tbuckley/cabot-search huggingface dataset:
Occupational Highway Transportation Deaths --- United States, 2003--2008
Authors: Mandy K Green, Robert Harrison, Kathy Leinenkugel, Claire B Nguyen, Meredith Towle, Todd Schoonover, Terry L Bunn, Joyce Northwood, Stephanie G Pratt, John R Meyers
Journal: MMWR Morbidity and Mortality Weekly Report (2011)

This article reports that highway transportation crashes are the leading cause of fatal injuries in the United States for both workers and the general population. The article describes how the prevention of work-related highway transportation deaths, and highway transportation deaths in general, are long-standing public health priorities. In order to assess the trends and help guide the prevention of occupational highway transportation deaths, the Centers for Disease Control (CDC) analyzed data from the Census of Fatal Occupational Injuries (CFOI) for the years 2003 through 2008. This analysis found a total of 8,173 workers died from highway transportation incidents during these years, which represents 24% of all fatal occupational injuries for the period. The annual average fatality rate for workers was 0.9 highway transportation deaths per 100,000 workers and that the rate decreased an average of 2.8% annually during the period. Workers employed in the trucking industry accounted for the greatest number (2,320) and highest rate of highway transportation deaths (19.6 per 100,000 workers). Public health, highway safety, labor, as well as state agencies, highway designers, and transportation-related associations need to work together to implement effective interventions in order to reduce the risk for highway transportation deaths for all workers. Employers should adopt, communicate, and enforce safety policies designed to reduce highway transportation deaths (e.g., requiring the use of safety belts in fleet vehicles, restricting cellular telephone use while driving, and allowing for adequate travel time), and ensure these policies are followed by employees.
Abstract P311: Tree Nut Consumption is Inversely Associated With Subclinical Atherosclerosis: The NHLBI Family Heart Study
Authors: Oyere K Onuma, Andrew Petrone, Jeremy Robbins, R. C Ellison, J. J Carr, Donna K Arnett, Steven C Hunt, J. M Gaziano, Luc Djousse
Journal: Circulation (2015)

Background: Epidemiologic and clinical trial data have demonstrated beneficial effects of nut consumption on cardiovascular risk factors and mortality. However, little is known about the association of nut consumption and subclinical atherosclerosis in the general population. Objective: To test the hypothesis that tree nut consumption is associated with a lower risk of subclinical atherosclerosis. Methods: We determined risk factors and tree nut consumption in a cross-sectional sample of 2297 participants from the NHLBI Family Heart Study without known coronary heart disease. Nut consumption was determined from a Food frequency questionnaire (FFQ) and participants were categorized into 3 groups according to their nut consumption (never/rare, less than once/week, and >= 1 time/week). The primary outcome was prevalent coronary calcification, defined as coronary artery calcium (CAC) score > 100 Agatston units (AU). We fitted generalized estimating equations (GEE) to calculate the prevalence odds ratios of co...
Abstract 18584: Filamin-A Mutations Causing Mitral Valve Prolapse Alters Integrin Expression and Causes Breakdown of Mechanotransduction
Authors: Muralidhar Padala, Marzieh H Zamani, Padmini Sarathchandra, Jean Merot, Julia Gorelik, Magdi H Yacoub, Adrian H Chester
Journal: Circulation (2014)

