tbuckley/cabot-search huggingface dataset:
Abstract 18263: Poor Handgrip Strength and Outcomes in Heart Failure. The Atlanta Cardiomyopathy Consortium
Authors: Anjan Deka, Song Li, Catherine N Marti, Gail Snell, Nina Caltabiano, Robert Cole, Divya Gupta, Sonjoy Laskar, Andrew L Smith, Javed Butler, Andreas P Kalogeropoulos, Vasiliki V Georgiopoulou
Journal: Circulation (2013)

Background: Handgrip strength test quantifies the amount of static force that the hand can squeeze around a dynamometer and is associated with increased mortality in middle-aged and older adults, and in patients with chronic diseases. The prognostic role of handgrip strength in heart failure (HF) has not been fully investigated. Methods: A hydraulic hand dynamometer was used to measure handgrip strength in 317 outpatients with HF enrolled in The Atlanta Cardiomyopathy Consortium (TACC) cohort study. Patients repeated the test 3 times in each hand and the average from both hands was used. We defined poor handgrip strength based on age- and gender-specific normative data. We evaluated the association between poor handgrip strength and major clinical event (death, heart transplant, left ventricular assist device) and healthcare resource utilization. Results: Baseline patient characteristics are presented in Table 1; 228 patients (71.9%) had poor handgrip strength. Total follow-up was 911 patient-years; 55 patients (17.4%) experienced a major clinical event. There was a total of 836 all-cause hospitalizations with an average length of stay of 4.7 days. Poor handgrip strength was not significantly associated with major clinical events (hazard ratio (HR) 1,19; 95% CI: 0.64 to 2,21; P=0.59). However, patients with poor strength had 42% higher hospitalization rate (95% CI: 1.3% to 98%; P=0.042) and spent 85% (95% CI: 10% to 210%; P=0.020) more days in the hospital. Average length of stay among patients with poor handgrip strength was 4.9 days vs. 4.2 days in those with preserved strength. Conclusion: Poor handgrip strength is highly prevalent among HF patients and is associated with higher healthcare resource utilization and length of stay.
Improving the Quality of Quality Improvement Reporting
Authors: Krislynn M. Mueck, Luke R. Putnam, Lillian S. Kao
Journal: JAMA Surgery (2016)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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 Surgery journal
Individualized Ranibizumab Regimen Driven by Stabilization Criteria for Central Retinal Vein Occlusion
Authors: Michael Larsen, Sebastian M. Waldstein, Francesco Boscia, Heinrich Gerding, Jordi Monés, Ramin Tadayoni, Siegfried Priglinger, Andreas Wenzel, Elizabeth Barnes, Stefan Pilz, William Stubbings, Ian Pearce
Journal: Ophthalmology (2016)

