tbuckley/cabot-search huggingface dataset:
Abstract P065: The Weight Loss by Using the Smartphone Application for People with Metabolic Abnormalities: A Randomized Controlled Trial
Authors: Jung Hyun Lee, Jee-Seon Shim, Hyungseon Yeom, Su Jin Lee, Hyeon Chang Kim
Journal: Circulation (2019)

Introduction: Obesity has been an important issue for global health. The use of the smartphone application might contribute to weight loss. However, there is still little evidence for the effectiveness among people without overt metabolic disorder. Hypothesis: We assessed the weight loss for people who used the smartphone application with and without personal coaching, with respect to people who did not use any. Methods: A total of 129 participants (aged 30-59 years; 63 men; 66 women) were recruited from the community-based cohort study in Korea during 2017-18. The inclusion criteria were as follows. 1) no cardiovascular disease; 2) no medication for hypertension, diabetes and dyslipidemia; 3) no current use of the application for behavior modification; 4) at least two components of metabolic syndrome (waist circumference ≥ 90/80 cm (men/women), SBP/DBP ≥ 135/85 mmHg, triglyceride ≥ 150 mg/dL, HDL cholesterol &lt; 40/50 mg/dL (men/women), and fasting glucose ≥ 100 mg/dL). Participants were educated for behavior modification and randomly assigned to three groups; CO (control, no use of the application), AO (the application only; without personal coaching) and APC (the application with personal coaching). The weight was measured during a screening examination and follow-up examinations at 1.5, 3 and 6 months from a start date. A linear mixed model including the data from participants who attended the follow-up examination at least once was used to assess the weight loss. Results: A total of 111 participants attended the follow-up examination at least once. The mean (±SD) weight of those at screening was 71.6±12.2 kg. The mean weight loss of participants after 6 months was 0.11±1.6 kg (p = 0.67) in CO, 0.34±2.8 kg (p = 0.45) in AO, and 0.96±2.2 kg (p =0.02) in APC. Compared with the weight loss in CO, there was no significant additional weight loss in AO (0.35 kg; p = 0.41, 0.60 kg after 3 months; p = 0.16 and 0.24 kg after 6 months; p = 0.58), however, there was significant additional weight loss in APC for 3 and 6 months later (0.51 kg after 1.5 months; p = 0.23, 0.93 kg after 3 months; p = 0.03 and 0.87 kg after 6 months; p = 0.04). Conclusions: The use of the application with personal coaching had the effect of losing weight. These results support that the use of the application can be useful for people with metabolic abnormalities that require weight loss.
Reply to Davide Rosati, Riccardo Lombardo, Cosimo De Nunzio, Constantino Leonardo, and Andrea Tubaro’s Words of Wisdom re: Transperineal Interstitial Laser Ablation of the Prostate, A Novel Option for Minimally Invasive Treatment of Benign Prostatic Obstruction. Eur Urol 2021;80:673–4
Authors: Gaetano De Rienzo, Paolo Minafra, Pasquale Ditonno
Journal: European Urology (2022)
How Ribosomes Translate Cancer
Authors: Sergey O. Sulima, Isabel J.F. Hofman, Kim De Keersmaecker, Jonathan D. Dinman
Journal: Cancer Discovery (2017)

Abstract A wealth of novel findings, including congenital ribosomal mutations in ribosomopathies and somatic ribosomal mutations in various cancers, have significantly increased our understanding of the relevance of ribosomes in oncogenesis. Here, we explore the growing list of mechanisms by which the ribosome is involved in carcinogenesis—from the hijacking of ribosomes by oncogenic factors and dysregulated translational control, to the effects of mutations in ribosomal components on cellular metabolism. Of clinical importance, the recent success of RNA polymerase inhibitors highlights the dependence on “onco-ribosomes” as an Achilles' heel of cancer cells and a promising target for further therapeutic intervention. Significance: The recent discovery of somatic mutations in ribosomal proteins in several cancers has strengthened the link between ribosome defects and cancer progression, while also raising the question of which cellular mechanisms such defects exploit. Here, we discuss the emerging molecular mechanisms by which ribosomes support oncogenesis, and how this understanding is driving the design of novel therapeutic strategies. Cancer Discov; 7(10); 1069–87. ©2017 AACR.
First International Breast Cancer Chemoprevention Workshop-Conference
Journal: JNCI Journal of the National Cancer Institute (1987)

