tbuckley/cabot-search huggingface dataset:
The Effects of Physiologic Amounts of Simple Sugars on Lipoprotein, Glucose, and Insulin Levels in Normal Subjects
Authors: Brenda M Bossetti, Lynn M Kocher, Janice F Moranz, James M Falko
Journal: Diabetes Care (1984)

Using a crossover design, eight healthy volunteers randomly received physiologic amounts (⅓ of each subject's total carbohydrate intake) of either fructose or sucrose as the primary source of simple sugar, incorporated into isocaloric diets comprised of typical American foods. After 7 and 14 days of consuming either of the two sugars, no change occurred in fasting glucose or insulin levels. In addition, total triglyceride, totalcholesterol, low-density-lipoprotein (LDL) cholesterol, and high-density-lipoprotein (HDL) cholesterol concentrations were unaltered. Since our study used conventional foods in normal eating patterns rather than contrived formulas or excessive amounts of simple sugar, our data indicate that there is no difference between sucrose or fructose on various lipid components or glucose and fasting insulin levels in the “real world” innormal subjects.
Eradication of Medullary Multiple Myeloma by CD4+ Cytotoxic Human T Lymphocytes Directed at a Single Minor Histocompatibility Antigen
Authors: Robbert M. Spaapen, Richard W.J. Groen, Kelly van den Oudenalder, Teun Guichelaar, Maureen van Elk, Tineke Aarts-Riemens, Andries C. Bloem, Gert Storm, Anton C. Martens, Henk M. Lokhorst, Tuna Mutis
Journal: Clinical Cancer Research (2010)

Abstract Purpose: The essential role of CD4+ T cells as helpers of anticancer immunity is indisputable. Little is known, however, about their capacity to serve as effector cells in cancer treatment. Therefore, we explored the efficacy of immunotherapy with sole CD4+ cytotoxic human T cells directed at a hematopoietic-restricted minor histocompatibility antigen (mHag). Experimental Design: In macrophage-depleted Rag2−/−γc−/− mice, which were also devoid of T, B, and natural killer cells, mHag-specific native T cells or tetanus toxoid (TT)-specific T cells transduced with the mHag-specific T-cell receptor (TCR) were injected to treat full-blown mHag+ human multiple myeloma tumors. Results: mHag-specific antitumor responses were achieved after injection of native or mHag-TCR-transduced T cells. Although the therapy completely eradicated the primary tumors in the bone marrow, it failed to control extramedullary relapses, even after repeated T-cell injections. Detailed analyses ruled out mHag or MHC downregulation as mechanisms of extramedullary tumor escape. Impaired T-cell survival in vivo or defective homing to the tumor site were also ruled out as mechanisms behind extramedullary relapses, because injections of TT-loaded antigen presenting cells could facilitate homing of long-term surviving T cells to s.c. tumor sites. Moreover, intratumoral treatment of extramedullary tumors with 3AB11 was also ineffective. Conclusions: Taken together, these results for the first time show the feasibility of immunotherapy of primary bone marrow tumors with sole CD4+ human T cells directed to a tumor-associated mHag. Extramedullary relapses, probably due to microenvironment-dependent inhibitory mechanisms, remain a challenging issue towards effective cellular immunotherapy of hematologic malignancies. Clin Cancer Res; 16(22); 5481–8. ©2010 AACR.
The Public Health Implications of the Cost-Effectiveness of Bariatric Surgery for Diabetes
Authors: Neda Laiteerapong, Elbert S. Huang
Journal: Diabetes Care (2010)

Bariatric surgery is one of the major breakthroughs in diabetes care to have emerged since the discovery of insulin. In the 15 years since the first observational study, clinical trials and observational studies of bariatric surgery in diabetic patients have confirmed the beneficial effects of surgery (1). Since 2000, guidelines from the National Institutes of Health (NIH) have recommended bariatric surgery as an option for obesity treatment in adults with a BMI ≥35 kg/m2 and a serious comorbid condition (2). In 2009, the Centers for Medicare & Medicaid Services officially announced it would cover bariatric surgery for beneficiaries with morbid obesity and type 2 diabetes. While bariatric surgery can be beneficial, it is an expensive intervention costing at least $13,000 in the first year (3). In light of its high costs and potential benefits, understanding the cost-effectiveness of bariatric surgery for diabetes is critical for policy discussions regarding any ongoing or additional public health investment in bariatric surgery. The cost-effectiveness of bariatric surgery for diabetes has been evaluated in prior studies, but these studies have been limited by simplistic diabetes models (4–6) with parameter inputs derived from individual trials (5). Only one previous study of Roux-en-Y gastric bypass has accounted for the future complications of diabetes (7,8), and only one study has been conducted from the perspective of the U.S. (7).

