tbuckley/cabot-search huggingface dataset:
Cervical Spine Injuries in Football
Authors: Hugh H. Hussey
Journal: JAMA (1976)

A recent issue of<i>Archives of Surgery</i>published a minisymposium on injuries of the cervical spine. A cue to the contents was given in the first sentence of Babcock's<sup>1</sup>introduction: "Spinal cord injury is one of the most devastating accidents that man can incur and still survive." Babcock<sup>2</sup>also described the thorough roentgenographic techniques that are necessary for identifying and classifying lesions according to mechanisms of injury. In turn, Stauffer and Rhoades<sup>3</sup>emphasized the importance of and described the individual methods for surgical stabilization of severe injuries. Feuer<sup>4</sup>categorized the types of traumatic vertebral deformities and the forms of resultant cord damage and explored the merits of surgical vs nonsurgical treatment. In sum, the symposium was concerned with severe and serious injuries of the cervical spine. Problems of less severe nature were neglected—a deficiency that is partly corrected in this issue ofThe Journal(p 1243)
Damages Against Casualty Officer
Authors: B. O. Dowdell, A. D. Charnley, P. D. Drinkwater, J. M. Reid, J. B. Eagles, E. Gledhill, J. M. Aitken, W. E. Thompson, B. Eagles, C. F. J. Carruthers, F. M. Fountain, W. S. Dickson, K. E. Marsh
Journal: BMJ (1953)
Initiation/promotion versus complete carcinogenicity in the rodent liver
Authors: John Ashby, B. M. Elliott, P. A. Lefevre, Jerry Styles, E. Longstaff
Journal: Environmental Health Perspectives (1983)

4-N-Pyrrolidinylazobenzene (4N) is a close structural analog of the rodent liver carcinogen 4-dimethylaminoazobenzene (DAB). This structural similarity led us to evaluate it for genotoxic activity in vitro. We observed activity for 4N and DAB in the BHK cell transformation assay and subsequently in the Salmonella mutation assay of Ames. By a curious chance, Scribner, Miller and Miller, probably prompted by the same structural similarity, had synthesized 4N in the 1960s and found it to be noncarcinogenic to the rodent liver using a bioassay test protocol that detected DAB as carcinogenic. These findings were only described following the publication of our observations made in vitro. The conflict that apparently exists between these data can be interpreted in two separate ways. (a) Scribner et al. have suggested that 4N may be a carcinogenic initiator as opposed to a complete carcinogen like DAB. They also suggested that promotion of 4N-treated rodents with phenobarbitone might lead to the production of liver tumors. (b) We have evaluated the simpler concept that the activities observed for 4N in vitro define a carcinogenic potential that is not realized in vivo due to its rapid detoxification, at least in rodents. The first of these explanations implies that pure carcinogenic initiators may form a separate class of genotoxic agents from complete carcinogens, and perhaps of greater interest, that 4N might provide a valuable model compound for the study of carcinogenic promotion in the rodent liver. The second explanation regards potential carcinogenicity as a single property that can be defined in vitro and which may or may not be expressed in vivo depending on the enzymic environments encountered by the test chemical. It is clearly important to evaluate these different propositions in order to aid progress in the study of carcinogenic promotion, especially in the rodent liver. The presentation will describe our recent studies in vitro and in vivo in this connection.
A piece of my mind. A difficult decision
Authors: J. L. Wright
Journal: JAMA (1993)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Ventricular systolic assessment in patients with dilated cardiomyopathy by preload-adjusted maximal power. Validation and noninvasive application.
Authors: T Sharir, M D Feldman, H Haber, A M Feldman, A Marmor, L C Becker, D A Kass
Journal: Circulation (1994)