Introduction: Mutations in the gene encoding Filamin-A, a cytoskeletal protein, were identified in patients with familial mitral valve prolapse(MVP). Mitral valves in these patients were floppy and appeared myxomatous, but the underlying mechanisms governing such changes are unclear. In this study, we sought to investigate the impact of these mutations on cultured cells in comparison with wild type Filamin-A, to delineate the mechanisms underlying MVP. Methods: Four immortal cell lines were established - Filamin-A KO, Filamin-A WT, G288R mutated Filamin-A, and P637Q mutated Filamin-A. Cells were cultured on plastic petri-dishes for a week, and at confluence the cells were imaged under a microscope, then their 3D morphology and mechanical stiffness measured with scanning ion conductance microscopy, and then the cells were assayed for integrins and counted using flow cytometry. Results: Filamin-A KO cells developed blebs on the surface, were flat and did not sufficiently attach to the cell culture substrate, while WT cells demonstrated excellent attachment and formed extensive lamellapodi and filipodia (Fig 1A). Both G288R and P637Q mutated cells had reduced extensions, with a cell structure that is small in circumference but large in height(Fig 1B). α1, α2, α3, α5, β1, β3, β4, α5β3, α2β1 integrin expression was drastically reduced in both G288R and P637Q mutations, compared to WT (Fig 1C1-C2). A 24 hour substrate attachment assay demonstrated 30% attachment of G288R cells were attached and viable, 50% of the P637Q cells were attached and viable, and 98% of WT cells were attached and viable, with similar results seen in gel contraction studies (Fig 1D). Conclusions: Filamin-A mutations associated with mitral valve prolapse seem to alter fundamental cellular mechanisms essential for cell attachment to matrix, motility and mechanotransduction.
The peripheral corneal melting syndrome and psoriasis: coincidence or association?
Authors: None Varma, None Woboso, None Lane, None Holt
Journal: British Journal of Dermatology (1999)

The peripheral corneal melting syndrome (PCMS) is a rare disease consisting of marginal corneal thinning that can progress to perforation. The PCMS carries a grave prognosis and it is of vital importance that dermatologists are aware that this may be responsible for a painful red eye in a patient with psoriasis. We highlight the features of the PCMS developing in an elderly woman with long‐standing psoriasis to increase awareness of its significance, and hypothesize that an association may exist between the two conditions. Only one previous report has been published in which the authors speculate on the possible association of this syndrome with psoriasis. That few other cases have been described is either a consequence of under‐reporting by both ophthalmologists and dermatologists unaware of a link or because the relationship between the syndrome and psoriasis is genuinely coincidental.
Abstract 12401: Soluble Fms-like Tyrosine Kinase 1 and Placental Growth Factor Ratio - A Novel Biomarker for Assessing Congestion and Angiogenesis in Children With Congenital Heart Disease
Authors: Masaya Sugimoto, Aya Kajihama, Kouichi Nakau, Hiroshi Azuma
Journal: Circulation (2013)

Background:  Serum levels of soluble fms-like tyrosine kinase 1 (sFlt-1), an antiangiogenic factor, and its binding protein, placental growth factor(PlGF), are altered in women with preeclampsia. Recently, the sFlt-1/PlGF ratio has been known to predict not only the occurrence of preeclampsia but also that of heart failure in adults. However, few reports have described the use of the sFlt-1/PlGF ratio for evaluating abnormal hemodynamic loads in children with congenital heart disease (CHD).   Methods:  Serum sFlt-1 and PlGF levels were determined in 20 children with atrial septal defects (ASD), 32 children with ventricular septal defects (VSD), 21 children with tetralogy of Fallot (ToF), 19 children who were Fontan candidates (Fontan), and 77 healthy controls. The pre- and post-surgical levels of sFlt-1 and PlGF were compared in the children with CHD.   Results:  The pre-surgical levels of the sFlt-1/PlGF ratios in the ASD, VSD, and Fontan children were significantly higher than those in the controls (Figure; white boxes). Furthermore, the sFlt-1/PlGF ratios were significantly decreased after surgical repair in the ASD and VSD children. In the ToF children, the serum sFlt-1/PlGF ratio was highest after palliative surgery (BT-shunt) and second highest after radical surgery (intra-cardiac repair) as compared to the pre-surgical levels (125 and 84 vs. 19, respectively). In the Fontan children, the serum sFlt-1/PlGF ratio was highest after palliative surgery (Glenn shunt) and much lower after radical surgery (Fontan procedure) as compared to the pre-surgical levels (170 and 12 vs. 136, respectively).   Conclusion:  Our study clearly demonstrated that the sFlt-1/PlGF ratio indicated congestive heart failure in children with CHD. In addition, the sFlt-1/PlGF ratio may indicate persistent cyanosis and angiogenesis in children after palliative surgery. These findings may prove useful in the management of CHD.
Iraq Targets Basic Health Needs
Authors: Rebecca Voelker
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
Abstract 2522: Development of GADD45β (growth arrest DNA damage-inducible gene 45 beta) agonists for the treatment of hepatocellular carcinoma (HCC)
Authors: Chiun Hsu, Da-Liang Ou, Kuen-Feng Chen, Zhong-Zhe Lin, Ann-Lii Cheng, Chung-Wai Shiau
Journal: Cancer Research (2014)

