tbuckley/cabot-search huggingface dataset:
Recurrent Dislocation of the Shoulder
Authors: Peter A. Casagrande
Journal: JAMA (1961)

This excellent monograph on recurrent dislocation of the shoulder is divided into 10 chapters: Historical Aspects, Anatomical Consideration, Clinical Features, Radiological Studies, Basic Lesions, Conservative Measures, Operative Procedures, Postoperative Measures, Followup Studies, and Summary and Conclusions. An added attraction is a unique stereoscopic compact viewer, which enables the reader to view anatomic lesions and operative approaches on 3-dimensional color discs. There are 5 of these stereo discs with adequate commentary in chapter 11 entitled "Stereo Appendix." Dr. Moseley has comprehensively covered the literature and has compiled a most complete bibliography. He reemphasizes the fact that recurrent disclocations of the shoulder are mainly due to a defect in the anterior capsular mechanism ( Bankhart lesion ). The next most important factor in recurrent dislocations is the posterolateral defect in the head of the humerus, which is frequently associated with some attrition of the anterior rim of the glenoid. He believes that almost 100%
Teratological research using in vitro systems. IV. Cells in culture.
Authors: J J Welsh
Journal: Environmental Health Perspectives (1987)

Several in vitro cellular systems designed to screen agents for teratogenic potential are described in this report. These assays were selected from a review of literature published through the spring of 1986 that generated over 100 references on teratological research using cell-based systems. Some of the assays have a broader application than others, but most require confirmation by one or more additional complementary tests because of the specificity of the teratogenic mechanism the assays are investigating. Included are systems that use analysis of tumor cell attachment; intercellular communication; growth of human embryonic palatal mesenchyme cells; progesterone production in porcine granulosa cells; differentiation of embryonic neural crest, limb bud, midbrain, and Drosophila cells; and differentiation of tumor cells. Because of the dynamic nature of cell culture work, the group of assays listed here should not be viewed as encompassing all cell systems of value with regard to teratogenicity testing; instead, the list represents several of the more prominent systems now being evaluated by the scientific community.
A False-Positive I-131 Whole-Body Scan in Chronic Parotitis
Authors: SUZY KIM, CHAN H. PARK, SEOK NAM YOON, KYUNGHOON HWANG
Journal: Clinical Nuclear Medicine (2001)

Although I-131 whole-body scanning is a useful method to evaluate and manage well-differentiated thyroid cancer, several causes of false-positive findings require careful evaluation. The authors describe a case of benign parotitis mimicking metastasis on an I-131 whole-body scan.
Demands on surgical inpatient services after mass mammographic screening.
Authors: L Holmberg, H O Adami, I Persson, T Lundstrom, L Tabar
Journal: BMJ (1986)

The changes in the demand for surgical inpatient care created by mammographic screening for breast cancer were analysed by comparing two counties, one with and one without a mass screening campaign. A comprehensive computerised register of inpatient care in the region was used. The results indicate that population based screening offered to women above 40 years and repeated every two to three years will increase the number of operations required for breast cancer and inpatient days by at least 150% during the initial screening round. During the second round the figures tend to return to previous levels. Of decisive importance for the demands on health service resources are the specificity of screening, the duration of the first screening round, and the age groups included.
Preventing Intimate Partner Violence
Authors: Kathryn E. Moracco, Thomas B. Cole
Journal: JAMA (2009)

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
Abstract 2624: Sodium butyrate induced cellular senescence and inhibited invasion of cancer cells with distinct mechanism.
Authors: Kazuyuki Itoh, Kiyoko Yoshioka, Hidemitsu Nakagawa
Journal: Cancer Research (2013)

