with phytohemagglutinin, inositol phosphates are produced at a rapid rate for 2 min and at a much slower rate thereafter. Stimulation of CD5 allows CD3-mediated production of inositol phosphates to be sustained at a brisk rate for greater than 20 min and augments the initial CD3-mediated increase in inositol trisphosphate and release of intracellular Ca2+. Thus, perturbation of CD5 by monoclonal antibody enhances the ability of the CD3-antigen receptor complex to couple to the inositol phospholipid pathway. This effect of CD5 is independent of any direct effect of the CD5 monoclonal antibody on the levels of inositol phosphates.
Pneumatosis Intestinalis-Reply
Authors: Stephen N. Martyak
Journal: JAMA (1976)

<h3>In Reply.—</h3> At the time of the submission of our brief report, we learned Drs Wilson and Passaro soon were going to describe the entity of bypass enteritis. Because their patients were febrile, seriously ill, and required extensive therapy to recover, while our patient was not ill but merely had roentgenographic changes, we questioned the relationship of the disorders. We should have more clearly stated that the episode our patient had may have been a mild form of enteritis. Our primary objective in reporting the case was to discourage use of the sigmoid colon as an implantation site for the defunctionalized bowel segment. In our patient, a relatively asymptomatic pneumatosis intestinalis developed after sigmoid placement. Bypass enteritis is reported to occur after sigmoid placement. (Wilson and Passaro note bacterial overgrowth with cecal placement but no enteritis.) These kinds of observations should raise question as to the possible detrimental effects of
A comparison of stable and 14C-labelled polyethylene glycol as volume indicators in the human jejunum
Authors: D. L. Wingate, R. J. Sandberg, S. F. Phillips
Journal: Gut (1972)

Polyethylene glycol (PEG plus (14)C-PEG) was measured turbidimetrically and by liquid scintillation counting to compare the validities of these methods during the use of PEG as a volume indicator of intestinal perfusion studies in man. Use of (14)C-PEG results yielded similar estimates of water absorption or secretion. The simplicity of (14)C counting offers practical advantages to the use of (14)C-PEG as a nonabsorbable marker for perfusion studies in man.
1050 TREATING RELAPSE WITH PEGINTERFERON ALFA-2A PLUS RIBAVIRIN AND AMANTADIN FOR EITHER 72 OR 48 WEEKS (IN PATIENTS WITH HCV-TYPE 1/3 INFECTION): RESULTS FROM THE TRELA-STUDY
Authors: P. Buggisch, S. Zeuzem, G. Teuber, B. Möller, A. Ehrhardt, C. Gelbmann, J. Encke, T. Pohle, M.P. Manns, S. Stoll, T. Berg
Journal: Journal of Hepatology (2009)
Hypolipidemic, anti-obesity, anti-inflammatory, anti-osteoporotic, and anti-neoplastic properties of amine carboxyboranes.
Authors: I H Hall, S Y Chen, K G Rajendran, A Sood, B F Spielvogel, J Shih
Journal: Environmental Health Perspectives (1994)

