tbuckley/cabot-search huggingface dataset:
Depressive Illness and Aggression in Belfast
Authors: H. A. Lyons
Journal: BMJ (1972)

An inverse relation has been suggested between the incidence of depressive illness and the opportunity to externalize aggressive behaviour. The riot situation in Belfast in 1969-70 provided an opportunity to study this hypothesis. The incidences of depressive illness in the city and a neighbouring peaceful rural county were compared over a number of years. Data regarding age, sex, area of the city, and type of depression were obtained. The city was divided into areas and four of these were studied in detail. Similar data were obtained for persons showing aggressive behaviour. There was a significant decrease in depressive illness in Belfast in both sexes and all age groups. This was more pronounced in males but the decrease was confined to those in social groups IV and V. The decrease was more significant in riot areas. The suicide rate fell by almost 50% and there was a noticeable increase in the rates of homicide and crimes of violence. In contrast the rural county showed a sharp increase in male depressives.
Mutations in the polyglutamine binding protein 1 gene cause X-linked mental retardation
Authors: Vera M Kalscheuer, Kristine Freude, Luciana Musante, Lars R Jensen, Helger G Yntema, Jozef Gécz, Abdelaziz Sefiani, Kirsten Hoffmann, Bettina Moser, Stefan Haas, Ulf Gurok, Sebastian Haesler, Beatriz Aranda, Arpik Nshedjan, Andreas Tzschach, Nils Hartmann, Tim-Christoph Roloff, Sarah Shoichet, Olivier Hagens, Jiong Tao, Hans van Bokhoven, Gillian Turner, Jamel Chelly, Claude Moraine, Jean-Pierre Fryns, Ulrike Nuber, Maria Hoeltzenbein, Constance Scharff, Harry Scherthan, Steffen Lenzner, Ben C J Hamel, Susann Schweiger, Hans-Hilger Ropers
Journal: Nature Genetics (2003)
THE INDICATIONS FOR AND METHODS OF EMPLOYING HYDROTHERAPY
Authors: J. M. ANDERS
Journal: JAMA (1924)

It is quite obvious from facts gathered by actual observation that the medical profession of America bestows too little attention on the subject of hydrotherapy, more particularly, perhaps, as it is related to the treatment of chronic complaints. As a consequence, there is a lack of familiarity with the principles and technic of hydriatics. It is hoped that this paper may serve to arouse greater interest in the subject as a whole, although it will be, as the title indicates, limited to a discussion, somewhat in detail, of the indications for and methods of utilizing water in the management of only a certain number of acute and chronic complaints. <h3>INDICATIONS FOR HYDROTHERAPY IN ACUTE INFECTIVE DISEASES</h3> Among the more common acute infectious complaints that are greatly benefited by the proper application of cold water are typhoid fever, lobar and lobular pneumonia, influenza and tonsillitis. In typhoid fever, the cold immersion
Bosentan Inhibits Transient Receptor Potential Channel Expression in Pulmonary Vascular Myocytes
Authors: Naomi Kunichika, Judd W. Landsberg, Ying Yu, Hideki Kunichika, Patricia A. Thistlethwaite, Lewis J. Rubin, Jason X.-J. Yuan
Journal: American Journal of Respiratory and Critical Care Medicine (2004)

Bosentan, a dual endothelin receptor blocker, has been used clinically to treat idiopathic pulmonary arterial hypertension (IPAH). However, the mechanism of its antiproliferative effect on pulmonary artery smooth muscle cells (PASMCs) remains unclear. A rise in cytoplasmic Ca2+ stimulates PASMC proliferation and the canonical transient receptor potential (TRPC) channels are an important pathway for Ca2+ entry during PASMC proliferation. Bosentan (20–50 μM) significantly inhibited endothelin-1– or platelet-derived growth factor (PDGF)–mediated PASMC growth and [3H]thymidine uptake. In PASMCs, endothelin-1 (1 μM) and PDGF (10 ng/ml) both upregulated protein expression of TRPC6, whereas bosentan markedly downregulated TRPC6 protein levels. Furthermore, TRPC6 expression in PASMCs from patients with IPAH was greater than in normal PASMCs, and the antiproliferative effect of bosentan was significantly enhanced in IPAH-PASMCs in comparison with normal PASMCs. These observations demonstrate that the antiproliferative effect of bosentan on PASMCs involves the downregulation of TRPC6 channels via a mechanism possibly independent of endothelin receptor blockade. The greater effect of bosentan on IPAH-PASMCs than on normal PASMCs suggests that increased TRPC6 expression and function may be involved in the overgrowth of PASMCs in patients with IPAH.
Abstract 2985: DNA-damage related histone marks can distinguish the anti-tumor effects of established and novel histone deacetylase inhibitors in ovarian cancer cells
Authors: Andrew J. Wilson, Ed Holson, Srividya Bhaskara, Jahred Carlise, Stuart L. Schreiber, Scott W. Hiebert, Dineo Khabele
Journal: Cancer Research (2010)

