tbuckley/cabot-search huggingface dataset:
Evaluation of the properties of Mineral Trioxide Aggregate mixed with Zinc Oxide exposed to different environmental conditions
Authors: B. Bolhari, N. Meraji, M. Rezazadeh Sefideh, P. Pedram
Journal: Bioactive Materials (2020)

Addition of zinc oxide (ZnO) to Mineral Trioxide Aggregate (MTA) has been shown to rectify tooth discoloration caused by Angelus MTA. This study evaluated the microhardness, compressive strength, calcium ion release and crystalline structures of MTA mixed with ZnO in different environmental conditions. Molds with a diameter of 4 mm and a height of 6 mm were used for compressive strength, calcium ion release and X-ray diffraction (XRD) evaluations. Molds with 6 mm diameter and 4 mm height were used for surface microhardness evaluations. Cements evaluated include Angelus MTA (Angelus, Brail), Angelus MTA + ZnO, ProRoot MTA (Dentsply Tulsa Dental, OK), and ProRoot MTA + ZnO. Each group was divided into 3 subgroups according to exposure conditions: normal saline (NS), phosphate buffered saline (PBS) or blood. After 7 days incubation, surface microhardness, compressive strength and XRD analysis was performed. Calcium ion release was evaluated after 3, 24 and 168h incubation using atomic absorption spectrophotometry. Data were analyzed by One Way Anova followed by the Tukey HSD Post hoc tests and T-Test. The significance level was set at 0.05. Addition of ZnO to Angelus and ProRoot MTA significantly decreased the compressive strength of these cements regardless of the environmental conditions (P < 0.001); however, it had no significant effect on their microhardness or calcium ion release. In conclusion, adding ZnO to Angelus and ProRoot MTA can adversely affect the compressive strength of Angelus and ProRoot MTA.
The Life and Death of Mammograms in Patients 75 Years and Older—To Screen or Not to Screen?
Authors: Joann G. Elmore, Q. Ngo-Metzger
Journal: JAMA Internal Medicine (2020)

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 Internal Medicine 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 Internal Medicine journal
Global evidence on occupational sun exposure and keratinocyte cancers: a systematic review
Authors: T. Loney, M.S. Paulo, A. Modenese, F. Gobba, T. Tenkate, D.C. Whiteman, A.C. Green, S.M. John
Journal: British Journal of Dermatology (2020)

Individual studies have suggested that the association between occupational exposure to solar ultraviolet radiation (UVR) and the development of keratinocyte cancers (KCs) may only be valid in populations of European ancestry living in certain geographical regions. Comparative global data are scarce and so this review aimed to summarize current evidence on the association between occupational exposure to solar UVR and the development of KCs, with a specific focus on geographical location and skin colour. Ovid MEDLINE, PubMed, Embase and Web of Science were searched for potentially relevant records. Extracted data were summarized by study, country and region. We included one prospective cohort study and 18 case–control studies (n = 15 233) from 12 countries in regions where the majority of the population is white skinned (Americas, Europe and Oceania). Eighteen of the 19 studies reported effect estimates suggesting an increased risk of basal cell carcinoma (BCC) and/or squamous cell carcinoma (SCC) among outdoor workers. Only 11 studies found a significantly increased risk and many had imprecise estimates. There was a significantly increased risk of BCC and SCC in individual studies in North America, Latin America and the Caribbean, Western Europe and Southern Europe, but not across regions or countries. Overall, 95% of studies reported higher risks among outdoor workers, although the increases in risk were statistically significant in just over half of the studies. Well-designed and sufficiently powered occupational case–control and cohort studies with adequate adjustment for confounding factors and other risk factors are required to provide more accurate risk estimates for occupational KC.
Abstract 18599: Drug-Eluting vs Bare-Metal Stents: Comparison of Incidence of Post-Procedure Bleeding Risk and In-hospital Mortality in Patients With Myocardial Infarction Who Had Percutaneous Coronary Intervention: A Nationwide Analysis Using the National Inpatient Database of 2014
Authors: Xin Wei, Ahmadreza Moradi, Parisa Toosi, Mariam Khandaker, Bing Yue, Sung E Lee, Yuzhou Liu, Angela Palazzo
Journal: Circulation (2017)