The amine-carboxyborane derivatives were shown to be effective antineoplastic/cytotoxic agents with selective activity against single-cell and solid tumors derived from murine and human leukemias, lymphomas, sarcomas, and carcinomas. The agents inhibited DNA and RNA synthesis in preference to protein synthesis in L1210 lymphoid leukemia cells. Inosine-monophosphate dehydrogenase apparently is a target site of the compounds; similar effects on phosphoribosyl-pyrophosphate amido transferase, orotidine-monophosphate decarboxylase, and both nucleoside and nucleotide kinases were observed. Deoxyribonucleotide pool levels were reduced in the cells; DNA strand scission was observed with the agents. In rodents, the amine carboxyboranes were potent hypolipidemic agents, lowering both serum cholesterol and triglyceride concentrations, in addition to lowering cholesterol content of very low-density lipoprotein and low-density lipoprotein (LDL) and elevating high-density lipoprotein (HDL) cholesterol concentrations. De novo regulatory enzymes involved in lipid synthesis were also inhibited (e.g., hypocholesterolemic 3-hydroxy-3-methyl-Coenzyme A reductase, acyl-Coenzyme A cholesterol acyltransferase, and sn-glycerol-3-phosphate acyltransferase). Concurrently, the agents modulated LDL and HDL receptor binding, internalization, and degradation, so that less cholesterol was delivered to the plaques and more broken down from esters and conducted to the liver for biliary excretion. Tissue lipids in the aorta wall of the rat were reduced and fewer atherosclerotic morphologic lesions were present in quail aortas after treatment with the agents. Cholesterol resorption from the rat intestine was reduced in the presence of drug. Genetic hyperlipidemic mice demonstrated the same types of reduction after treatment with the agents. The agents would effectively lower lipids in tissue based on the inhibition of regulatory enzymes in pigs. These findings should help improve domestic meat supplies from fowl and pigs. The amine-carboxyboranes were effective anti-inflammatory agents against septic shock, induced edema, pleurisy, and chronic arthritis at 2.5 to 8 mg/kg. Lysosomal and proteolytic enzyme activities were also inhibited. More significantly, the agents were dual inhibitors of prostaglandin cyclooxygenase and 5'-lipoxygenase activities. These compounds also affected cytokine release and white cell migration. Subsequent studies showed that the amine-carboxyboranes were potent anti-osteoporotic agents reducing calcium resorption as well as increasing calcium and proline incorporation into mouse pup calvaria and rat UMR-106 collagen.
Abnormal intragastric distribution of food during gastric emptying in functional dyspepsia patients.
Authors: L E Troncon, R J Bennett, N K Ahluwalia, D G Thompson
Journal: Gut (1994)

Although delayed gastric emptying is found in some patients with functional dyspepsia, there seems to be little relation between rate of emptying and symptoms. This study examined the hypothesis that food maldistribution rather than gastric stasis may equate to symptoms in such patients and used scintigraphic techniques to quantify the partition of gastric contents between proximal and distal stomach during gastric emptying. Eleven patients with functional dyspepsia characterised by chronic severe postprandial bloating without organic abnormality, and 12 healthy volunteers, ingested a standard meal labelled with technetium-99M (99mTc). Serial images of the gastric area in anterior and posterior projections were taken for 90 minutes, regions of interest for proximal, distal, and total stomach were defined, and activity time curves were derived from the geometric means of anterior and posterior counts. Total emptying in patients (median: 46 minutes; range: 30-76) was not significantly different from controls (45 minutes; 28-58) and only three showed delayed gastric emptying. In controls, food remained predominantly in the proximal half of the stomach after ingestion and then redistributed to the distal half. In the patients, however, initial activity in the proximal half after ingestion (48%; 40-65) was significantly lower (p < 0.05) than in controls (60%; 39-73) and distributed more fully to the distal half of the stomach with a peak distal activity (56%; 34-58), which was consistently higher than in controls (36%; 33-42) (p < 0.05). It is concluded that this subgroup of functional dyspepsia patients show abnormal intragastric distribution of food, independent of gastric emptying rate.
Biochemical and functional characterization of xenoreactive natural antibodies in hu-PBL-SCID mice.
Authors: B Naziruddin, R Shiroki, S Shishido, T Howard, T Mohanakumar
Journal: Journal of Clinical Investigation (1996)

An in vivo model system to understand the mechanism of xenograft rejection was established using human peripheral blood leukocyte-reconstituted SCID (hu-PBL-SCID) mice. Human xenoreactive natural antibodies (XNA), of IgM and IgG subtypes, capable of binding to pig aortic endothelial cells (PAEC) were detected in the sera of hu-PBL-SCID by ELISA and flowcytometric methods. Western blot analysis of PAEC lysates showed that IgM and IgG XNA from hu-PBL-SCID recognized xenoantigens with similar molecular mass as those recognized by XNA from normal human serum (NHS). This result demonstrated that hu-PBL-SCID contained XNA representing the same repertoire as that of the NHS. XNA from NHS and hu-PBL-SCID were also able to induce intracellular Ca2+ signals in cultured PAEC several fold above the basal level. This result revealed their functional similarity and demonstrated for the first time that XNA in the absence of C can activate PAEC, which may lead to the pathology of xenograft rejection. In vivo, PAEC transplanted under the kidney capsule of hu-PBL-SCID mice showed deposition of human IgM and mouse C. In summary, the present study demonstrates that hu-PBL-SCID can serve as a useful model to characterize innate immunity against xenograft.
β-catenin activated hepatocellular adenoma
Authors: Hyun Hee Chu, Woo Sung Moon
Journal: Clinical and Molecular Hepatology (2013)