<h3>Purpose</h3> To assess the 12-month efficacy and safety profile of an individualized regimen of ranibizumab 0.5 mg driven by stabilization criteria in patients with macular edema secondary to central retinal vein occlusion (CRVO). <h3>Design</h3> A 24-month, prospective, open-label, single-arm, multicenter study. <h3>Participants</h3> Three hundred fifty-seven patients. <h3>Methods</h3> Patients were treated with monthly ranibizumab 0.5-mg injections (minimum of 3 injections) until stable visual acuity (VA) was maintained for 3 consecutive months. Thereafter, ranibizumab 0.5 mg was dosed as needed if monthly monitoring indicated a loss of VA resulting from disease activity. <h3>Main Outcome Measures</h3> Mean change from baseline at month 12 in best-corrected VA (BCVA; primary end point) and safety over 12 months. The efficacy of this regimen in subgroups categorized by baseline BCVA score, CRVO duration, or presence of macular ischemia (exploratory analysis). <h3>Results</h3> At baseline, the mean BCVA was 53.0 letters and mean CRVO duration was 8.9 months (median, 2.4 months). Ranibizumab 0.5-mg treatment resulted in a statistically significant mean gain in BCVA from baseline at month 12 of 12.3 letters (standard deviation [SD], 16.72 letters; <i>P</i> < 0.0001). The mean number of ranibizumab injections up to month 12 was 8.1 (SD, 2.77). At month 12, mean BCVA gains were similar with or without macular ischemia at baseline (11.6 vs. 12.1 letters); the mean BCVA gain was higher with baseline CRVO duration of less than 3 months (13.4 letters) than with a longer duration (≥3–<9 months, 11.1 letters; ≥9 months, 10.9 letters). Patients with lower baseline BCVA had larger mean BCVA gains at month 12 than those with higher baseline BCVA (≤39/40–59/≥60 and 18.0/12.7/8.9 letters, respectively), although the absolute BCVA at month 12 was higher with higher baseline BCVA. No new ocular or nonocular safety events were observed. <h3>Conclusions</h3> An individualized dosing regimen of ranibizumab 0.5 mg driven by stabilization criteria for up to 12 months resulted in significant BCVA gain in a broad population of patients with macular edema secondary to CRVO, including those with macular ischemia at baseline. The safety findings were consistent with those reported in previous ranibizumab studies in patients with CRVO.
Company reneges on promise to cut price of toxoplasmosis drug
Authors: Owen Dyer
Journal: BMJ (2015)

Turing Pharmaceuticals, the company that drew condemnation from all sides in the United States two months ago when it bought the toxoplasmosis drug pyrimethamine (Daraprim) and raised the price by over 5000%,1 has abandoned a commitment to lower the drug’s list price by Christmas, instead opting to reduce the price charged to hospitals and offering expanded support to patients who lack health insurance or financial resources.

The changes were dismissed as “window dressing” by the HIV Medicine Association. “This medication can be made for pennies. They need to reduce the price to what it was before,” said the virologist Carlos Del Rio, the group’s chairman, in a statement. …
The Vernacular of Risk — Rethinking Direct-to-Consumer Advertising of Pharmaceuticals
Authors: Jeremy A. Greene, Elizabeth S. Watkins
Journal: New England Journal of Medicine (2015)

Interview with Dr. Christopher Robertson on the FDA’s new draft guidelines on direct-to-consumer pharmaceutical advertising. (07:33)Download Missing from the debate over proposed new rules for direct-to-consumer drug advertising is a broader perspective on the vernacular of risk, as something fundamental to the origins of the category of prescription drugs and their regulation over the past half-century.
Patients to test whether new technologies help manage conditions
Authors: Gareth Iacobucci
Journal: BMJ (2016)

The NHS in England is to try out new ways to equip patients with medical technologies in their home, as it seeks to improve the care of older patients, people with long term conditions, and people with mental health problems.

A new scheme, known as NHS Innovation Test Beds, will see the NHS partnering with leading technology firms such as Verily (formerly Google Life Sciences), IBM, and Philips to test the effectiveness of issuing devices such as wearable monitors for patients to use at home. The plan was due to be announced …
Preventive approach of allergic reaction to oxaliplatin
Authors: M. Suenaga, N. Mizunuma, T. Watanabe, K. Hatake, T. Muto
Journal: Journal of Clinical Oncology (2006)