Abstract Induction of GADD45β expression, which is associated with cellular stress response and apoptosis regulation, in HCC cells was found to correlate with sensitivity of sorafenib, the standard molecular targeted therapy for advanced HCC. In this study, we use this GADD45β induction as a screening platform to identify novel agents for HCC treatment from sorafenib derivatives that lack RAF kinase inhibition activity. GADD45β expression in Huh-7 cells was measured by quantitative RT-PCR. Cell viability was examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was examined by flow cytometry. Signal transduction pathways in cells were assessed by western blotting. In vivo anti-tumor efficacy was tested in mouse xenograft models using Huh7 and Huh7R cells, the latter had acquired resistance to sorafenib. Pharmacokinetic studies were done in Sprague-Dawley rat model. The compound SC-20, which had a N-(4-(quinolin-4-yloxy)phenyl)benzamide scaffold, showed greater GADD45β induction than other derivatives. The nitro group on the quinolone ring of SC-20 was considered important in GADD45β induction. SC-20 induced more prominent apoptosis and inhibition of proliferation in Huh7 cells than sorafenib, independent of MEK/ERK signaling activity in Huh7 cells. SC-20 showed more prominent GADD45β induction and better antitumor activity than sorafenib in both Huh-7 and Huh7R xenograft models and good safety. Pharmacokinetic studies indicated that SC-20 had long plasma half-life (22.5 ± 0.51 hours), low water solubility, high (&amp;gt; 99%) plasma protein binding, and inhibited CYP2C9 and 2C19. GADD45β agonists warrant further development for HCC treatment. (supported by NSC 101-2325-B-002 -039, NSC 101-2321-B-002 -014, NSC 102-2325-B-002 -038) Citation Format: Chiun Hsu, Da-Liang Ou, Kuen-Feng Chen, Zhong-Zhe Lin, Ann-Lii Cheng, Chung-Wai Shiau. Development of GADD45β (growth arrest DNA damage-inducible gene 45 beta) agonists for the treatment of hepatocellular carcinoma (HCC). [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2522. doi:10.1158/1538-7445.AM2014-2522
Abstract 2444: Prevalence and Role of Autoantibodies Against Beta 1- Adrenoceptor in Children with Dilated Cardiomyopathy
Authors: Mara Pilati, Claudia Saffirio, Rachele Adorisio, Manuela Pardeo, GianFranco Bottazzo, Stephen P Sanders, M. Giulia Gagliardi
Journal: Circulation (2006)

Background: Autoimmunity seems to have a role in the pathogenesis of dilated cardiomyopathy (DCM). Autoantibodies against beta 1 adrenoceptors have been identified in 30 to 90 % adult pts and their...
Peptide‐Based Proteasome Inhibitors in Anticancer Drug Design
Authors: Nicola Micale, Kety Scarbaci, Valeria Troiano, Roberta Ettari, Silvana Grasso, Maria Zappalà
Journal: Medicinal Research Reviews (2014)