In this issue of Diabetes Care , Hoerger et al. (9) address many of these deficits in the existing literature and report on the most rigorously conducted cost-effectiveness analysis of bariatric surgery for diabetes to date. Using the Centers for Disease Control-Research Triangle Institute (CDC-RTI) Diabetes Cost-Effectiveness Model, the authors modeled the potential lifetime effects of bariatric surgery on diabetes by estimating rates of diabetes remission and relapse, as well as diabetes complications, …
Aurora-A, a Negative Prognostic Marker, Increases Migration and Decreases Radiosensitivity in Cancer Cells
Authors: Zhong Guan, Xian-ren Wang, Xiao-feng Zhu, Xue-fei Huang, Jie Xu, Li-hui Wang, Xiang-bo Wan, Zi-jie Long, Jian-nan Liu, Gong-kan Feng, Wenlin Huang, Yi-xin Zeng, Fu-jin Chen, Quentin Liu
Journal: Cancer Research (2007)

Abstract Centrosomal Aurora-A (Aur-A) kinase ensures proper spindle assembly and accurate chromosome segregation in mitosis. Overexpression of Aur-A leads to centrosome amplification, aberrant spindle, and consequent genetic instability. In the present study, Aur-A was found to be overexpressed in laryngeal squamous cell carcinoma (LSCC). Moreover, Aur-A expression was adversely correlated with median survival, and further identified as a potential independent factor for disease prognosis. Suppression of Aurora kinase activity chemically or genetically led to LSCC Hep2 cell cycle arrest and apoptotic cell death. Importantly, we found that Aur-A increases cell migration and this novel function was correlated with Akt1 activation. The enhanced cell migration induced by Aur-A overexpression could be abrogated by either small-molecule Akt1 inhibitor or short interfering RNA. VX-680, a selective Aurora kinase inhibitor, decreased Akt1 phosphorylation at Ser473 and inhibited cell migration, but failed to do so in constitutive active Akt1 (myr-Akt1)–overexpressed cells. Moreover, our data suggested that overexpression of Aur-A kinase might also contribute to radioresistance of LSCC. Inhibiting Aur-A by VX-680 induced expression of p53 and potently sensitized cells to radiotherapy, leading to significant cell death. Ectopic overexpression of Aur-A, however, reduced p53 level and rendered cells more resistant to irradiation. Taken together, we showed that Aur-A kinase, a negative prognostic marker, promotes migration and reduces radiosensitivity in laryngeal cancer cells. [Cancer Res 2007;67(21):10436–44]
Polyelectrolyte complex micelles by self-assembly of polypeptide-based triblock copolymer for doxorubicin delivery
Authors: Jeong Hwan Kim, Thiruganesh Ramasamy, Tuan Hiep Tran, Ju Yeon Choi, Hyuk Jun Cho, Chul Soon Yong, Jong Oh Kim
Journal: Asian Journal of Pharmaceutical Sciences (2014)

Polyelectrolyte complex micelles were prepared by self-assembly of polypeptide-based triblock copolymer as a new drug carrier for cancer chemotherapy. The triblock copolymer, poly(l-aspartic acid)-b-poly(ethylene glycol)-b-poly(l-aspartic acid) (PLD-b-PEG-b-PLD), spontaneously self-assembled with doxorubicin (DOX) via electrostatic interactions to form spherical micelles with a particle size of 60–80 nm (triblock ionomer complexes micelles, TBIC micelles). These micelles exhibited a high loading capacity of 70% (w/w) at a drug/polymer ratio of 0.5 at pH 7.0. They showed pH-responsive release patterns, with higher release at acidic pH than at physiological pH. Furthermore, DOX-loaded TBIC micelles exerted less cytotoxicity than free DOX in the A-549 human lung cancer cell line. Confocal microscopy in A-549 cells indicated that DOX-loaded TBIC micelles were transported into lysosomes via endocytosis. These micelles possessed favorable pharmacokinetic characteristics and showed sustained DOX release in rats. Overall, these findings indicate that PLD-b-PEG-b-PLD polypeptide micelles are a promising approach for anti-cancer drug delivery.
Randomised controlled trial of Helicobacter pylori testing and endoscopy for dyspepsia in primary
Authors: B C Delaney
Journal: BMJ (2001)