Hepatocellular adenoma (HCA) is a benign liver tumor composed of hepatocytes.1 HCA represents a heterogeneous entity, and is subclassified into four groups according to genotype and phenotype: hepatocyte nuclear factor (HNF) 1α-inactivated HCA, β-catenin-activated HCA, inflammatory HCA, and unclassified HCA.1 Theses subtypes vary greatly in their clinical and pathological features. Identifying the HCA subtype is important because it represents a way to understand the prognosis of HCA in terms of hepatocellular carcinoma (HCC) transformation. We present a case of β-catenin-activated HCA and discuss the histopathological findings with a review of the literature.
Diabetes, Insulin Secretion, and the Pancreatic Beta-Cell Mitochondrion
Authors: D Langin
Journal: New England Journal of Medicine (2001)

The mitochondrion of the insulin-secreting pancreatic islet cell is a biochemical beehive in which the products of glucose oxidation influence the secretion of insulin. Work with cultured islets has shown that a mitochondrial ion carrier termed uncoupling protein 2 (UCP2 ) affects glucose-stimulated insulin levels. A recent report demonstrated that in mice with a disabled UCP-2 gene, insulin secretion was enhanced and blood levels of glucose were reduced. When the gene was knocked out in ob/ob mice, which are obese, insulin-resistant, and diabetic, insulin secretion increased and the hyperglycemia was ameliorated.
Why Does Not the Stomach Digest Itself?
Authors: Lester R. Dragstedt
Journal: JAMA (1961)

The stomach normally does not digest itself because of a mechanism which regulates gastric secretion. This checks the secretion of gastric juice before the content becomes sufficiently corrosive to damage the mucosa. Pure gastric juice can destroy the mucosa and produce a peptic ulcer. An ulcer forms when gastric secretion is stimulated by agencies other than food and when its buffering effect is absent or inadequate.
Long-Term Consequences of Opiate Dependence
Authors: Charles P. O'Brien, George E. Woody, A. Thomas McLellan
Journal: New England Journal of Medicine (1981)

Opiate dependence has been a problem in America for over 100 years. It drew the editorial attention of 19th-century writers,1 and that interest has continued to the present. Thus, a historical approach such as that taken by Musto and Ramos in this issue of the Journal is particularly interesting. Their article reflects how changing attitudes in society can influence the medical treatment of this serious problem. They report the first long-term follow-up of an opiate-maintenance clinic that operated in New Haven from 1918 to 1920. In some ways their findings are consistent with those of other studies, in that evidence . . .
DNA single-strand breaks and cytotoxicity induced by chromate(VI), cadmium(II), and mercury(II) in hydrogen peroxide-resistant cell lines.
Authors: K Tsuzuki, M Sugiyama, N Haramaki
Journal: Environmental Health Perspectives (1994)

The induction of cytotoxicity and DNA single-strand breaks by chromium(VI), cadmium(II), and mercury(II) were compared in H2O2-resistant Chinese hamster ovary (CHO(R)) cells and parental (CHO(P)) cells. Using a colony-forming assay, CHO(R) cells were found to be significantly more resistant than CHO(P) cells to the cytotoxicity caused by CdCl2 and HgCl2, but not to that caused by Na2CrO4. However, the DNA single-strand breaks produced by each of these metals were significantly lower in the CHO(R) cells. With respect to chromium reduction, the level of chromium(V) in CHO(R) cells was decreased. The role of intracellular active oxygen in the heavy metal-induced DNA damage and cytotoxicity is discussed.