Abstract The identification of the key role of the eukaryotic 26S proteasome in regulated intracellular proteolysis and its importance as a target in many pathological conditions wherein the proteasomal activity is defective (e.g., malignancies, autoimmune diseases, neurodegenerative diseases, etc.) prompted several research groups to the development of specific inhibitors of this multicatalytic complex with the aim of obtaining valid drug candidates. In regard to the anticancer therapy, the peptide boronate bortezomib (Velcade®) represents the first molecule approved by FDA for the treatment of multiple myeloma in 2003 and mantle cell lymphoma in 2006. Since then, a plethora of molecules targeting the proteasome have been identified as potential anticancer agents and a few of them reached clinical trials or are already in the market (i.e., carfilzomib; Kyprolis®). In most cases, the design of new proteasome inhibitors (PIs) takes into account a proven peptide or pseudopeptide motif as a base structure and places other chemical entities throughout the peptide skeleton in such a way to create an efficacious network of interactions within the catalytic sites. The purpose of this review is to provide an in‐depth look at the current state of the research in the field of peptide‐based PIs, specifically those ones that might find an application as anticancer agents.
Establishment of radiation resistant esophageal carcinoma cell lines and signal transduction pathways involved
Authors: Xiaochun Zhang, Ritsuko Komaki, James D. Cox, Bingliang Fang, Joe Y. Chang
Journal: Cancer Research (2006)

4405  Purpose: Radiation therapy plays a crucial role for the management of locally advanced esophageal cancer. However, 75% of patients still have residual disease after standard definitive radiotherapy. Dose escalation of radiation didn’t improve local control and survival indicating radiation resistance. The mechanism of this critical clinical issue remain unclear. To explore the molecular mechanisms involved in radiation resistant esophageal cancer cells after fractionated radiotherapy, we established radiation resistant esophageal carcinoma cell lines and analyzed possible signal transduction pathways involved. Material and methods: Radiation resistant esophageal cancer cell lines were established by fractionated radiation. Five pairs of esophageal squamous carcer cell lines and two pair of adenocarcinoma cell lines were treated with continuous 2 Gy fractionated irradiation to total dose 60 Gy. The parental cells were subjected to identical trypsinisation, re-plating, and culture conditions but were not irradiated. The radiation sensitivity of both paretnal cell lines and radiation resistant cell lines was determined by clonogenic assay after exposure to graded single doses of radiation (0–10 Gy).Cell cycle distribution and sub-G1 DNA accumulation study after exposure to 6 Gy of irradiation using FACS. The alternation of signal transduction pathways was studied using Western blot. Results: Total of six radiation resistant cells lines have been established. One pair of the cell lines (parental Seg-1 and radiation resistant Seg-1R) were adenocarcinoma, the most common cell type in the United States. Clonogenic assay showed significant increase in radiation resistance (up to 25-fold, P
Global Alliance against Chronic Respiratory Diseases
Authors: J. Bousquet, R. Dahl, N. Khaltaev
Journal: Allergy (2007)

Hundreds of millions of people of all ages suffer from chronic respiratory diseases which include asthma and respiratory allergies, chronic obstructive pulmonary disease, occupational lung diseases and pulmonary hypertension. More than 500 million patients live in developing countries or in deprived populations. Chronic respiratory diseases are increasing in prevalence. Although the cost of in action is clear and unacceptable, chronic respiratory diseases and their risk factors receive in sufficient attention from the health care community, government officials, media, patients and families. The Fifty‐Third World Health Assembly recognized the enormous human suffering caused by chronic diseases and requested the World Health Organization (WHO) Director General to give priority to the prevention and control of chronic diseases, with special emphasis on developing countries. This led to the formation of the WHO Global Alliance against Chronic Respiratory Diseases (GARD). GARD is a voluntary alliance of organizations, institutions and agencies working towards a common vision to improve global lung health according to local needs. GARD is developed in a stepwise approach using the following three planning steps: estimate population need and advocate action; formulate and adopt policy; and identify policy implementation steps.
Informing Patients of Uncertainty in Clinical Trials—Reply
Authors: Benjamin Djulbegovic
Journal: JAMA (2001)

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
Array-based comparative genomic hybridization of uterine leiomyosarcoma
Authors: Jeong Eun Park, Hyun-Jung Kim, Su-Mi Bae, Jang Heub Kim, Tae Chul Park, Eun Kyung Park, Dong Chun Park, Woong Shick Ahn
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