First International Breast Cancer Chemoprevention Workshop-Conference Get access JNCI: Journal of the National Cancer Institute, Volume 79, Issue 1, July 1987, Page 198, https://doi.org/10.1093/jnci/79.1.198-c Published: 01 July 1987
FEVER THERAPY
Journal: Annals of Internal Medicine (1943)

Article1 June 1943FEVER THERAPYGORDON B. TAYLOE, M.D., F.A.C.P.GORDON B. TAYLOE, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-18-6-968 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWithin recent years more than 600 articles have been written on artificial hyperpyrexia and more than 50 diseases have been allegedly treated by this method of therapy. It is not my intention to condemn any fever producing method used, to criticize any member of the profession for using any particular type of fever therapy which he may prefer and can best use, or to offer artificial fever therapy as a panacea for the correct and proper treatment for all diseases. I do intend briefly to review the current literature on the subject, to describe the method of treatment I have...Bibliography1. EWALTEBAUGH JRFS: Treatment of dementia paralytica: A five year comparative study of artificial fever therapy and therapeutic malaria in 232 cases, Jr. Am. Med. Assoc., 1941, cxvi, 2474-2477. CrossrefGoogle Scholar2. HUNTLEY WB: Syphilis treated with fever therapy in penal institutions, Arch. Phys. Therap., 1941, xxii, 667-673. Google Scholar3. NEYMANN CA: Artificial fever produced by physical means; its development and application, 1938, Charles C. Thomas, Springfield, Ill., p. 28, fig. 6. Google Scholar4. KRUSEN FH: Physical medicine, 1941, W. B. Saunders, Philadelphia, Pa., p. 122. Google Scholar5. TURVILLEFETTER WHF: Experiences with fever therapy at the Philadelphia Naval Hospital, U. S. Naval Med. Bull., 1943, xli, 431-441. Google Scholar6. KENDELLROSESIMPSON HWDLWM: Artificial fever versus combined fever-chemotherapy in gonococcic infections, Arch. Phys. Therap., 1941, xxii, 103-110. Google Scholar7. WENGATZBOAKCARPENTER HFRACM: The bactericidal effect of sulfanilamide on the gonococcus in vitro, Jr. Bact., 1938, xxxv, 36. Google Scholar8. PRICKMANBENNETTKRUSEN LERLFH: Treatment of brucellosis by physically induced hyperpyrexia, Proc. Staff Meet. Mayo Clin., 1938, xiii, 321-328. Google Scholar9. KRUSEN FH: Personal Communication. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: (MC) U. S. Navy Philadelphia, Pennsylvania*Presented before the Fifth Annual Round-up of Eastern Pennsylvanians of the American College of Physicians, U. S. Naval Hospital, Philadelphia, Pa., October 23, 1942.(NOTE: Authorization has been obtained from the Surgeon General for publication.) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1943Volume 18, Issue 6Page: 968-973KeywordsFeversHyperthermiaSurgeons ePublished: 1 December 2008 Issue Published: 1 June 1943 PDF downloadLoading ...
European cancer mortality predictions for the year 2022 with focus on ovarian cancer
Authors: M. Dalmartello, C. La Vecchia, P. Bertuccio, P. Boffetta, F. Levi, E. Negri, M. Malvezzi
Journal: Annals of Oncology (2022)