Abstract Sodium butyrate (SB) -C-4 saturated fatty acid (short-chain fatty acids) present in the human bowel membrane in the quite high concentration (2 mM) as food metabolites. It was previously reported that SB showed anti-tumor effect as HDAC inhibitor, however, the precise mechanism has not been elucidated yet. Here, we focused on the role of SB on cancer cell growth, motility and invasion. Physiological concentration of SB (0.25-4 mM) induced inhibition of cell growth (2D), colony formation in soft agar, in vitro motility and invasiveness with Boyden chamber and wound healing assay in a dose-dependent fashion using human fibrosarcoma (HT1080), glioblastoma (A172) cells and rat mammary Walker 256 cells. SB also affected the morphology of HT1080, A172 and Walker 256 cells, namely spread out with marked stress fibers bridging focal adhesions. Phosphorylation levels of focal adhesion kinase (Y577 and Y397 sites) were increased but that of myosin light chain (S19 site) was not altered. All of these biological effects of SB were reversible, and recovered after withdrawal. In contrast, HDAC inhibitor trichostatinA inhibited cancer cell growth irreversibly but not affected motility, invasiveness and morphology. In addition, HT1080 and A172 cells treated with SB showed positivity for senescence-associated β-gal (SA-β gal) staining with elevated expression levels of p53 and p21 proteins in a time and dose-dependent manner. In contrast, mRNA level of p21 was sharply declined after the treatment with SB. Knocking down of p21 protein expression by siRNA reversed both the growth inhibition and positivity for SA-β gal staining but not the inhibition of invasiveness. Thus p21 was required for cellular senescence but not for the decrease in motility induced by SB. Further, proteasome inhibitor, MG132 decreased the cellular growth and inhibited motility and invasiveness of the HT1080 and A172 cells, and showed similar all these biological effects of SB. Finally, intrathecal administration of SB effectively inhibited the invasion of Walker256 cells into the brain and elongated the animal (rat) survival in vivo. Collectively, SB inhibited growth with induced cellular senescence, inhibited invasion by distinct mechanism, and thus would be a good candidate for anti-invasive therapy without severe adverse effects. Citation Format: Kazuyuki Itoh, Kiyoko Yoshioka, Hidemitsu Nakagawa. Sodium butyrate induced cellular senescence and inhibited invasion of cancer cells with distinct mechanism. [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 2624. doi:10.1158/1538-7445.AM2013-2624
American Diabetes Association Evidence-Based Nutrition Principles and Recommendations Are Not Based on Evidence
Authors: Thomas M.S. Wolever
Journal: Diabetes Care (2002)

Patients With Type 1 Diabetes1,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] not only regulates calcium metabolism but also modulates the immune system.Some reports have suggested that 1,25(OH) 2 D 3 helps to prevent the development of type 1 diabetes.The association between the vitamin D receptor (VDR) genotype and susceptibility to type 1 diabetes has been examined, but a definitive conclusion has not yet been reached (1,2).We examined the VDR genotype in juvenile Japanese patients with type 1 diabetes.A total of 108 diabetic patients (41 boys and 67 girls, age of onset 0.4 -18 years with a median age of 8.9) and 120 nonrelated nondiabetic subjects were studied.Three polymorphic restriction fragment-length polymorphisms (RFLPs), i.e., Fok I, ApaI, and TaqI, were genotyped by PCR-RFLP method.The genotype or allele frequencies were compared statistically by the 2 test.The significance of differences in each genotype for the age of onset was tested with the Mann-Whitney U test.Among the patients, the FF (n ϭ 50) and tt (n ϭ 5) genotypes were found relatively frequently, and aa (n ϭ 46) was infrequent compared with those in control subjects, but these differences were not statistically significant (P ϭ 0.14, 0.18, and 0.38 for FF, tt, and aa genotypes, respectively).There was also no significant difference in the allele frequency of each polymorphism, although the incidence of the F allele tended to be higher in the diabetic patients (P ϭ 0.051).Concerning the age of onset of diabetes, patients with the ff genotype (n ϭ 12, median 5.2 years, range 1.7-11.0)were significantly younger at onset than those with FF (n ϭ 50, 9.7 years, 0.4 -15.9, P ϭ 0.01) or Ff (n ϭ 46, 8.9 years, 0.9 -18.0,P ϭ 0.03).No significant association was observed between the TaqI or ApaI genotype and the age of onset.The ff genotype has been reported to be associated with a lower expression of VDR mRNA and reduced inhibition of phytohemagglutinin-stimulated growth of peripheral blood mononuclear cells.Thus, the Fok I genotype may influence the rate of the progression of insulitis by modifying the autoimmune process, which may have led to the significant difference in the age of onset.The relatively high frequency of the F allele in diabetic patients, which has also been found in Japanese adult diabetic patients (2), is apparently inconsistent with this observation.A possible explanation is that the impact of Fok I polymorphism may not be strong enough to prevent the progression of autoimmune insulitis into overt diabetes and thus does not influence susceptibility to the disease itself.In conclusion, VDR gene polymorphism does not appear to have a strong enough impact to clearly influence susceptibility to the disease itself, but Fok I polymorphism might influence the age of onset of diabetes in juvenile Japanese diabetic patients.
Tumor Protein 53–Induced Nuclear Protein 1 Is a Major Mediator of p53 Antioxidant Function
Authors: Carla E. Cano, Julien Gommeaux, Sylvia Pietri, Marcel Culcasi, Stéphane Garcia, Mylène Seux, Sarah Barelier, Sophie Vasseur, Rose P. Spoto, Marie-Josèphe Pébusque, Nelson J. Dusetti, Juan L. Iovanna, Alice Carrier
Journal: Cancer Research (2008)