Abstract The majority of epithelial ovarian carcinomas harbor molecular alterations in DNA-damage response genes. Epithelial ovarian cancers are surprisingly sensitive to DNA-damaging platinum-based (cisplatin or carboplatin) chemotherapy, suggesting that the dependencies of ovarian cancers on impaired DNA-damage response pathways can be harnessed for therapeutic purposes. Our group and others have shown that histone deacetylase (HDAC) inhibitors are promising anti-tumor agents, particularly when combined with DNA-damaging drugs in ovarian cancer cells. In this study, H2AX phosphorylation (pH2Ax), a known histone mark of DNA damage and other histone marks related to DNA damage and repair pathways, including the newly recognized acetylated lysine K56 on histone 3 (H3K56ac) were used to distinguish the biological effects of a unique and diverse panel of clinically utilized and novel HDAC inhibitors. Ovarian cancer cell lines with diverse molecular alterations, including mutations in p53, Brca1, Akt, Ras, and overexpression of MDR1, were utilized in these screens. The HDAC inhibitors that induced the highest levels of pH2Ax produced the greatest anti-tumor effects (growth inhibition and apoptosis). Furthermore, a screen of DNA-damage response histone marks led to the selection of novel HDAC inhibitors that exerted synergistic anti-tumor effects when combined with cisplatin and other DNA-damaging drugs. Taken together, our results support a role of HDAC inhibitors in the treatment of ovarian cancer and suggest that pH2Ax is a potential surrogate biomarker of the efficacy of HDAC inhibitor combination therapy with DNA-damaging agents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2985.
A novel method for the direct fabrication of growth factor-loaded microspheres within porous nondegradable hydrogels: Controlled release for cartilage tissue engineering
Authors: Kara L. Spiller, Yu Liu, Julianne L. Holloway, Suzanne A. Maher, Yilin Cao, Wei Liu, Guangdong Zhou, Anthony M. Lowman
Journal: Journal of Controlled Release (2011)
Racial Differences in BRCA Testing
Authors: Sharon Hensley Alford, Judy Mouchawar
Journal: JAMA (2005)

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
A comparative analysis of antegrade and retrograde conduction patterns in man.
Authors: M Akhtar, A N Damato, W P Batsford, J N Ruskin, J B Ogunkelu
Journal: Circulation (1975)

Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.
Metabolic effects of substrates on the isolated guinea-pig heart in relation to arrhythmias during reperfusion
Authors: S. C DENNIS, D. J HEARSE, D J. COLTART
Journal: Cardiovascular Research (1982)

Mechanisms whereby glucose reduces the incidence of pyruvate induced reperfusion arrhythmias in isolated guinea-pig hearts have been investigated. Alterations in cytoplasmic ATP/ADP ratios, creatine phosphate and glycogen were excluded as possible mechanisms. Likewise, data are presented that appear to be at variance with the proposition that glycolytically derived ATP may play a special role in the maintenance of electrical stability. To explain the anti-arrhythmic effects of glucose in terms of this thesis it is necessary to invoke compartmentation of glycolysis. A correlation between the incidence of arrhythmias and glycolytic ATP production can only exist if the contributions to glycolytic flux from glucose and glycogen utilisation can be regarded as separate.
Pancreatic exocrine function in severe human chronic renal failure.
Authors: C Owyang, L J Miller, E P DiMagno, J C Mitchell, V L Go
Journal: Gut (1982)