Cancer mortality rates, though not absolute numbers of deaths, have been decreasing over the last three decades in Europe.We estimated projections and the number of avoided deaths for total cancer mortality and 10 major cancer sites, between 1989 and 2022, for the European Union (EU), the UK, France, Germany, Italy, Poland and Spain using cancer death certification and population data since 1970 from the World Health Organization and Eurostat.In the EU, we predict 1 269 200 cancer deaths in 2022; corresponding age-standardized rates (world) fall 6% to 126.9 deaths/100 000 in men and 4% to 80.2/100 000 women since 2017. Male lung cancer is expected to fall 10% reaching 30.9/100 000. The rise in female lung cancer mortality slowed (+2% to 13.8/100 000). We estimated 369 000 (23%) avoided deaths in 2022 alone and a total of 5 394 000 (12%) deaths since the peak rate in 1988. Stomach, colorectal, breast and prostate cancers showed substantial declines, between 5% and 16% over the past 5 years. Pancreatic cancer remained stable in men (8.1/100 000) and rose 3% in women (5.9/100 000), becoming the third cause of cancer mortality in the EU (87 300 deaths), overtaking breast cancer (86 300 deaths). The fall in uterine cancers slowed down (-4%) to 4.7/100 000. Bladder cancer fell 9% in men, but was stable in women. Leukaemias fell more than 10%. Ovarian cancer mortality declined over the past decade in all considered countries. EU predicted rates were 4.3/100 000 (-13%) all ages, 1.2/100 000 (-26%) at 20-49, 15.3/100 000 (-11%) at 50-69 and 32.3/100 000 (-11%) at 70-79 years.We predicted additional declines in cancer mortality rates for 2022. The slowdown in female lung cancer mortality reflects some levelling of smoking in women. Favourable ovarian cancer trends are likely to continue and are largely attributable to the spreading oral contraceptive use and some impact of improved diagnosis and management.
Group 3 innate lymphoid cells produce the growth factor HB-EGF to protect the intestine from TNF-mediated inflammation
Authors: Lei Zhou, Wenqing Zhou, Ann M. Joseph, Coco Chu, Gregory G. Putzel, Beibei Fang, Fei Teng, Mengze Lyu, Hiroshi Yano, Katrin I. Andreasson, Eisuke Mekada, Gerard Eberl, Gregory F. Sonnenberg
Journal: Nature Immunology (2022)
Immuno-proteomic profiling reveals aberrant immune cell regulation in the airways of individuals with ongoing post-COVID-19 respiratory disease
Authors: Bavithra Vijayakumar, Karim Boustani, Patricia P. Ogger, Artemis Papadaki, James Tonkin, Christopher M. Orton, Poonam Ghai, Kornelija Suveizdyte, Richard J. Hewitt, Sujal R. Desai, Anand Devaraj, Robert J. Snelgrove, Philip L. Molyneaux, Justin L. Garner, James E. Peters, Pallav L. Shah, Clare M. Lloyd, James A. Harker
Journal: Immunity (2022)

Some patients hospitalized with acute COVID-19 suffer respiratory symptoms that persist for many months. We delineated the immune-proteomic landscape in the airways and peripheral blood of healthy controls and post-COVID-19 patients 3 to 6 months after hospital discharge. Post-COVID-19 patients showed abnormal airway (but not plasma) proteomes, with an elevated concentration of proteins associated with apoptosis, tissue repair, and epithelial injury versus healthy individuals. Increased numbers of cytotoxic lymphocytes were observed in individuals with greater airway dysfunction, while increased B cell numbers and altered monocyte subsets were associated with more widespread lung abnormalities. A one-year follow-up of some post-COVID-19 patients indicated that these abnormalities resolved over time. In summary, COVID-19 causes a prolonged change to the airway immune landscape in those with persistent lung disease, with evidence of cell death and tissue repair linked to the ongoing activation of cytotoxic T cells.
Management of Dyslipidemia in Adults With Diabetes
Journal: Diabetes Care (2002)