Introduction: Limited data are available on the effects of drug-eluting stents (DES) versus bare-metal stents (BMS) on rates of post-procedural bleeding and in-hospital mortality among patients who...
Human monoclonal antibodies block the binding of SARS-CoV-2 spike protein to angiotensin converting enzyme 2 receptor
Authors: Xiangyu Chen, Ren Li, Zhiwei Pan, Chunfang Qian, Yang Yang, Renrong You, Jing Zhao, Pinghuang Liu, Leiqiong Gao, Zhirong Li, Qizhao Huang, Lifan Xu, Jianfang Tang, Qin Tian, Wei Yao, Li Hu, Xiaofeng Yan, Xinyuan Zhou, Yuzhang Wu, Kai Deng, Zheng Zhang, Zhaohui Qian, Yaokai Chen, Lilin Ye
Journal: Cellular and Molecular Immunology (2020)

According to the World Health Organization (WHO) newly updated situation report on March 18th, 2020, the coronavirus disease 2019 (COVID-19) pandemic has confirmed 191,127 cases and claimed 7807 deaths worldwide. 16][7][8] Although the mortality rate of COVID-19 is significantly lower than that of SARS-CoV infection, SARS-CoV-2 shows much higher human-to-human transmission rate, rapidly leading to a global pandemic declared by WHO on March 11th, 2020. 9 Currently, there are no approved prophylactic vaccines or therapeutic drugs that are specific to COVID-19.Blocking monoclonal antibodies (mAbs), due to their extraordinary antigen specificity, are one of the best candidates for neutralizing virus infection. 10,11Therefore, identifying and cloning blocking mAbs that can specifically target surface viral proteins to block the viral entry to host cells is a very attractive approach for preventing and treating COVID-19, in particular when effective vaccines and therapeutics are unavailable in the outbreak of the COVID-19 pandemic.We then sought to identify and clone blocking mAbs from the memory B cell repertoire of recently recovered COVID-19 patients to prevent the entry of COVID-19 virus to the host cells.3][14][15] The S protein of SARS-CoV-2 consists of two subunits, S1 and S2.To engage host cell receptor human angiotensinconverting enzyme 2 (hACE2), shared by both SARS-CoV and SARS-CoV-2, S protein undergoes dramatic conformational
Preprint servers: a ‘rush to publish’ or ‘just in time delivery’ for science?
Authors: Alan Robert Smyth, Claire Rawlinson, Gisli Jenkins
Journal: Thorax (2020)

At the time of writing, the WHO has declared COVID-19 a pandemic and healthcare systems around the world face the biggest public health challenge for a generation. As never before, the clinical and scientific communities, governments and the public need access to robust data to facilitate evidence-based decision-making. The foundation of a reliable research literature is effective peer review. However, in the last decade, there has been debate over the effectiveness of peer review. Research in the field has shown that prestigious journals reject manuscripts which go on to be highly cited elsewhere.1 The peer review process introduces considerable delay in making research findings publicly available2 and yet there is no correlation between the number of rounds of manuscript review and revision and the subsequent citation count for the paper.1 

The stage is therefore set for the entrance of a new actor—the preprint server. A recent article (posted as a preprint) identified almost 50 preprint servers, open research bundles or other disruptive technologies which have entered the field in recent years.3 The distinctive feature of preprint servers is that they do not undertake peer review but restrict scrutiny to basic screening and legal checks, such as for plagiarism. However, preprint servers do allow online comments from the scientific community—a form …
Phase II study of volociximab (M200), an α5β1 anti-integrin antibody in metastatic melanoma
Authors: L. D. Cranmer, A. Y. Bedikian, A. Ribas, S. O’Day, A. Forero-Torres, S. Yazji, J. M. Kirkwood
Journal: Journal of Clinical Oncology (2006)