Patients with chronic renal failure have an abnormal immunoreactive gastrointestinal hormone profile, which is characterised by raised fasting serum concentrations of hormones that have antagonistic effects on exocrine pancreatic function. In addition, in this present study we have found that in renal insufficiency cholecystokinin disappears slowly from the plasma after a constant intravenous infusion of the hormone (p = 0.05 compared with healthy subjects). To evaluate whether the stimulatory or inhibitory hormones have a predominant effect, pancreatic exocrine function under conditions of mannitol perfusion of the duodenum and continuous intravenous cholecystokinin stimulation was studied in eight patients who had severe chronic renal failure and eight age-matched and sex-matched control subjects. Compared with healthy subjects, patients with renal insufficiency had hypersecretion of trypsin in response both to mannitol perfusion of the duodenum and to cholecystokinin stimulation (p less than 0.05). No significant differences in lipase secretion were noted between the patients with renal insufficiency and control subjects. These findings are consistent with the hypothesis that, of the abnormally raised fasting serum concentrations of gastrointestinal hormones found in renal insufficiency, hormones that stimulate rather than inhibit pancreatic exocrine function predominate. Secondly, the dissociation between trypsin and lipase outputs in chronic renal failure may suggest a differential trophic influence of stimulatory hormones -- that is, hypercholecystokininaemia -- on pancreatic exocrine enzyme secretion.
Distribution of Alexithymic Characteristics within an Adult Outpatient Population
Authors: Robert J. Feiguine, Nelson F. Jones, Peter A. Kasse
Journal: Psychotherapy and Psychosomatics (1988)

Utilizing the MMPI Alexithymia Scale (MMPI-AS), a retrospective study was undertaken to determine the distribution of alexithymia within an outpatient population. Approximately 7.64% of the outpatient population displayed the alexithymic trait. Analysis of alexithymia by sex revealed that 10.61% of males and 5.13% of females evidenced alexithymia. This does not correspond with other studies on the distribution of alexithymia within other nonpsychosomatic populations. Issues regarding the measurement instrument, distribution of alexithymia, as well as areas for further investigation are addressed.
Diabetes mellitus related bone metabolism and periodontal disease
Authors: Ying-Ying Wu, E Xiao, Dana T Graves
Journal: International Journal of Oral Science (2015)

Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide. Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus. Alveolar bone loss is one of the main outcomes of periodontitis, and diabetes is among the primary risk factors for periodontal disease. In this review, we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects, focusing on alveolar bone loss. Bone remodelling begins with osteoclasts resorbing bone, followed by new bone formation by osteoblasts in the resorption lacunae. Therefore, we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts. The negative impact of diabetes on bone quantity and quality can lead to an increased risk of fractures and severe gum disease. Dana Graves from the University of Pennsylvania in Philadelphia and colleagues reviewed the mechanisms behind bone loss in people with diabetes and the link to severe gum disease (periodontitis). Diabetes reduces bone-forming cells and bone turnover, while enhancing the number of cells that break down and absorb bone tissue back into the body. These changes in bone metabolism increase the risk of fracture and severe periodontitis. Diabetes is one of the main risk factors for periodontitis, people with diabetes being three to four times more likely to have the disease. This higher risk is most likely due to an exaggerated immune and inflammatory response to the bacteria responsible for gum disease.
NON-SURGICAL TREATMENT OF CIRRHOSIS OF THE LIVER
Authors: N. S. DAVIS
Journal: JAMA (1913)

active under bromid perfusion, but our series of experiments is nol complete enough to state whether or not there is local change in sensitiveness to vagus control.EXPERIMENTS ON THE ISOLATED MAMMALIAN HEART From the therapeutic point of view, read ions of the warm-blooded hear! to the bromids is of more interest perhaps than the reactions of the cold-blooded heart.We have made a number of tests by a method which depends on coronary perfusion. [solated cai hearts were maintained under a perfusion oí :l parts chlorid- Ringer's solution, and 1 pari cat hlood.A carefully balanced bromid-Ringer's diluted wilh Ihe same amount of cal blood was used for testing the bromids.The warm-blooded heart is inure sensitive lo the bro- mids than is the cold-blooded hear!.Our tesis have nol heen absolutely constant.Oui oí thirteen experiments three showed primary acceleration of rale, which is generally obtained in the cold-blooded heart.The remaining experiments show primary depression in rale.In all experiments Hiere was a depression of amplitude, [f Ihe bromid perfusion was for only a relatively short period then there followed a gradual but slow recovery in both rate and amplitude on renewing Ihe normal lunger's and blood.In long bromid perfusions arhyth- niia often sets in which may be removed wilh chloridllingcr's blood. DISCUSSION OF RESULTSIn summarizing these results one mus!admit that the inorganic bromids are relatively indifferent to such organs as the heart of the cold-blooded vertebrates.On the hearts oí warni-blooded animals the bromids are in the long run sharply depressant whether they he meas- ured by rale or by amplitude.If the bromids are com- bined wilh bases in strictly physiologically balanced solutions they are relatively non-toxic, especially to car- diac muscle.On the other hand, if the sails are used without reference to the physiologie balance oí bases it often happens that react ions oí Ihe heart are relatively misleading, owing not to the primary toxicity of the bromid anion hut to the influence oí (lie base or cation.This is particularly true of potassium bromid.Looking over the literature we cannot escape the conclusion that many of the so-called bromid therapeutic effects are distinctly chargeable to the base with which Ihe bromid has been combined.Correlation between Complexion and Resistance to Auto- Intoxication.-1should like to call attention to the extraor-
New Biocide with Both <i>N</i>‐Chloramine and Quaternary Ammonium Moieties Exerts Enhanced Bactericidal Activity
Authors: Lingdong Li, Tianyun Pu, George Zhanel, Nan Zhao, Werner Ens, Song Liu
Journal: Advanced Healthcare Materials (2012)