Abstract p53 exerts its tumor suppressor function mainly through transcriptional induction of target genes involved in several processes, including cell cycle checkpoints, apoptosis, and regulation of cell redox status. p53 antioxidant function is dependent on its transcriptional activity and proceeds by sequential induction of antioxidant and proapoptotic targets. However, none of the thus far renowned p53 targets have proved able to abolish on their own the intracellular reactive oxygen species (ROS) accumulation caused by p53 deficiency, therefore pointing to the existence of other prominent and yet unknown p53 antioxidant targets. Here, we show that TP53INP1 represents such a target. Indeed, TP53INP1 transcript induction on oxidative stress is strictly dependent on p53. Mouse embryonic fibroblasts (MEF) and splenocytes derived from TP53INP1-deficient (inp1−/−) mice accumulate intracellular ROS, whereas overexpression of TP53INP1 in p53-deficient MEFs rescues ROS levels to those of p53-proficient cells, indicating that TP53INP1 antioxidant function is p53 independent. Furthermore, accumulation of ROS in inp1−/− cells on oxidant challenge is associated with decreased expression of p53 targets p21/Cdkn1a, Sesn2, TAp73, Puma, and Bax. Mutation of p53 Ser58 (equivalent to human p53 Ser46) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser58 phosphorylation is implicated in this process. In addition, TP53INP1 deficiency results in an antioxidant (N-acetylcysteine)-sensitive acceleration of cell proliferation. Finally, TP53INP1 deficiency increases oxidative stress–related lymphoma incidence and decreases survival of p53+/− mice. In conclusion, our data show that TP53INP1 is a major actor of p53-driven oxidative stress response that possesses both a p53-independent intracellular ROS regulatory function and a p53-dependent transcription regulatory function. [Cancer Res 2009;69(1):219–26]
IN VITRO TRANSFORMATION BY THE ADENOVIRUS-SV40 HYBRID VIRUSES
Authors: H. J. Igel, P. H. Black
Journal: The Journal of Experimental Medicine (1967)

Tumors induced with hamster kidney cells transformed by the adeno 2-, adeno 3-, adeno 7-, and adeno 12-SV40 hybrid viruses, and by adenovirus type 12, were examined histologically. The tumors induced with adeno 2-, adeno 3-, and adeno 7-SV40-transformed cells were similar to tumors induced with SV40-transformed hamster kidney cells but contained cells intermediate in morphology between SV40 and adenovirus tumor cells and occasionally contained nests of adenovirus-like cells. Cells transformed by the adeno 12-SV40 hybrid and by adenovirus type 12 gave rise to morphologically similar tumors. The results suggest that both viral genomes are operative in hybrid-transformed cells but that one genome is apparently responsible for the predominant morphology of the tumor. Evidence that the morphology of a single transformed target cell is determined by the transforming genome was discussed.
Adrenal failure complicating status asthmaticus in steroid-treated patients.
Authors: A. H. el-Shaboury
Journal: BMJ (1966)