BACKGROUND Noninvasive cardiac-specific analysis of contractile function in patients with dilated heart failure remains problematic. This study tests whether maximal power divided by the square of end-diastolic volume (PWRmx/EDV2, or preload-adjusted PWRmx) can provide such assessment. METHODS AND RESULTS To validate the load insensitivity of the PWRmx index and determine its response to contractile change, 24 subjects with chronic dilated cardiomyopathy underwent invasive pressure-volume catheterization study using the conductance catheter technique. Preload was transiently reduced by 30% using balloon occlusion of the inferior vena cava, and afterload impedance was lowered by 50%, induced by a bolus injection of nitroglycerin. Contractile state was varied by intravenous dobutamine, verapamil, or esmolol. PWRmx was calculated from the simultaneous product of ventricular pressure and rate of volume change (dV/dt), the latter derived from the volume catheter signal. PWRmx varied directly with preload but was minimally influenced by afterload. However, PWRmx/EDV2 was not significantly altered by either loading change. PWRmx/EDV2 did vary with contractility, correlating closely with changes in the end-systolic pressure-volume relation (r = .91, P &lt; .001). To test the noninvasive application of this index, 12 additional patients were studied, with PWRmx/EDV2 derived from nuclear ventriculography combined with a novel method to measure central arterial pressures. Subjects received intravenous nitroprusside or dobutamine in random order. Ejection fraction increased similarly with both agents (+42.9 +/- 8.9% for dobutamine and +29.4 +/- 5.3% for nitroprusside, both P &lt; .01). In contrast, PWRmx/EDV2 did not significantly change with nitroprusside but increased by 126 +/- 16.1% with dobutamine (P &lt; .01). CONCLUSIONS Preload-adjusted PWRmx is a steady-state index of ventricular systolic function that is sensitive to inotropic state and minimally influenced by physiological changes in afterload impedance or volume load. It appears useful for noninvasive cardiac-specific analysis of acute drug effects.
Direct reprogramming of mouse fibroblasts to cardiomyocyte-like cells using Yamanaka factors on engineered poly(ethylene glycol) (PEG) hydrogels
Authors: Amanda W. Smith, Jake D. Hoyne, Peter K. Nguyen, Dylan A. McCreedy, Haytham Aly, Igor R. Efimov, Stacey Rentschler, Donald L. Elbert
Journal: Biomaterials (2013)
Abstract 572: Proline-rich acidic protein 1 (PRAP1), a novel mitotic arrest deficient 1 (MAD1) interacting partner, suppresses mitotic checkpoint signaling in hepatocellular carcinoma.
Authors: Karen MF Sze, Glanice K. Chu, Queenie HY Mak, Irene OL Ng
Journal: Cancer Research (2013)

Abstract DNA aneuploidy or chromosomal instability is commonly observed in major types of human cancers, and one of the causes for chromosomal instability is defective mitotic checkpoint signaling in cells. Loss of mitotic checkpoint contributes to chromosomal instability, leading to carcinogenesis. The mitotic checkpoint monitors the status of kinetochore-microtubule attachment and delays the onset of anaphase until all kinetochores have been attached with microtubules. Mitotic arrest deficient 1 (MAD1) is key component in mitotic checkpoint signaling. We previously identified a novel isoform of MAD1, which we named MAD1β (Sze et al. Cancer Res 2008;68:9194-9201). In this study, using yeast-two hybrid screening, we have identified a novel MAD1 interacting partner, proline-rich acidic protein 1 (PRAP1). The function of PRAP1 is largely unknown. Hence, we investigated its role in mitotic checkpoint signaling in hepatocellular carcinoma (HCC). We demonstrated the physical interaction between PRAP1, MAD1 and MAD1β in yeast-two hybrid screening and with co-immunoprecipitation assay. Both MAD1 and MAD1β proteins were co-immunoprecipitated with PRAP1. Moreover, we stably expressed PRAP1 in two HCC cell lines, BEL-7402 and SMMC-7721, which have competent mitotic checkpoints. We observed that stable expression of PRAP1 induced impairment in mitotic checkpoint (P &amp;lt; 0.01). After treatment with either colcemid or nocodazole, the PRAP1-stably expressing BEL-7402 and SMMC-7721 cells showed significantly lower mitotic indices as compared with the corresponding vector control cells. Ectopic expression of PRAP1 also resulted in chromosome bridge formation (P&amp;lt; 0.01) and aberrant chromosome numbers (P &amp;lt; 0.001) in these cell lines. All these cellular changes contributed to chromosomal instability. Interestingly, ectopic expression PRAP1 led to significant underexpression of MAD1 but not MAD1β in HCC cells. Taken altogether, our data indicate that PRAP1 is an interacting partner of MAD1 and may have functions of degrading MAD1 and in turn suppressing mitotic checkpoint signaling in HCC. (This study was partly funded by a Hong Kong Research Grants Council GRF grant [HKU 772608]) Citation Format: Karen MF Sze, Glanice K. Chu, Queenie HY Mak, Irene OL Ng. Proline-rich acidic protein 1 (PRAP1), a novel mitotic arrest deficient 1 (MAD1) interacting partner, suppresses mitotic checkpoint signaling in hepatocellular carcinoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 572. doi:10.1158/1538-7445.AM2013-572
Vascular Inflammation Evaluated by [18F]-Fluorodeoxyglucose Positron Emission Tomography Is Associated With the Metabolic Syndrome
Authors: Nobuhiro Tahara, Hisashi Kai, Sho-ichi Yamagishi, Minori Mizoguchi, Hiroyuki Nakaura, Masatoshi Ishibashi, Hayato Kaida, Kenkichi Baba, Naofumi Hayabuchi, Tsutomu Imaizumi
Journal: Journal of the American College of Cardiology (2007)
Rural Medical Care
Authors: Robert Oseasohn
Journal: JAMA (1971)