Considering the rise of antibiotic resistance, the development of new antibacterial agents with improved biocidal functions is urgently required. In this study, ionic 5,5-dimethylhydantoin (DMH) analogues containing either a quaternary ammonium moiety (2)-4) or a phosphonate functional group (5),-6), were designed and synthesized to investigate the possible enhancing effect of quaternary ammonium moieties on the antibacterial performance of N-chloramines. These ionic DMH analogues were converted to their N-chloramine counterparts either in free form or after being covalently immobilized on a polymer surface via the "click" chemistry method. In the subsequent antimicrobial assessment against multi-drug-resistant Escherichia coli (MDR-E. coli) and methicillin-resistant Staphylococcus aureus (MRSA), chlorinated 2 and 3, the cyclic N-chloramines with a structural cation, exhibited distinctly enhanced biocidal functions in solution and after immobilization on surfaces.
Abstract A33: The role of microRNA-181a in TGF-β-mediated breast cancer progression
Authors: Molly A. Taylor, William P. Schiemann
Journal: Cancer Research (2012)

Abstract Transforming growth factor-beta (TGF-β) is a multifunctional cytokine that functions to inhibit breast cancer development in the normal mammary epithelium by inducing cell cycle arrest, and maintaining microenvironmental homeostasis through extracellular matrix (ECM) deposition and remodeling. Mammary tumorigenesis causes a loss in TGF-β-mediated cytostasis and leads to a switch in TGF-β function, whereby TGF-β promotes epithelial-mesenchymal transition (EMT), proliferation, invasion and metastasis. This switch in TGF-β function, from tumor suppressor to tumor promoter, is referred to as the “TGF-β paradox” and occurs through molecular mechanisms that remain incompletely understood. Moreover, this switch in TGF-β function is often accompanied by desmoplastic and fibrotic reactions, leading to the formation of a more rigid microenvironment, which in and of itself has been associated with tumor progression. We have shown that tissue compliance and extracellular matrix rigidity mediate how cells sense and respond to TGF-β. Indeed, we can recapitulate the “TGF-β paradox” by exposing metastatic breast cancer cells to compliant ECM signals, which reinstates the cytostatic activities of TGF-β. As a possible mechanism for the influence of matrix rigidity on TGF-β signaling, we sought to define the miRNA expression profiles induced by TGF-β in metastatic cells as compared to their non-metastatic counterparts when grown in either compliant or rigid conditions. We show that ECM rigidity regulates the miRNA expression signature induced by TGF-β in breast cancer cells. From this miRNA signature, we have identified the miR-181 family as a miR family that is highly upregulated in metastatic cells in response to TGF-β. Additionally, over-expression of a miR-181a mimic enhances TGF-β-mediated invasion. Conversely, treating cells with a hairpin inhibitor directed against miR-181a inhibits TGF-β-mediated invasion, EMT, and survival signaling. Furthermore, inhibition of miR-181a abrogates pulmonary outgrowth and enhances overall survival in vivo. Collectively, our findings identify the miR-181a family as a novel effector of TGF-β-driven tumor progression and suggest that measures capable of diminishing miR-181a levels may alleviate breast cancer progression. [FY09-DOD-BCRP-Predoctoral Traineeship Award]. Citation Format: Molly A. Taylor, William P. Schiemann. The role of microRNA-181a in TGF-β-mediated breast cancer progression [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer; 2012 Jan 8-11; Miami Beach, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(2 Suppl):Abstract nr A33.