<h3>Abstract</h3> <b>Objective:</b> To determine the cost effectiveness of a strategy of near patient <i>Helicobacter pylori</i> testing and endoscopy for managing dyspepsia. <b>Design:</b> Randomised controlled trial. <b>Setting:</b> 31 UK primary care centres. <b>Participants:</b> 478 patients under 50 years old presenting with dyspepsia of longer than four weeks duration. <b>Interventions:</b> Near patient testing for <i>H pylori</i> and open access endoscopy for patients with positive results. Control patients received acid suppressing drugs or specialist referral at general practitioner9s discretion. <b>Main outcome measures:</b> Cost effectiveness based on improvement in symptoms and use of resources at 12 months; quality of life. <b>Results:</b> 40% of the study group tested positive for <i>H pylori</i>. 45% of study patients had endoscopy compared with 25% of controls. More peptic ulcers were diagnosed in the study group (7.4% <i>v</i> 2.1%, P=0.011). Paired comparison of symptom scores and quality of life showed that all patients improved over time with no difference between study and control groups. No significant differences were observed in rates of prescribing, consultation, or referral. Costs were higher in the study group (£367.85 <i>v</i> £253.16 per patient). <b>Conclusions:</b> The test and endoscopy strategy increases endoscopy rates over usual practice in primary care. The additional cost is not offset by benefits in symptom relief or quality of life. <h3>What is already known on this topic</h3> Patients younger than 50 without <i>H pylori</i> infection are unlikely to have treatable disease detected at endoscopy Such patients can be managed by acid suppression and reassurance alone Test and endoscopy (referral of patients testing positive for <i>H pylori</i>in primary care) has been recommended as a way to reduce endoscopic workload <h3>What this paper adds</h3> Applying a test and endoscopy strategy increased the endoscopy referral rate from 25% to 40% The strategy produced no significant differences in symptoms or quality of life compared with usual management The increased costs of this strategy cannot be justified
Association between dietary folate intake and clinical outcome in head and neck squamous cell carcinoma
Authors: D. Kawakita, K. Matsuo, F. Sato, I. Oze, S. Hosono, H. Ito, M. Watanabe, Y. Yatabe, N. Hanai, Y. Hasegawa, K. Tajima, S. Murakami, H. Tanaka
Journal: Annals of Oncology (2011)
End-Stage Renal Disease due to Diabetes Among Southwestern American Indians, 1990–2001
Authors: Nilka Ríos Burrows, Andrew S. Narva, Linda S. Geiss, Michael M. Engelgau, Kelly J. Acton
Journal: Diabetes Care (2005)

OBJECTIVE—This study assesses trends in the incidence of diabetes-related end-stage renal disease (ESRD) among southwestern American Indians (SWAIs). RESEARCH DESIGN AND METHODS—Using the U.S. Renal Data System, we obtained the total number of new cases of treated ESRD in which diabetes was the primary cause of renal failure in 1990 through 2001. The incidence of diabetes-related ESRD was calculated using census population figures and estimates of the SWAI population with diabetes, then age-adjusted to the 2000 U.S. population. RESULTS—Between 1990 and 2001, the annual number of new patients starting treatment for diabetes-related ESRD in the SWAI total population increased from 154 to 320, and the age-adjusted diabetes-related ESRD incidence per 10,000 population increased 34% (6.2–8.3 per 10,000 people). However, after adjusting for the increasing number of people with diabetes in the SWAI population between 1993 and 2001, the age-adjusted incidence of diabetes-related ESRD among SWAIs with diabetes decreased 31%, from 80.4 to 55.8 per 10,000 people with diabetes. It decreased for both sexes and in all age-groups. CONCLUSIONS—The increasing incidence of diabetes-related ESRD in the SWAI population parallels the growing prevalence of diabetes. However, since 1993 diabetes-related ESRD incidence decreased in the SWAI population with diabetes, consistent with national trends. This may reflect the reduction in risk factors and improvements in diabetes care practices in Indian communities.
Re: Impact of Stromal Sensitivity on Radiation Response of Tumors
Authors: W. Budach
Journal: JNCI Journal of the National Cancer Institute (1998)