A system was designed to provide medical care to families in a rural community by means of a physician's assistant linked to an urban medical center. Medical services were defined in collaboration with the community. The assistant, a registered nurse and local resident, was trained to make observations, communicate, and act under physician supervision. The system has been operating for two years and has given care to over 500 families.
Hormonal and Metabolic Effects of Enalapril Treatment in Hypertensive Subjects With NIDDM
Authors: M Peter Moore, Teresa W Elliott, M Gary Nicholls
Journal: Diabetes Care (1988)

The effects of enalapril treatment on blood glucose, insulin, and C-peptide levels and effects on the reninangiotensin aldosterone system were studied in 22 hypertensive patients with non-insulin-dependent diabetes. After a 4-wk run-in period during which all previous antihypertensive drugs were discontinued, treatment was commenced with one daily dose of 10 mg enalapril. The dose was adjusted upward at 3-wk intervals to a maximum of 40 mg daily. In 3 subjects, addition of a thiazide diuretic was required after 9 wk of treatment. At completion of run-in and after 9 and 13 wk of treatment, subjects had blood samples drawn after fasting and 2 h after a standardized 1.6-mJ mixed meal. Mean fasting blood glucose at the end of the run-in period was 8.3 ± 0.5 mM and at study completion was 7.3 ± 0.4 mM. Mean postprandial blood glucose was 10.8 ±1.0 mM before treatment and 9.8 ± 0.7 mM at study completion. The changes in fasting and postprandial blood glucose levels were not significant (P = .06 and P = .15, respectively). There was no significant change in glycosylated hemoglobin levels. Fasting and meal-stimulated insulin and C-peptide levels were not altered by enalapril treatment. Treatment was associated with a sustained reduction in plasma angiotensin-converting enzyme activity, an increase in plasma renin activity, reduced plasma aldosterone levels, and significant reductions in supine, seated, and standing arterial blood pressures. There was a small rise in mean plasma potassium from 4.0 ± 0.09 to 4.2 ± 0.09 mM after 3 wk of treatment, but after 9 wk, potassium levels had returned to pretreatment levels. Plasma creatinine levels did not change.
Demonstration of Specific Binding of Cocaine to Human Spermatozoa
Authors: Ricardo A. Yazigi
Journal: JAMA (1991)

Exposure of males to cocaine has been linked to abnormal development of their offspring. To investigate the possible role of sperm, this study examined the interaction of cocaine with human spermatozoa. Washed sperm were incubated with tritiated cocaine (6.7 nmol/L) with or without unlabeled cocaine (670 μmol/L), and the samples were filtered and the remaining radioactivity quantitated. The specific binding was optimal at 20 minutes and 23°C. Competition studies with tritiated cocaine (3.4 to 66.6 nmol/L) indicated the presence of approximately 3.6× 10<sup>3</sup>binding sites per cell, with a high affinity receptor dissociation constant (K<sub>d</sub>= 12.6 nmol/L). Cocaine concentrations as high as 670 μmol/L had no detectable effect on either the motility or viability of the cells. These results support the hypothesis that the sperm may act as a vector to transport cocaine into an ovum. This novel mechanism could be involved in the abnormal development of offspring of cocaine-exposed males. (<i>JAMA</i>. 1991;266:1956-1959)
Insulin Withholding for Weight Control in Women With Diabetes
Authors: Melanie M Biggs, Monica Ramirez Basco, Gayle Patterson, Philip Raskin
Journal: Diabetes Care (1994)