Though pathological studies have shown that administration of adrenal steroids can cause adrenocortical atrophy in experi mental animals (Ingle, 1938 ; Winter et al., 1950 ; Rawls et al., 1954 ; Holub et al., 1959) and in man (Sprague et al., 1950, 1951 ; Salassa et al., 1953 ; Bennett, 1954 : Stoner and Whiteley, 1954), biochemical studies have revealed that the adrenal glands are capable of responding satisfactorily to corticotrophin (A.C.T.H.) stimulation despite many years of steroid therapy (Fredell et al., 1955 ; Larzelere et al., 1957 ; Carreon et al., 1960 ; Andersson and Kjerulf, 1961 ; Robinson et al., 1962 ; Savage et al., 1962 ; Brinck-Johnsen et ed., 1963 ; Treadwell et al., 1963). Even when a subnormal increase in plasma 17-hydroxysteroids (17-OHCS ; cortisol) is found during an infusion of A.C.T.H., a significant increase has been recorded with more prolonged adrenal stimulation (Eik-Nes et al., 1955 ; Christy et al., 1956 ; Sandberg et al, 1957 ; Krusius and Oka, 1958 ; Landon et al., 1965). There do not appear to be any reports on adrenal function during attacks of status asthmaticus in patients receiving long term steroid therapy. The present paper describes the plasma 17-OHCS response to the administration of A.C.T.H. in 17 such patients with status asthmaticus.
Reply to the Letters to the Editor from Bach and Silvestri
Authors: Claudia I. Henschke
Journal: Clinical Cancer Research (2008)

In Response: In response to Drs. Silvestri and Bach, it was clearly stated that all eight patients with clinical stage I lung cancer who had no treatment died of lung cancer in our response to the letters to the editor in the New England Journal of Medicine (1). The details of the procedures for obtaining the cause and timing of deaths have already been given (2). In his editorial, Dr. Aisner noted the importance of following those who had no treatment for their lung cancer. This continues as a critical aspect of the I-ELCAP as it shows the natural course of screen-detected lung cancer in the absence of treatment. Surely we need to continue to accumulate additional patients without treatment or with delayed treatment as they are identified. Beyond this, we address potential “overdiagnosis” in several ways (2) by (a) requiring growth of nodules &lt;15 mm before biopsy, (b) having an expert pathology panel review all pathology specimens, and (c) following those who have no treatment or who delay their treatment. Ultimately, the benefit of screening comes from the opportunity to provide for early treatment and, in the absence of performing a trial that randomly assigns patients with screen-diagnosed lung cancer to immediate versus delayed treatment, our quasi-experimental design provides this information.The I-ELCAP study provides a new paradigm for performing screening research by studying the diagnostic and prognostic issues separately (3). This approach has advantages over the traditional screening randomized control trial. Far from being a “case series” as suggested by Dr. Silvestri, each screenee is enrolled according to a common protocol (4) and is followed for all rounds of screening to determine whether they have lung cancer, either diagnosed by the screening or by prompting of symptoms between the screenings. Once a person is diagnosed with cancer, they are followed to learn the curability of each relevant subtype of cancer. Curability is estimated by finding the asymptote on the Kaplan-Meier survival curve (2). It is well known that once screening stops, the deaths will start occurring at the same rate as in the absence of screening, and these deaths do not contribute to the knowledge of the benefit of screening.Dr. Bach is concerned that we referred to an article we wrote that explains the time delay before a mortality reduction can be seen in a breast cancer–screening program (5). We used the Malmo breast cancer randomized screening trial to show that the benefit of early treatment provided by screening was only seen some 8 years after the start of screening, and only as long as screening continued. This article was recognized as the turning point in the mammography controversy in 2002 where failure to understand this delay in the benefit nearly led to a change in public policy (6, 7). This article is particularly on point with regard to the Bach et al. article in JAMA (8) where the focus is on mortality reduction in the early years of follow-up where no reduction is to be expected.
ENORMOUS CARDIAC DISTENTION
Authors: George L. Kessler
Journal: JAMA (1926)