8011 Background: Integrin α5β1 has been reported to be unregulated in metastatic melanoma and in tumor angiogenesis. A critical survival step in angiogenesis is the ligation of fibronectin in the extracellular matrix to α5β1 on endothelial cells. M200 is an IgG4 chimeric monoclonal antibody targeting α5β1, inducing apoptosis of proliferating endothelial cells. M200 activity is independent of growth factor stimulus, suggesting that binding of fibronectin to α5β1 occurs downstream of growth factor signalling, and is possibly a final common pathway for the development of neovasculature. Methods: This is a multicenter, open label, single cohort, pilot phase II study of 40 patients (pts) in metastatic melanoma. Pts received M200 10 mg/kg IV every 2 weeks with DTIC 1g/m 2 monthly until disease progression. Pts were evaluated for efficacy every 8 weeks by objective response using RECIST criteria. Additional evaluations included pharmacokinetics and immunogenicity profile. An independent data safety monitoring board was utilized to review safety data. Results: A total of 40 pts have been enrolled to date. All pts were evaluable for safety and 30 pts for objective response using ITT population. Median age was 58.8 years, with 26 (65%) male. ECOG score was 0–1 in 37 (92%) pts. Up to 14 doses of M200 (median 4 doses) and 7 doses of DTIC (median 2) have currently been administered, with dosing continuing. Thirty-one (77.5%) pts have had at least 1 AE with 8 (20%) pts at least 1 SAE. The most frequent adverse events for M200 were nausea 17.5%, constipation 10% and vomiting 10% and for DTIC were nausea 35%, vomiting 20% and pyrexia 15%. Fifteen SAE’s with 2 possibly related to M200 including hypertension and deep vein thrombosis. Four pts died in the study, all with progressive disease (PD). Best overall response at 8 weeks was stable disease (SD) in 16/30 pts and PD in 14/30 pts. Median time to progression was 72 days. Conclusions: M200 appears to be well tolerated at 10 mg/kg Q2W in combination with DTIC. [Table: see text]
Effect of Pre and Post-Transplantation Responses on Outcome of Multiple Myeloma Patients: CR and near-CR Should Not Be Considered as Equivalent Prognostic Markers. Results of a PETHEMA/Gem Prospective Study
Authors: Juan José Lahuerta, Maria Victoria Mateos, Joaquin Martínez-López, Laura Rosinol, Anna Sureda, Javier de la Rubia, José García-Laraña, Rafael Martínez-Martínez, Miguel-Teodoro Hernández-García, Dolores Carrera, Juan Besalduch, Felipe de Arriba, Jose-Maria Ribera, Lourdes Escoda, María-Belen Hernández-Ruiz, Javier García-Frade, Concepción Rivas-González, Adrian Alegre, Joan Blade, J.F. San Miguel
Journal: Blood (2008)
Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation
Authors: Jennifer M Felton, David A Dorward, Jennifer A Cartwright, Philippe MD Potey, Calum T Robb, Jingang Gui, Ruth W Craig, Jürgen Schwarze, Christopher Haslett, Rodger Duffin, Ian Dransfield, Christopher D Lucas, Adriano G Rossi
Journal: Thorax (2020)

Eosinophils are key effector cells in allergic diseases. Here we investigated Mcl-1 (an anti-apoptotic protein) in experimental allergic airway inflammation using transgenic overexpressing human Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor. Overexpression of Mcl-1 exacerbated allergic airway inflammation, with increased bronchoalveolar lavage fluid cellularity, eosinophil numbers and total protein, and an increase in airway mucus production. Eosinophil apoptosis was suppressed by Mcl-1 overexpression, with this resistance to apoptosis attenuated by cyclin-dependent kinase inhibition which also rescued Mcl-1-exacerbated allergic airway inflammation. We propose that targeting Mcl-1 may be beneficial in treatment of allergic airway disease.
Abstract 12965: New Treatment Concept for Spinal Cord Ischemic Injury With Nanobubble Technology
Authors: Masaaki Naganuma, Yuriko Saiki, Makoto Takahashi, Naoya Terao, Hiroki Takaya, Tomoyuki Suzuki, Yusuke Suzuki, Ichiro Yoshioka, Goro Takahashi, Masatoshi Akiyama, Kiichiro Kumagai, Osamu Adachi, Akira Horii, Yoshikatsu Saiki
Journal: Circulation (2018)

Introduction: Spinal cord ischemic injury (SCII) is one of the disastrous complications related with aortic operation. We previously reported the usefulness of prophylactic spinal cavity irrigation...
Myeloid Cell–Derived TGFβ Signaling Regulates ECM Deposition in Mammary Carcinoma via Adenosine-Dependent Mechanisms
Authors: Georgii Vasiukov, Tatiana Novitskaya, Andries Zijlstra, Philip Owens, Fei Ye, Zhiguo Zhao, Harold L. Moses, Timothy Blackwell, Igor Feoktistov, Sergey V. Novitskiy
Journal: Cancer Research (2020)