RATIONALE FOR TREATMENTOF DYSLIPIDEMIA -The rationale for the treatment of diabetic dyslipidemia is discussed in detail in the American Diabetes Association (ADA) technical review "Management of Dyslipidemia in Adults With Diabetes" (1).Type 2 diabetes is associated with a two-to fourfold excess risk of coronary heart disease (CHD).Although the degree of glycemia in diabetic patients is strongly related to the risk of microvascular complications (retinopathy and renal disease), the relation of glycemia to macrovascular disease in type 2 diabetes is more modest.The finding of increased cardiovascular risk factors before the onset of type 2 diabetes also suggests that aggressive screening for diabetes combined with improved glycemic control alone will not be likely to completely eliminate excess risk of CHD in type 2 diabetic patients.Clearly, a multifactorial approach to prevention of CHD in type 2 diabetes will be necessary. PREVALENCE OF DYSLIPIDEMIAIN TYPE 2 DIABETES -The most common pattern of dyslipidemia in type 2 diabetic patients is elevated triglyceride levels and decreased HDL cholesterol levels.The concentration of LDL cholesterol in type 2 diabetic patients is usually not significantly different from nondiabetic individuals.Diabetic patients may have elevated levels of non-HDL cholesterol (LDL plus VLDL).However, type 2 diabetic patients typically have a preponderance of smaller, denser LDL particles, which possibly increases atherogenicity even if the absolute concentration of LDL cholesterol is not significantly increased.Lastly, as shown in the technical review (1), the median triglyceride level in type 2 diabetic patients is Ͻ200 mg/dl (2.30 mmol/l), and 85-95% of patients have triglyceride levels below 400 mg/dl (4.5 mmol/l).As in nondiabetic individuals, lipid levels may be affected by factors unrelated to glycemia or insulin resistance, such as renal disease, hypothyroidism, and the frequent occurrence of genetically determined lipoprotein disorders (e.g., familial combined hyperlipidemia and familial hypertriglyceridemia).These genetic disorders may contribute to the severe hypertriglyceridemia seen in some patients with diabetes.Furthermore, use of alcohol and estrogen may also contribute to hypertriglyceridemia.
Three-Drug Regimen Bests Chemo in NSCLC
Journal: Cancer Discovery (2021)

A three-drug regimen containing the CTLA4 inhibitor tremelimumab plus the PD-L1 inhibitor durvalumab and chemotherapy may be an effective first-line treatment strategy for patients with metastatic non-small cell lung cancer. In the phase III POSEIDON trial, the combination significantly extended progression-free survival and overall survival compared with chemotherapy alone.
Reply
Authors: Jonathan G. Stine, Ian R. Schreibman, Alison J. Faust, Jessica Dahmus, Benjamin Stern, Christopher Soriano, Gloriany Rivas, Breianna Hummer, Scot R. Kimball, Nathaniel R. Geyer, Vernon M. Chinchilli, Kathryn Schmitz, Christopher Sciamanna
Journal: Hepatology (2022)