This case should prove of interest, as I was unable to find any to compare with it in the literature: P. M., a married woman, aged 31, a Jewess, was of good habits and had had no diseases of childhood, except at the age of 8, an attack of tonsillitis; this was followed by streptococcic arthritis, which cleared up and never returned, but left the patient with a stenosis of the mitral valve. The history up until the time I first saw her was indefinite. She consulted me at 14 years of age for palpitation and indigestion. The physical examination at that time showed a heart of enormous hypertrophy and dilatation, with auricular fibrillation, mitral stenosis, aortic systolic murmur and tricuspid regurgitation. There was a slight icteric tint to the skin, and the liver was about three finger-breadths below the border of the ribs; urinalysis gave negative results; no edema
<i>In Vivo</i> X-Ray Imaging Reveals Improved Airway Surface Hydration after a Therapy Designed for Cystic Fibrosis
Authors: Kaye S. Morgan, Martin Donnelley, Nigel Farrow, Andreas Fouras, Naoto Yagi, Yoshio Suzuki, Akihisa Takeuchi, Kentaro Uesugi, Richard C. Boucher, Karen K. W. Siu, David W. Parsons
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

Kaye S. Morgan, Martin Donnelley, Nigel Farrow, Andreas Fouras, Naoto Yagi, Yoshio Suzuki, Akihisa Takeuchi, Kentaro Uesugi, Richard C. Boucher, Karen K. W. Siu, David W. Parsons
Pharmacokinetics and pharmacodynamic action of budesonide in early- and late-stage primary biliary cirrhosis
Authors: Wolfgang Hempfling, Frank Grunhage, Karin Dilger, Christoph Reichel, Ulrich Beuers, Tilman Sauerbruch
Journal: Hepatology (2003)

Budesonide has been discussed as a potential treatment option in primary biliary cirrhosis (PBC). Therefore, we studied the pharmacokinetics and pharmacodynamics of budesonide in patients with PBC stage I/II and stage IV. Twelve patients with early PBC stage I/II and 7 patients with PBC stage IV under continuous treatment with ursodeoxycholic acid (UDCA) were enrolled in an exploratory trial. Each patient received oral budesonide for 3 weeks at weekly increasing dosages of 3 mg once to thrice per day. Budesonide and cortisol plasma levels, urinary cortisol excretion, serum liver tests, and immunoglobulins were determined on days 1, 7, and 21 of the study. Patients with PBC stage IV showed significantly higher peak plasma concentrations (4.9 ± 3.5 vs. 1.5 ± 0.4 ng/mL; P &lt; .05) and areas under the plasma concentration–time curves (AUC) (23.2 ± 16.8 vs. 5.1 ± 1.4 hours · ng/mL, P &lt; .01, total AUC extrapolated to infinity [AUC 0–∞ ]) after a single dose of 3 mg budesonide when compared with patients with PBC stage I/II. Equally, AUC of budesonide were significantly increased under a multiple dose regimen on day 21 (14.0 ± 11.6 vs. 5.0 ± 1.9 hours · ng/mL, P &lt; .01, AUC at steady state from dosing time to 8 hours [AUC ss,0–8 h ]). Higher levels of budesonide were related to a significant decrease in plasma cortisol and reduction of urinary cortisol excretion in patients with stage IV disease. Two patients with stage IV disease developed portal vein thrombosis (PVT). In conclusion, administration of budesonide leads to markedly elevated plasma levels in cirrhotic patients with PBC associated with serious adverse drug reactions. Thus, further evaluation of combined treatment with UDCA may be considered in early–stage PBC but not in cirrhotic patients with PBC.