13574 Background: Oxaliplatin is a well-known platinum compound as a key agent of FOLFOX regimen, the world standard chemotherapy in colorectal cancer. Allergic reaction due to oxaliplatin is a chronic adverse event regarded as almost type I allergy. In our institute, we have also experienced allergic reaction including severe cases and started to apply practical preventive approach to the patients treated with FOLFOX regimens. Methods: Preventive approach was as follows: 40mg of famotidine and 8mg of dexamethasone before oxaliplatin infusion were given to all patients from the initial cycle and 50mg of diphenhydramine after cycle 4. Further intensive anti-allergic procedure was performed for the patients who showed any allergic reactions against initial preventive approach. Increased dose of dexamethasone to 20mg and diphenhydramine were administered before oxaliplatin infusion and oxaliplatin was prolonged from 2 up to 4 hours for patients with grade 1, 2 allergic reactions (CTCAE v3.0). Treatment was discontinued in patients with severe grade 3 adverse events. Results: 139 patients received FOLFOX regimens during 6 months. 15 patients (10.8%) presented with allergic reaction, 11 (73.3%) of those were grade 1, 2 and the other 4 (26.7%) were grade 3. Immediate discontinuation of oxaliplatin infusion and administration of antihistaminic drugs, steroid or rapid infusion were routine proceeding, and almost of the patients entirely recovered within 2 hours. 9 patients were re-exposed to oxaliplatin using the preventive approach and grade1 reaction appeared in 3 patients (33.3%) again. Conclusions: Our initial preventive approach was effective to reduce the incidence of allergy, severe adverse events. And further intensive anti-allergic procedure contributed to re-expose to oxaliplatin. No significant financial relationships to disclose.
Aspergillus PCR in serum for the diagnosis, follow-up and prognosis of invasive aspergillosis in neutropenic and nonneutropenic patients
Authors: S. Imbert, L. Gauthier, I. Joly, J.-Y. Brossas, M. Uzunov, F. Touafek, S. Brun, D. Mazier, A. Datry, F. Gay, A. Fekkar
Journal: Clinical Microbiology and Infection (2016)
The prognostic value of preoperative <i>helicobacter pylori </i>infection in resected gastric cancer.
Authors: Lauren McLendon Postlewait, Malcolm Hart Squires, David A. Kooby, George A. Poultsides, Sharon M. Weber, Mark Bloomston, Ryan C. Fields, Timothy M. Pawlik, Konstantinos Ioannis Votanopoulos, Carl Richard Schmidt, Aslam Ejaz, Alexandra W. Acher, David J. Worhunsky, Neil Saunders, Doug S. Swords, Linda X. Jin, Clifford Suhyun Cho, Kenneth Cardona, Charles A. Staley, Shishir Kumar Maithel
Journal: Journal of Clinical Oncology (2015)

137 Background: Limited data exist on the prognostic implication of pre-operative Helicobacter pylori (H. pylori) infection in gastric adenocarcinoma (GAC). Our aim was to assess the association of H. pyloriwith recurrence and survival in patients undergoing resection of GAC. Methods: All patients who underwent curative intent resection for GAC from 2000 to 2012 at seven academic institutions comprising the US Gastric Cancer Collaborative were included. 30-day mortalities were excluded. Survival analyses were conducted with Kaplan Meier log rank and multivariate Cox regression. Primary endpoints were recurrence-free survival (RFS) and overall survival (OS). Results: Of 965 patients, 559 met inclusion criteria and had documented pre-operative H. pylori testing. 18.6% (n=104) of patients tested positive for H. pylori pre-operatively. Data regarding treatment of H. pylori was not available. H. pylori infection was associated with younger age (62.1 vs 65.1 years; p=0.041), distal tumor location (82.7% vs 71.9%; p=0.033), and receipt of adjuvant radiation therapy (47.0% vs 34.9%; p=0.032). There were no significant differences in ASA class, margin status, Grade, PNI, LVI, or nodal metastases. The distribution of TNM stage I-III was similar between the two groups. H. pylori status was not associated with tumor recurrence. However, pre-operative H. pylori infection was associated with longer OS (84.3 mo vs 44.2 mo; p=0.008). When accounting for differences in age, tumor location, and delivery of radiation therapy, H. pylori infection persisted as a positive prognostic factor for OS (HR 0.60; CI 0.40-0.91; p = 0.016). Conclusions: Patients with and without preoperative H. pylori infection had no significant differences in adverse pathologic factors including positive margin, high grade, lymph node metastases, or advanced TNM stage. Despite similar disease presentation, pre-operative H. pylori infection was independently associated with improved overall survival. Further studies examining the interaction between H. pylori and tumor immunology and genetics are needed to better understand the relationship between H. pylori and survival in gastric cancer.
MicroRNA-10a/10b represses a novel target gene mib1 to regulate angiogenesis
Authors: Xin Wang, Chang Chun Ling, Liping Li, Yinyin Qin, Jialing Qi, Xiaoyu Liu, Bo You, Yunwei Shi, Jie Zhang, Qiu Jiang, Hui Xu, Cheng Sun, Yiwen You, Renjie Chai, Dong Liu
Journal: Cardiovascular Research (2016)