Abstract TGFβ plays a crucial role in the tumor microenvironment by regulating cell–cell and cell–stroma interactions. We previously demonstrated that TGFβ signaling on myeloid cells regulates expression of CD73, a key enzyme for production of adenosine, a protumorigenic metabolite implicated in regulation of tumor cell behaviors, immune response, and angiogenesis. Here, using an MMTV-PyMT mouse mammary tumor model, we discovered that deletion of TGFβ signaling on myeloid cells (PyMT/TGFβRIILysM) affects extracellular matrix (ECM) formation in tumor tissue, specifically increasing collagen and decreasing fibronectin deposition. These changes were associated with mitigated tumor growth and reduced metastases. Reduced TGFβ signaling on fibroblasts was associated with their proximity to CD73+ myeloid cells in tumor tissue. Consistent with these findings, adenosine significantly downregulated TGFβ signaling on fibroblasts, an effect regulated by A2A and A2B adenosine receptors. METABRIC dataset analysis revealed that patients with triple-negative breast cancer and basal type harbored a similar signature of adenosine and ECM profiles; high expression of A2B adenosine receptors correlated with decreased expression of Col1 and was associated with poor outcome. Taken together, our studies reveal a new role for TGFβ signaling on myeloid cells in tumorigenesis. This discovered cross-talk between TGFβ/CD73 on myeloid cells and TGFβ signaling on fibroblasts can contribute to ECM remodeling and protumorigenic actions of cancer-associated fibroblasts. Significance: TGFβ signaling on fibroblasts is decreased in breast cancer, correlates with poor prognosis, and appears to be driven by adenosine that accelerates tumor progression and metastasis via ECM remodeling.
Quality of life intervention for men with biochemical recurrence of prostate cancer
Authors: W. Tan, S. Ames, A. Gretchen, R. Stone, T. Rizzo, E. Covil, J. Olmos, M. M. Clark, T. Rummans
Journal: Journal of Clinical Oncology (2006)

18585 Background: The Quality of life (QOL) and psychosocial needs of the 30–40% of prostate cancer patients who experience biochemical recurrence are not known. The impact of having a rising PSA, anticipation of undergoing PSA testing, and living with prostate cancer may increase psychological distress and decrease QOL. Aim: to evaluate the psychosocial treatment needs of men with biochemical recurrence of prostate cancer (br-PCa) and to develop a treatment to address these needs. Methods: 28 men with br-PCa, 58–87 years, were enrolled. A qualitative research approach was used, consisting of six, 2 hour, semi-structured, focus groups containing 4–6 men per group. Data were content coded and grouped into categories following the structure of the focus group guide. The major conceptual themes were then summarized by 2 independent reviewers. Discrepancies were discussed with a third researcher until a consensus was reached. These results were used to guide development of a multi-disciplinary quality of life intervention. Results: Participants defined QOL as the ability to stay active both physically and mentally without limitation in the performance of usual activities. There was a consensus that prostate cancer led to substantial anxiety related to PSA testing, treatment side effects, and fear of recurrence. Participants were enthusiastic about receiving adjuvant multidisciplinary treatment for prostate cancer focusing on anxiety management, nutrition, exercise, management of treatment side effects, and medical education. Participants desired a male group leader and feedback was mixed regarding whether spouses should be involved. Conclusions: Men with br-PCa report experiencing substantial anxiety and were enthusiastic about receiving a structured intervention to these needs. Based on our findings an intervention has been developed and is currently being compared to usual care. No significant financial relationships to disclose.
α-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment
Authors: Md. Razaul Karim, Elly E. Liao, Jaekwang Kim, Joyce Meints, Hector Martell Martinez, Olga Pletnikova, Juan C. Troncoso, Michael K. Lee
Journal: Molecular Neurodegeneration (2020)