Irradiation of tumors causes the death of both parenchymal tumor cells as well as normal tissue stromal cells (e.g., endothelium, connective tissue). However, it has been difficult to distinguish the contributions to overall tumor response after irradiation from the two compartments. The development of the severe combined immunodeficient (SCID) mouse provides a model in which the contribution of stromal cell responses to ionizing radiation to overall tumor response can be defined, because its normal tissue cells are extremely radiosensitive. Therefore, the results of irradiation of tumors in radiation-sensitive (SCID) and radiation-resistant hosts can be compared, and the contribution of the normal tissue stroma clarified.Our purpose was to investigate the effects of radiation-induced stromal cell damage on tumor cell death, using tumor growth delay (GD) and local control (complete and permanent regression of the irradiated tumor) as end points.Tumor GD and local control experiments were performed in SCID, athymic, and C3H mice. Sixty SCID and 60 nude mice for each of three human tumor cell lines (HGL9, HSTS26, HCT15) and for each of five murine cell lines (FSC1, FSC2, FSM1, FSM2, E01) and 60 SCID and 60 C3H mice for the FSa2 spontaneous C3H sarcoma were studied. Neoplasms were produced by injection of 10(6) cells from in vitro tissue cultures into the flanks of donor mice; after tumors had grown, experimental neoplasms were produced by transplanting 2- to 3-mm fragments into recipient mice. Animals were randomly assigned to various groups when tumors reached average volumes of 120 mm3. Graded, single-dose x irradiations (15-115 Gy, dose rate about 7 Gy/min) were given under acutely hypoxic conditions. Tumors were scored one to two times per week until recurrence.The x-ray doses needed to achieve local control in 50% of the animals (tumor control doses, TCD50) ranged from 45.1 to 58.0 Gy for human tumors and from 36.3 to 114.0 Gy for murine tumors. On average, the TCD50 values in SCID mice were only about 3.5% lower than values in nude or C3H mice. The amount of GD defined at 66% of the TCD50 for the various groups was, however, 27% longer in the SCID mice (P = .004).While the three-fold higher radiation sensitivity of the normal tissue stromal cells in the SCID mice did not alter the percentage of tumors controlled by x irradiation in the SCID mouse hosts as compared with other hosts, there appear to be significant differences in GD. Radiation-induced stromal cell damage does not significantly contribute to tumor cell death; however, it can prolong the interval of tumor regression.
Cardiovascular disease and cancer compete for the outcome of death
Authors: G. Irving
Journal: BMJ (2014)

Life is a game of multiple competing risks, and problems arise when we forget that death is a single, non-repetitive event usually attributable to one cause.1 Doctors often consider issues of competing risks when caring for patients with multimorbid chronic disease. For example, it’s not uncommon for a GP to ask, “Will my …
Gene Expression Profiling of Localized Esophageal Carcinomas: Association With Pathologic Response to Preoperative Chemoradiation
Authors: Rajyalakshmi Luthra, Tsung-Teh Wu, Madan G. Luthra, Julie Izzo, Enrique Lopez-Alvarez, Li Zhang, Jaime Bailey, Jeffrey H. Lee, Robert Bresalier, Asif Rashid, Stephen G. Swisher, Jaffer A. Ajani
Journal: Journal of Clinical Oncology (2005)