MicroRNA-10 (miR-10) was originally shown to regulate angiogenesis by directly modulating the levels of membrane-bound fms-related tyrosine kinase 1 (mflt1) and its soluble splice isoform sflt1 post-transcriptionally in zebrafish. Given that flt1 knockdown incompletely rescues the angiogenic phenotypes in miR-10 morphants, flt1 is unlikely to be the only important target of miR-10 in endothelial cells (ECs). It will be interesting to investigate new mechanism responsible for angiogenic defect induced by miR-10 knockdown. Firstly, we demonstrated that miR-10a and miR-10b (miR-10a/10b) were highly enriched in embryonic zebrafish ECs using deep sequencing, Taqman polymerase chain reaction, and in situ hybridisation. Subsequently, we proved that loss of miR-10a/10b impaired blood vessel outgrowth through regulating tip cell behaviours. Mib1 was identified as a potential direct target of miR-10a/10b through in silicon analysis and in vitro luciferase sensor assay. In vivo reporter assay in zebrafish embryos confirmed the binding of miR-10 with 3′-UTR of zebrafish mib1. Furthermore, inhibition of mib1 and Notch signaling rescued the angiogenic defects in miR-10-deficient zebrafish embryos. In addition, we provided evidences that miR-10 regulates human ECs behaviour through targeting Mib1 as well. Taken together, these results indicate that miR-10 regulates the angiogenic behaviour in a Notch-dependent manner by directly targeting mib1.
Incidence, Risk Factors and Allogeneic Stem Cell Transplant Outcomes In Chronic Sclerotic Gvhd: T-Cell Depletion Is Preventive and Peripheral Blood Stem Cellis a Risk Factor, But Not HLA-Mismatch With No Adverse Impact On Transplant Outcomes
Authors: Jieun Uhm, Nada Hamad, Mohamed Shanavas, Fotios V. Michelis, Vikas Gupta, John Kuruvilla, Hans A. Messner, Jeffrey H. Lipton, Dennis Dong Hwan Kim
Journal: Blood (2013)
Phase III randomized trial of high-dose chemotherapy (HDC) and peripheral blood stem cell (PBSC) support as consolidation in patients (pts) with advanced ovarian cancer (AOC): 5-year follow-up of a GINECO/FNCLCC/SFGM-TC study
Authors: H. Cure, C. Battista, J. P. Guastalla, M. Fabbro, N. Tubiana, H. Bourgeois, B. Lioure, B. Chiurazzi, D. Paraiso, E. Pujade-Lauraine
Journal: Journal of Clinical Oncology (2004)