OBJECTIVE To provide a description of the clinical characteristics that distinguish individuals who withhold insulin for weight control from those who do not. Some individuals with insulin-dependent diabetes mellitus (IDDM) control their weight by withholding insulin and purging excessive calories. This process places patients at risk for developing severe hyperglycemia, diabeticketoacidosis, and increases the risk of long-term complications of diabetes. RESEARCH DESIGN AND METHODS Forty-two women with IDDM, ages 16–40, were interviewed and divided into two groups: insulin withholders (IWs) and non-insulin withholders (non-IWs). These groups were compared on physiological, behavioral, psychological, and psychiatric variables. RESULTS Compared with non-IWs, patients who withheld insulin to control their weight exhibited poorer glycemic control, reported more negative attitudes toward diabetes, were more likely to have pathological scores on the Eating Disorder Inventory 2, and were more likely to report current or past symptoms of anorexia or bulimia nervosa. IWs were also more likely to report lying to physicians about their degree of compliance with their diabetes regimens. CONCLUSIONS The results of this study indicated that IWs exhibit more symptoms associated with the spectrum of eating disorders than non-IWs. This study showed that insulin withholding for weight control not only exists, but is associated with some maladaptive symptoms and behaviors that need to be addressed by diabetes treatment teams.
Elevated Proinsulin Levels Related to Islet Cell Antibodies in First-Degree Relatives of IDDM Patients
Authors: Giatgen A Spinas, Ole Snorgaard, Svend G Hartling, Martin Oberholzer, Willi Berger
Journal: Diabetes Care (1992)

Objective To assess whether proinsulin levels are elevated in first-degree relatives of insulin-dependent diabetes mellitus (IDDM) patients and whether there is a relationship between proinsulin levels and the occurrence of immunological markers. Research Design and Methods Fasting proinsulin concentrations were measured in 85 first-degree relatives (54 siblings, 20 parents, 11 children) of IDDM patients and in 90 age- and weight-matched control subjects with no family history of diabetes mellitus. Results Fasting proinsulin levels (median, 25th, and 75th percentiles) were 8 pM (range 3.2–14 pM) in first-degree relatives and 1.7 pM (range 1.7–4 pM) in control subjects (P &amp;lt;0.0001). Proinsulin was significantly elevated in siblings (7.2 pM, range 3.8–15 pM; P &amp;lt;0.0001), parents (9.8 pM, range 6.4–13 pM; P &amp;lt;0.0001), and children (6.6 pM, range 1.8–12 pM, P = 0.04) compared with control subjects but without differences between these groups. Islet cell antibody positive (ICA+) IDDM relatives had significantly higher proinsulin levels than ICA- (16 pM; range 7.2–25 vs. 6.9 pM, range 3.1–12 pM; P = 0.02). There was no difference between individuals with and without insulin autoantibodies. No difference in proinsulin levels was observed if the relatives were subdivided according to HLA-DR sharing with the diabetic proband. Conclusions Fasting proinsulin concentrations were raised not only in siblings but also in parents and children of IDDM patients. Because proinsulin is more elevated in ICA+ than in ICA− subjects, increased proinsulin levels could reflect minor β-cell damage due to previous immunological attack.
Loss of Neural Cell Adhesion Molecule Induces Tumor Metastasis by Up-regulating Lymphangiogenesis
Authors: Ivana Crnic, Karin Strittmatter, Ugo Cavallaro, Lucie Kopfstein, Lotta Jussila, Kari Alitalo, Gerhard Christofori
Journal: Cancer Research (2004)

Reduced expression of neural cell adhesion molecule (NCAM) has been implicated in the progression to tumor malignancy in cancer patients. Previously, we have shown that the loss of NCAM function causes the formation of lymph node metastasis in a transgenic mouse model of pancreatic beta cell carcinogenesis (Rip1Tag2). Here we show that tumors of NCAM-deficient Rip1Tag2 transgenic mice exhibit up-regulated expression of the lymphangiogenic factors vascular endothelial growth factor (VEGF)-C and -D (17% in wild-type versus 60% in NCAM-deficient Rip1Tag2 mice) and, with it, increased lymphangiogenesis (0% in wild-type versus 19% in NCAM-deficient Rip1Tag2 mice). Repression of VEGF-C and -D function by adenoviral expression of a soluble form of their cognate receptor, VEGF receptor-3, results in reduced tumor lymphangiogenesis (56% versus 28% in control versus treated mice) and lymph node metastasis (36% versus 8% in control versus treated mice). The results indicate that the loss of NCAM function causes lymph node metastasis via VEGF-C- and VEGF-D-mediated lymphangiogenesis. These results also establish Rip1Tag2;NCAM-deficient mice as a unique model for stochastic, endogenous tumor lymphangiogenesis and lymph node metastasis in immunocompetent mice.
Hispanics with End-Stage Renal Disease
Authors: C. Craig Tisher
Journal: Annals of Internal Medicine (1994)