We appreciate the summary and interpretation of the findings of our NASHFit Trial by Zanetto et al.[1] This was the first study investigating how exercise can mitigate thrombotic risk in patients with NASH. We found that the plasma level of plasminogen activator inhibitor (PAI)‐1 was significantly decreased following 20 weeks of exercise training, independent of obesity or body composition. These findings are important because patients with NASH have increased rates of thromboembolism.[2] Decreasing PAI‐1, which is abnormal and leads to impaired fibrinolysis (clot breakdown) in NASH, would be expected to lessen thromboembolism and its subsequent morbidity and mortality. PAI‐1 is an established biomarker of thrombotic complications across multiple populations, including those with metabolic disease. In patients with NASH, there is a large body of evidence demonstrating increased PAI‐1 level in a dose‐dependent fashion across all disease stages.[3] We previously demonstrated that PAI‐1 level was much greater in liver transplant candidates with NASH cirrhosis and that PAI‐1 level normalizes within 1 week following transplantation.[4] However, our study was underpowered to detect an association between PAI‐1 and thromboembolism. To date, we are unaware of any prospective studies linking PAI‐1 to thrombotic events exclusively in patients with NASH. In this letter, Zanetto et al. provide new evidence to support PAI‐1 as a biomarker of thromboembolism in NASH. In their post hoc analysis of 26 patients with NASH cirrhosis, PAI‐1 level was significantly greater in the 5 patients who developed venous thromboembolism, independent of other components of the fibrinolytic system. Although interpretation of these results needs to be performed cautiously given the relatively small sample size consisting largely of male patients with decompensated cirrhosis, the findings are nonetheless promising and provide additional evidence linking impaired fibrinolysis to thrombotic events in NASH. We look to future prospective studies to validate these findings and confirm that PAI‐1 remains a relevant thrombotic biomarker in patients with NASH across all stages of disease. CONFLICT OF INTEREST Dr. Stine received grants from Novo Nordisk, Noom, Inc., AstraZeneca and Grifols. AUTHOR CONTRIBUTIONS All authors contributed in the following manner and (1) drafted the article or revised it critically for important intellectual content and (2) provided final approval of the version to be published.
Combined IL-2, agonistic CD3 and 4-1BB stimulation preserve clonotype hierarchy in propagated non-small cell lung cancer tumor-infiltrating lymphocytes
Authors: Parin Shah, Marie-Andrée Forget, Meredith L Frank, Peixin Jiang, Donastas Sakellariou-Thompson, Lorenzo Federico, Roohussaba Khairullah, Chantal Alexia Neutzler, Ignacio Wistuba, Chi-Wan B Chow, Yan Long, Junya Fujimoto, Shiaw-Yih Lin, Anirban Maitra, Marcelo V Negrao, Kyle Gregory Mitchell, Annikka Weissferdt, Ara A Vaporciyan, Tina Cascone, Jack A Roth, Jianjun Zhang, Boris Sepesi, Don L Gibbons, John V Heymach, Cara L Haymaker, Daniel J McGrail, Alexandre Reuben, Chantale Bernatchez
Journal: Journal for ImmunoTherapy of Cancer (2022)

Adoptive cell transfer (ACT) of tumor-infiltrating lymphocytes (TIL) yielded clinical benefit in patients with checkpoint blockade immunotherapy-refractory non-small cell lung cancer (NSCLC) prompting a renewed interest in TIL-ACT. This preclinical study explores the feasibility of producing a NSCLC TIL product with sufficient numbers and enhanced attributes using an improved culture method.TIL from resected NSCLC tumors were initially cultured using (1) the traditional method using interleukin (IL)-2 alone in 24-well plates (TIL 1.0) or (2) IL-2 in combination with agonistic antibodies against CD3 and 4-1BB (Urelumab) in a G-Rex flask (TIL 3.0). TIL subsequently underwent a rapid expansion protocol (REP) with anti-CD3. Before and after the REP, expanded TIL were phenotyped and the complementarity-determining region 3 β variable region of the T-cell receptor (TCR) was sequenced to assess the T-cell repertoire.TIL 3.0 robustly expanded NSCLC TIL while enriching for CD8+ TIL in a shorter manufacturing time when compared with the traditional TIL 1.0 method, achieving a higher success rate and producing 5.3-fold more TIL per successful expansion. The higher proliferative capacity and CD8 content of TIL 3.0 was also observed after the REP. Both steps of expansion did not terminally differentiate/exhaust the TIL but a lesser differentiated population was observed after the first step. TIL initially expanded with the 3.0 method exhibited higher breadth of clonotypes than TIL 1.0 corresponding to a higher repertoire homology with the original tumor, including a higher proportion of the top 10 most prevalent clones from the tumor. TIL 3.0 also retained a higher proportion of putative tumor-specific TCR when compared with TIL 1.0. Numerical expansion of TIL in a REP was found to perturb the clonal hierarchy and lessen the proportion of putative tumor-specific TIL from the TIL 3.0 process.We report the feasibility of robustly expanding a T-cell repertoire recapitulating the clonal hierarchy of the T cells in the NSCLC tumor, including a large number of putative tumor-specific TIL clones, using the TIL 3.0 methodology. If scaled up and employed as a sole expansion platform, the robustness and speed of TIL 3.0 may facilitate the testing of TIL-ACT approaches in NSCLC.
Black Mn-containing layered double hydroxide coated magnesium alloy for osteosarcoma therapy, bacteria killing, and bone regeneration
Authors: Dongdong Zhang, Shi Cheng, Ji Tan, Juning Xie, Yu Zhang, Shuhan Chen, Huihui Du, Shi Qian, Yuqing Qiao, Feng Peng, Xuanyong Liu
Journal: Bioactive Materials (2022)