5006 Background: Phase II studies have suggested that HDC is most effective in chemosensitive AOC pts with low tumor burden. Methods: We compared the disease free-survival (DFS), overall survival (OS) and toxicity of women with AOC randomized after second-look surgery (SLS) to receive either HDC Carboplatin-Cyclophosphamide and PBSC support (Cb 400 mg/m2/d and Cy 1500 mg/m2/d x 4 days) or 3 cycles of conventional-dose maintenance (CDM) (q4w, Cb 300 mg/m2, Cy 500 mg/m2). Eligibility criteria were: age <60 yrs, FIGO stage III-IV, disease responsive to 4 - 6 cycles of a platinum-based first-line chemotherapy, tumor size <2 cm at the end of the SLS or a pathological complete response (pCR) but high-risk factors. Results: Between 07/1995 to 10/2000, 110 pts were enrolled, 57 in the HDC and 53 in the CDM arm. Pts characteristics were well balanced between the 2 arms. Half of the pts received paclitaxel in first-line. Nine pts had Stage IV and 101 pts stage III with at SLS: pCR (39%), microscopic (20%) and macroscopic (41%) disease. In the HDC arm, 1 pt was ineligible and 11 (20%) did not receive the HDC because of poor PBSC mobilization (n= 7), pt refusal (n=3) or early relapse (n=1). Median time to neutrophil and platelet recovery was 11 days. Two pts died from toxic myocarditis and renal insufficiency respectively. Median follow-up is 60 months. At time of analysis, 94 pts have relapsed and 63 have died. DFS and OS were not significantly different between the 2 arms. Median DFS and OS from randomization were 12.2 (95% CI: 7.3–17.1) and 42.5 (95% CI: 28.8–56.6) months in the CDM arm, and were 17.5 (95% CI: 5.2–29.9) (p=.22) and 49.7 (95% CI: 29.9–69.4) (p=.43) months in the HDC arm, respectively. Conclusions: These data do not support high-dose consolidation chemotherapy in AOC. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Amgen
Pre-operative hyperfractionated radiotherapy and concurrent 5-FU/cisplatin for locally advanced esophageal cancer - the impact of 18-F-fluoro-deoxy-D-glucose (FDG) positron emission tomography staging
Authors: M. R. Farmer, E. Levine, C. Ho, G. Mishra, S. Melin, J. Lovato, K. Geisinger, T. Oaks, P. Clark, A. W. Blackstock
Journal: Journal of Clinical Oncology (2005)

4074
953 INDOCYANINE GREEN CLEARANCE AS A MARKER OF DECOMPENSATION AND CLINICALLY SIGNIFICANT PORTAL HYPERTENSION IN PATIENTS WITH LIVER CIRRHOSIS
Authors: L. Turco, F. Azzaroli, F. Buonflglioli, A. Lisotti, P. Cecinato, M. Montagnani, C. Calvanese, F. Lodato, R. GolfierP, A. Colecchia, D. Festi, G. Mazzella
Journal: Journal of Hepatology (2011)
Aspartate β‐hydroxylase modulates cellular senescence through glycogen synthase kinase 3β in hepatocellular carcinoma
Authors: Yoshifumi Iwagami, Chiung‐Kuei Huang, Mark J. Olsen, John‐Michael Thomas, Grace Jang, Miran Kim, Qiushi Lin, Rolf I. Carlson, Carl E. Wagner, Xiaoqun Dong, Jack R. Wands
Journal: Hepatology (2015)

Aspartate β‐hydroxylase (ASPH) is an enzyme overexpressed in human hepatocellular carcinoma (HCC) tumors that participates in the malignant transformation process. We determined if ASPH was a therapeutic target by exerting effects on cellular senescence to retard HCC progression. ASPH knockdown or knockout was achieved by short hairpin RNAs or the CRISPR/Cas9 system, respectively, whereas enzymatic inhibition was rendered by a potent second‐generation small molecule inhibitor of ASPH. Alterations of cell proliferation, colony formation, and cellular senescence were evaluated in human HCC cell lines. The potential mechanisms for activating cellular senescence were explored using murine subcutaneous and orthotopic xenograft models. Inhibition of ASPH expression and enzymatic activity significantly reduced cell proliferation and colony formation but induced tumor cell senescence. Following inhibition of ASPH activity, phosphorylation of glycogen synthase kinase 3β and p16 expression were increased to promote senescence, whereas cyclin D1 and proliferating cell nuclear antigen were decreased to reduce cell proliferation. The mechanisms involved demonstrate that ASPH binds to glycogen synthase kinase 3β and inhibits its subsequent interactions with protein kinase B and p38 upstream kinases as shown by coimmunoprecipitation. In vivo experiments demonstrated that small molecule inhibitor treatment of HCC bearing mice resulted in significant dose‐dependent reduced tumor growth, induced phosphorylation of glycogen synthase kinase 3β, enhanced p16 expression in tumor cells, and promoted cellular senescence. Conclusions: We have identified a new mechanism that promotes HCC growth and progression by modulating senescence of tumor cells; these findings suggest that ASPH enzymatic activity is a novel therapeutic target for HCC. (H epatology 2016;63:1213–1226)
Characterization of novel putative tumor suppressor gene, DLC2 (deleted in liver cancer 2), in hepatocellular carcinoma
Authors: HY Leung, YP Ching, CM Wong, Dch Ng, D Jin, Iol Ng
Journal: Cancer Research (2004)