Letters1 November 1994Hispanics with End-Stage Renal DiseaseC. Craig Tisher, MDC. Craig Tisher, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-121-9-199411010-00034 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:On behalf of the members of the National Institutes of Health Consensus Panel that addressed morbidity and mortality in dialysis, I thank Drs. Radecki and Nissenson for drawing our attention to published data that support the clinical impression referred to in the consensus statement that Hispanics are somewhat over-represented among treated patients with end-stage renal disease. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1994Volume 121, Issue 9Page: 723-724KeywordsHispanic peopleMedical dialysisMorbidityMortalityRenal failure ePublished: 15 August 2000 Issue Published: 1 November 1994 Copyright & PermissionsCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Investigation of intestine function during acute viral hepatitis using combined sugar oral loads.
Authors: G Parrilli, R Cuomo, G Nardone, G Maio, C M Izzo, G Budillon
Journal: Gut (1987)

One fifth of all cases of A virus hepatitis (AVH) have symptoms of gastroenteritis at the onset. This study investigated the mediated intestinal absorption of D-xylose (D-xyl) and 3-o-methyl-D-glucose (3-omG) and the non-mediated permeation of lactulose (Lacl, mol wt 342) and L-rhamnose (L-rh, mol wt 164) during acute and remission phases of AVH. Ten patients with AVH were given an oral load containing these sugars (5 g D-xyl: 2.5 g 3-omG, 1 g L-rh, 5 g lacl in 250 ml water) once during the acute phase and again during remission. The same load was given once to a group of 22 healthy controls. The mean concentration of D-xyl in urine and the ratio of D-xyl to 3-omG in plasma and urine were normal in both the AVH phases, ruling out intestinal malabsorption even in the acute phase. This study showed a significant increase in non-mediated permeation to Lacl, but not to L-rh, during the acute phase. These data indicate that the barrier function of the intestine is compromised in AVH infection while the absorptive function is not. An abnormally low concentration of D-xyl and 3-omG in plasma at one hour was found in all patients during the acute phase. This finding cannot be explained by alterations in intestinal absorption, but could be accounted for by increased space distribution of the sugars because of increased diffusion into tissue cells and/or expansion of the extracellular space by fluid retention.
THE PRODUCTION OF PARTIAL LIVER INSUFFICIENCY IN RABBITS
Authors: Philip D. McMaster, D. R. Drury
Journal: The Journal of Experimental Medicine (1929)

A rapid and simple method for the production of marked liver insufficiency in rabbits has been described. The necessary operation can be carried out by an unassisted operator in a few minutes. The method should further the study of liver physiology. The changes as concerns blood sugar, urea formation, and uric acid metabolism would appear to be the same in the rabbit suffering from hepatic insufficiency as in the dog.
Hyperglucagonemia and insulin-mediated glucose metabolism.
Authors: S Del Prato, P Castellino, D C Simonson, R A DeFronzo
Journal: Journal of Clinical Investigation (1987)

The effect of chronic physiologic hyperglucagonemia on basal and insulin-mediated glucose metabolism was evaluated in normal subjects, using the euglycemic insulin clamp technique (+50, +100, and +500 microU/ml). After glucagon infusion fasting glucose increased from 76 +/- 4 to 93 +/- 2 mg/dl and hepatic glucose production (HGP) rose from 1.96 +/- 0.08 to 2.25 +/- 0.08 mg/kg X min (P less than 0.001). Basal glucose oxidation after glucagon increased (P less than 0.05) and correlated inversely with decreased free fatty acid concentrations (r = -0.94; P less than 0.01) and decreased lipid oxidation (r = -0.75; P less than 0.01). Suppression of HGP and stimulation of total glucose disposal were impaired at each insulin step after glucagon (P less than 0.05-0.01). The reduction in insulin-mediated glucose uptake was entirely due to diminished non-oxidative glucose utilization. Glucagon infusion also caused a decrease in basal lipid oxidation and an enhanced ability of insulin to inhibit lipid oxidation and augment lipid synthesis. These results suggest that hyperglucagonemia may contribute to the disturbances in glucose and lipid metabolism in some diabetic patients.