Abstract Background Studies link c-Abl activation with the accumulation of pathogenic α-synuclein (αS) and neurodegeneration in Parkinson’s disease (PD). Currently, c-Abl, a tyrosine kinase activated by cellular stress, is thought to promote αS pathology by either directly phosphorylating αS or by causing autophagy deficits. Methods αS overexpressing transgenic (Tg) mice were used in this study. A53T Tg mice that express high levels of human mutant A53TαS under the control of prion protein promoter. Two different approaches were used in this study. Natural aging and seeding model of synucleinopathy. In seeding model, intracortical/intrastriatal (IC/IS) stereotaxic injection of toxic lysates was done using tissue lysates from end-stage symptomatic mice. In this study, nilotinib and pifithrin-α was used as a c-Abl and p53 inhibitor, respectively. Both Tg and non-transgenic (nTg) mice from each group were subjected to nilotinib (10 mg/kg) or vehicle (DMSO) treatment. Frozen brain tissues from PD and control human cases were analyzed. In vitro cells study was implied for c-Abl/p53 genetic manipulation to uncover signal transduction. Results Herein, we show that the pathologic effects of c-Abl in PD also involve activation of p53, as c-Abl activation in a transgenic mouse model of α-synucleinopathy (TgA53T) and human PD cases are associated with the increased p53 activation. Significantly, active p53 in TgA53T neurons accumulates in the cytosol, which may lead to inhibition of autophagy. Thus, we hypothesized that c-Abl-dependent p53 activation contributes to autophagy impairment in α-synucleinopathy. In support of the hypothesis, we show that c-Abl activation is sufficient to inhibit autophagy in p53-dependent manner. Moreover, inhibition of either c-Abl, using nilotinib, or p53, using pifithrin-α, was sufficient to increase autophagic flux in neuronal cells by inducing phosphorylation of AMP-activated kinase (AMPK), ULK1 activation, and down-regulation of mTORC1 signaling. Finally, we show that pharmacological attenuation of c-Abl activity by nilotinib treatment in the TgA53T mouse model reduces activation of p53, stimulates autophagy, decreases accumulation αS pathology, and delays disease onset. Conclusion Collectively, our data show that c-Abl activation by α-synucleinopathy causes p53 dependent autophagy deficits and both c-Abl and p53 represent therapeutic target for PD.
High somatostatin receptor expression and efficacy of somatostatin analogues in patients with metastatic Merkel cell carcinoma*
Authors: T. Akaike, J. Qazi, A. Anderson, F.S. Behnia, M.M. Shinohara, G. Akaike, D.S. Hippe, H. Thomas, S.R. Takagishi, K. Lachance, S.Y. Park, E.S. Tarabadkar, J.G. Iyer, A. Blom, U. Parvathaneni, H. Vesselle, P. Nghiem, S. Bhatia
Journal: British Journal of Dermatology (2020)

Merkel cell carcinoma (MCC) is an aggressive, high‐grade, cutaneous neuroendocrine tumour (NET). Agents blocking programmed death 1/programmed death ligand 1 have efficacy in metastatic MCC (mMCC), but half of patients do not derive durable benefit. Somatostatin analogues (SSAs) are commonly used to treat low‐ and moderate‐grade NETs that express somatostatin receptors (SSTRs). To assess SSTR expression and the efficacy of SSAs in mMCC, a high‐grade NET. Methods In this retrospective study of 40 patients with mMCC, SSTR expression was assessed radiologically by somatostatin receptor scintigraphy (SRS; n = 39) and/or immunohistochemically when feasible (n = 9). Nineteen patients (18 had SRS uptake in MCC tumours) were treated with SSA. Disease control was defined as progression‐free survival (PFS) of ≥ 120 days after initiation of SSA. Thirty‐three of 39 patients (85%) had some degree (low 52%, moderate 23%, high 10%) of SRS uptake. Of 19 patients treated with SSA, seven had a response‐evaluable target lesion; three of these seven patients (43%) experienced disease control, with a median PFS of 237 days (range 152–358). Twelve of 19 patients did not have a response‐evaluable lesion due to antecedent radiation; five of these 12 (42%) experienced disease control (median PFS of 429 days, range 143–1757). The degree of SSTR expression (determined by SRS and/or immunohistochemistry) did not correlate significantly with the efficacy endpoints. In contrast to other high‐grade NETs, mMCC tumours appear frequently to express SSTRs. SSAs can lead to clinically meaningful disease control with minimal side‐effects. Targeting of SSTRs using SSA or other novel approaches should be explored further for mMCC.