5495 

The aim of this study was to identify novel genomic regions and specific target genes using a genome-wide array-based comparative genomic hybridization (array-CGH) analysis in uterine leiomyosarcoma (ULMS). Genomic DNA alterations were analyzed in 15 cases of ULMS (Age, 46s; Range in 28s-64s) from KangNam St Mary’s Hospital of the Catholic University of Korea. The paraffin-fixed tissue samples were microdissected under microscope and DNA was extracted. Array-based CGH and genomic PCR were carried out with statistical analyses such as hierarchical clustering and Gene Ontology. All of 15 cases of ULMS showed specific gains (8.4%) and losses (16.6%). The analysis limit of average gains and losses was 40%. Interestingly, we found out increasing of a variety genetic variations (39.3% in gains; 42.9% in losses) in FIGO stage IV compared with early stage (Ia 35.7%, Ic 17.1%, IIa 25%, IIIa 39.3% in gains; Ia 21.4%, Ic 21.1%, IIa 25%, IIb 17.9%, IIIa 32.1%) of ULMS. In our results showed that losses of 13q segments were more frequent among cases with ULMS. The region at 13q22.3, which contains the tumor suppressor gene EDNRB , showed losses in 67% of the cases. Alterations of EDNRB are frequent in a wide range of malignancies, in leiomyosarcoma as well as in other soft-tissue sarcomas. The regions of high level of gain were 1q23.3, 7p14.2, 7q34, 7q35, 7q36.3, 13q34, and 16p13.3. And the regions of homozygous loss were 2q21.1, 2q22.1, 2p23.2, 12q23.3, 4q21.22, 4q34.3, 11q24.2, 12q23.3, 13q13.1, 13q21.33, and 14q24.3. Representative frequently gained BAC clones encoded genes were HDAC9, CRR9, SOX18, PTPRN2, SKI, SOLH, and KIAA1199 . The genes encoded by frequently lost BAC clones were LOC150516 and AMY2A. Some of the most significant over expressed genes are involved in cellular pathways: Cell proliferation (e.g. SIL ), development (e.g. SKI ), cell communication (e.g. RAC2 ), transport (e.g. CAPS ), and regulation of transcription (e.g. SOLH ). Notably, high frequencies of identified specific genes including EDNRB in ULMS may significantly associate with an important role in the lymph node metastasis and advanced tumor stage of these ULMS. The present study using array-CGH analyses sought a deeper elucidation of the specific genomic alterations related to ULMS. The high resolution of array-CGH combined with human genome database would give a chance at identifying relevant target genes.
Magnetic resonance imaging measurement of gray matter volume reductions in HIV dementia
Authors: E H Aylward, P D Brettschneider, J C McArthur, G J Harris, T E Schlaepfer, J D Henderer, P E Barta, A Y Tien, G D Pearlson
Journal: American Journal of Psychiatry (1995)

The authors recently reported smaller basal ganglia volumes for patients with HIV-associated dementia than for HIV-infected patients without dementia and a seronegative comparison group. The purpose of the current study was to determine whether HIV dementia is associated with volume reductions in other brain regions.The authors measured volumes of CSF and gray and white tissue on cranial magnetic resonance images from homosexual men who were 1) infected with HIV with HIV-associated dementia complex, 2) infected with HIV without dementia, and 3) HIV seronegative.Results suggest that loss of white matter occurs with HIV infection and is more severe in HIV-positive patients with dementia than in those without dementia. There was some generalized volume reduction in gray matter in HIV-positive demented patients, although group differences did not reach significance when adjusted for age. Volume of posterior cortex, however, was significantly smaller among HIV-positive patients with dementia than in either remaining group. There were no significant differences between HIV-positive nondemented patients and HIV-negative subjects in these regions.In conjunction with findings from previous research, the authors conclude that HIV dementia is associated with specific gray matter volume reduction in basal ganglia and posterior cortex, as well as with generalized volume reduction of white matter.