3310  Deleted in liver cancer 2 (DLC2) gene, a putative tumour suppressor gene located at chromosome 13q12.3, was first identified by our group (Ching et al., J Biol Chem 2003;278:10824-10830). The DLC2 gene has striking homology to another tumor suppressor gene, DLC1, located at chromosome 8p22-8p21.3. DLC2 encodes a Rho GTPase activating protein (RhoGAP) with GAP activity specific for RhoA and Cdc42. The chromosomal region of the DLC2 gene shows frequent deletion with loss of heterozygosity in human hepatocellular carcinoma (HCC). By RT-PCR analysis, DLC2 is also frequently underexpressed in HCCs compared with the corresponding nontumorous livers. These suggest that the DLC2 gene may play a role in liver carcinogenesis. In this study, we aimed to further characterize DLC2 biochemically and functionally. From the bioinformatics search of DLC2 gene in humans, we found that there were four different isoforms of DLC2 gene, which we designate as DLC2α, β, γ, and δ. The four isoforms of DLC2 gene were identified in silico. With RT-PCR using four pairs of isoform specific primers performed on 10 HCC cell lines, DLC2α, γ, and δ were found to be expressed in all hepatoma cell lines tested, with different levels of expression. In contrast, the mRNA expression of the DLC2β isoform could be detected in only 4 of these 10 HCC cell lines. Direct sequencing of the PCR products of these isoforms confirmed the presence of these isoforms. In addition, we analyzed the localization and the in vivo function of DLC2 gene. Transfection of DLC2α and DLC2γ into Swiss3T3 cells showed their predominant cytoplasmic localization. Interestingly, over-expression of DLC2α and DLC2γ induced morphological alterations in the transfected Swiss3T3 cells. The shape of transfected Swiss3T3 cells was changed from angular and spindle to round when compared with the non-transfected parent cells. Confocal microscopy revealed that the morphological changes were associated with remarkable inhibition of actin stress fiber formation. In conclusion, these results were in keeping with the functions of DLC2 as a RhoGAP and that it induced morphological alterations through regulation of cytoskeletal reorganization. DLC2 likely exerts its tumor suppressor function partly via its RhoGAP function to inhibit RhoA activity, resulting in suppression of stress fiber formation. Further studies on the functional characterization of the different isoforms of DLC2 may give insight into its tumor suppressor function.
Management of Perianal Crohn's Disease
Authors: J H Hobbiss, Philip F Schofield
Journal: Journal of the Royal Society of Medicine (1982)

Symptomatic anal disease (excluding skin tags) was observed in 49 out of 151 successive patients treated for Crohn's disease. Two main types of anal disease were encountered: anal ulceration (23 patients) and anal abscesses and fistulae (26 patients). The ulcer group rarely required local surgical treatment. In the fistula group, a low tract was demonstrated and laid open in 20 patients. The healing times after operation in these patients were compared with those of 18 patients with non-Crohn's fistula-in-ano treated by the same method. No significant difference between the two groups could be demonstrated. Surgical treatment of low fistula-in-ano may be undertaken in patients with Crohn's disease, provided the bowel disease is under adequate control.