Osteosarcoma (OS) tissue resection with distinctive bactericidal activity, followed by regeneration of bone defects, is a highly demanded clinical treatment. Biodegradable Mg-based implants with desirable osteopromotive and superior mechanical properties to polymers and ceramics are promising new platforms for treating bone-related diseases. Integration of biodegradation control, osteosarcoma destruction, anti-bacteria, and bone defect regeneration abilities on Mg-based implants by applying biosafe and facile strategy is a promising and challenging topic. Here, a black Mn-containing layered double hydroxide (LDH) nanosheet-modified Mg-based implants was developed. Benefiting from the distinctive capabilities of the constructed black LDH film, including near-infrared optical absorption and reactive oxygen species (ROS) generation in a tumor-specific microenvironment, the tumor cells and tissue could be effectively eliminated. Concomitant bacteria could be killed by localized hyperthermia. Furthermore, the enhanced corrosion resistance and synergistic biofunctions of Mn and Mg ions of the constructed black LDH-modified Mg implants significantly facilitated cell adhesion, spreading and proliferation and osteogenic differentiation in vitro, and accelerated bone regeneration in vivo. This work offers a new platform and feasible strategy for OS therapeutics and bone defect regeneration, which broadens the biomedical application of Mg-based alloys.
Tcof1 haploinsufficiency promotes early T cell precursor-like leukemia in NrasQ61R/+ mice
Authors: Zhi Wen, Remington Finn, Xin Gao, Lin Li, Alexander Hebert, Erik A. Ranheim, Yun Zhou, Grant Yun, Jeroen P. Roose, Joshua J. Coon, Rita Shiang, Renren Wen, Menggang Yu, Demin Wang, Jing Zhang
Journal: Leukemia (2022)
NF-κB perturbation reveals unique immunomodulatory functions in Prx1 <sup>+</sup> fibroblasts that promote development of atopic dermatitis
Authors: Kang I. Ko, Jean J. Merlet, Brett P. DerGarabedian, Huang Zhen, Yoko Suzuki-Horiuchi, Matthew L. Hedberg, Eileen Hu, Anh T. Nguyen, Stephen Prouty, Faizan Alawi, Matthew C. Walsh, Yongwon Choi, Sarah E. Millar, Ashley Cliff, Jonathon Romero, Michael R. Garvin, John T. Seykora, Daniel Jacobson, Dana T. Graves
Journal: Science Translational Medicine (2022)

Skin is composed of diverse cell populations that cooperatively maintain homeostasis. Up-regulation of the nuclear factor κB (NF-κB) pathway may lead to the development of chronic inflammatory disorders of the skin, but its role during the early events remains unclear. Through analysis of single-cell RNA sequencing data via iterative random forest leave one out prediction, an explainable artificial intelligence method, we identified an immunoregulatory role for a unique paired related homeobox-1 (Prx1) + fibroblast subpopulation. Disruption of Ikkb –NF-κB under homeostatic conditions in these fibroblasts paradoxically induced skin inflammation due to the overexpression of C-C motif chemokine ligand 11 (CCL11; or eotaxin-1) characterized by eosinophil infiltration and a subsequent T H 2 immune response. Because the inflammatory phenotype resembled that seen in human atopic dermatitis (AD), we examined human AD skin samples and found that human AD fibroblasts also overexpressed CCL11 and that perturbation of Ikkb –NF-κB in primary human dermal fibroblasts up-regulated CCL11. Monoclonal antibody treatment against CCL11 was effective in reducing the eosinophilia and T H 2 inflammation in a mouse model. Together, the murine model and human AD specimens point to dysregulated Prx1 + fibroblasts as a previously unrecognized etiologic factor that may contribute to the pathogenesis of AD and suggest that targeting CCL11 may be a way to treat AD-like skin lesions.