Patients with localized esophageal carcinoma have a 5-year survival rate of less than 20%. Patients are often treated similarly (ie, with preoperative chemoradiotherapy) but the outcomes vary greatly. Chemoradiotherapy and surgery can result in significant undesirable consequences. Currently, however, there are no tools to help select optimum therapy. We hypothesized that gene expression profiling could provide clues and biomarkers for selection of therapy.Pretreatment endoscopic cancer biopsies from 19 patients (16 with adenocarcinoma, two with squamous cell carcinoma, and one with adenosquamous carcinoma) enrolled onto a preoperative chemoradiotherapy protocol were profiled using oligonucleotide microarrays. Surgical specimens following therapy were assessed for the degree of pathologic response. On the basis of array data, selected genes were analyzed by polymerase chain reaction.Unsupervised hierarchical cluster analysis segregated the cancers into two molecular subtypes, each consisting 10 and nine specimens, respectively. Most cancers (five of six) that had pathologic complete response (pathCR) clustered in molecular subtype I. Subtype II, with one exception, consisted cancers that had less than pathCR (< pathCR). Using a combination marker approach, levels of PERP, S100A2, and SPRR3 allowed discrimination of pathCR from < pathCR with high sensitivity and specificity (85%). Pathway analysis identified apoptotic pathway as one of the key functions downregulated in molecular type II in comparison with type I.These encouraging, albeit preliminary, data suggest that expression profiling may distinguish cancers with different pathologic outcome. This is the first report to show subtypes of esophageal cancers with distinct molecular signatures. The potential of PERP, S100A2, and SPRR3 as biomarkers of pathCR warrants further validation.
Smoking as a Modifiable Risk Factor for Type 2 Diabetes in Middle-Aged Men
Authors: S. Goya Wannamethee, A. Gerald Shaper, Ivan J. Perry
Journal: Diabetes Care (2001)

OBJECTIVE—To examine the effects of cigarette smoking, giving up smoking, and primary or secondary pipe or cigar smoking on the risk of type 2 diabetes. RESEARCH DESIGN AND METHODS—A prospective study followed 7,735 men aged 40–59 years from general practices in 24 British towns for an average of 16.8 years. Incident cases of physician-diagnosed diabetes were ascertained by repeated postal questionnaires and systematic reviews of primary care records. RESULTS—A total of 290 incident cases of diabetes were found in 7,124 men with no history of diabetes, coronary heart disease, or stroke. Cigarette smoking was associated with a significant increase in risk of diabetes, even after adjustment for age, BMI, and other potential confounders. The benefit of giving up smoking was only apparent after 5 years of smoking cessation, and risk reverted to that of never-smokers only after 20 years. The risk of diabetes in those who switched from smoking cigarettes to pipe or cigars remained equal to the risk in continuing cigarette smokers. Men who gave up smoking during the first 5 years of follow-up showed significant weight gain and subsequently higher risk of diabetes than continuing smokers. CONCLUSIONS—Cigarette smoking is an independent and modifiable risk factor for type 2 diabetes. Smoking cessation is associated with weight gain and a subsequent increase in risk of diabetes, but in the long term, the benefits of giving up smoking outweigh the adverse effects of early weight gain.
Cellular adhesion molecules on vascular smooth muscle cells
Authors: M Braun
Journal: Cardiovascular Research (1999)

Several studies during the last years have shown that, in addition to endothelial cells, vascular smooth muscle cells also express the cellular adhesion molecules ICAM-1 and VCAM-1 in atherosclerosis, restenosis and transplant vasculopathy. In vitro studies have characterized stimulatory and inhibitory factors that regulate the expression of ICAM-1 and VCAM-1 on cultured smooth muscle cells. There is evidence for a role of adhesion molecules on smooth muscle cells for leukocyte accumulation and activation of mononuclear cells. Some recent data suggest that the expression of adhesion molecules on smooth muscle cells are cell cycle-dependent and influence smooth muscle cell proliferation and differentiation. Therefore, ICAM-1 and VCAM-1 on smooth muscle cells may contribute to the inflammatory reaction in the vascular wall and may actively be involved in the progression and stability of atherosclerotic plaques.
Orthostatic Intolerance and Tachycardia Associated with Norepinephrine-Transporter Deficiency
Authors: John R. Shannon, Nancy L. Flattem, Jens Jordan, Giris Jacob, Bonnie K. Black, Italo Biaggioni, Randy D. Blakely, David Robertson
Journal: New England Journal of Medicine (2000)

Orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, and syncope and associated with postural tachycardia and plasma norepinephrine concentrations that are disproportionately high in relation to sympathetic outflow. We tested the hypothesis that impaired functioning of the norepinephrine transporter contributes to the pathophysiologic mechanism of orthostatic intolerance.
Resuscitation Equipment Board for Nurseries and Delivery Rooms
Authors: J. Michael Clark
Journal: JAMA (1976)

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