tbuckley/cabot-search huggingface dataset:
Human Peripheral Blood-Derived CD31+Cells Have Robust Angiogenic and Vasculogenic Properties and Are Effective for Treating Ischemic Vascular Disease
Authors: Sung-Whan Kim, Hyongbum Kim, Hyun-Jai Cho, Jung-Uek Lee, Rebecca Levit, Young-sup Yoon
Journal: Journal of the American College of Cardiology (2010)
Role of the Phonocardiogram in Evaluation of the Severity of Mitral Stenosis and Detection of Associated Valvular Lesions
Authors: BORYS SURAWICZ, CHARLES MERCER, HENRYK CHLEBUS, JOHN T. REEVES, FRANK C. SPENCER
Journal: Circulation (1966)

The phonocardiogram was correlated with hemodynamic measurements and with the results of surgical exploration in 141 patients with pure or dominant mitral stenosis. The study revealed the following results: 1. A diastolic murmur at the apex was absent in only two of 141 patients. [see figure in the PDf file] 2. The opening snap (OS) was absent in 29% of all patients and in 10% of patients with pure mitral stenosis and noncalcified mitral valve. The most important single factor contributing to the absence of an OS was calcification of the mitral valve. Other factors included young age and associated aortic stenosis or mitral insufficiency. 3. There was no significant correlation between the (Q-1)-(2-OS) interval (PCG index) and the diastolic pressure gradient across mitral valve at rest. The correlation between the PCG index and the calculated mitral valve area (MVA), and the diastolic pressure gradient across the mitral valve during exercise was significant ( P &lt;0.05). 4. The PCG index correctly predicted whether the MVA was smaller or greater than 1.2 cm 2 in 85% of patients with pure mitral stenosis but in only 57% of patients with associated lesions. The MVA was less than 1.2 cm 2 in 36 of 39 patients with pure mitral stenosis in whom the PCG index ranged from +2 to +6. Of 42 operated patients with pure mitral stenosis, the PCG estimate was correct in 36. The PCG index did not underestimate MVA in any of the operated patients. 5. In a group of patients with the same left atrial (LA) pressure, the 2-OS interval was longer in patients with low cardiac output. The relation between the 2-OS interval and the cardiac output could explain in part the lack of correlation between LA pressure and 2-OS interval and the smaller number of correct estimates of MVA made by the 2-OS interval as compared to the Q-1 interval and the PCG index. 6. There was no significant correlation between the amplitude of the first sound at the apex and the severity of mitral stenosis. Several patients with associated mitral insufficiency had a first sound of high amplitude. 7. There was no significant correlation between the amplitude of the sound of pulmonary valve closure (P 2 ) and the pulmonary artery pressure. P 2 amplitude was significantly greater in slender patients. 8. An apical systolic murmur was recorded in 48% of patients with pure mitral stenosis. The longer the murmur, the greater was the likelihood of associated mitral insufficiency. A pansystolic murmur at the apex usually indicated an associated mitral or tricuspid insufficiency.
Physiogenomic resources for rat models of heart, lung and blood disorders
Authors: Renae L Malek, Hong-ying Wang, Anne E Kwitek, Andrew S Greene, Nirmal Bhagabati, Gretta Borchardt, Lisa Cahill, Tracey Currier, Bryan Frank, Xianping Fu, Michael Hasinoff, Eleanor Howe, Noah Letwin, Truong V Luu, Alexander Saeed, Hedieh Sajadi, Steven L Salzberg, Razvan Sultana, Mathangi Thiagarajan, Jennifer Tsai, Kathleen Veratti, Joseph White, John Quackenbush, Howard J Jacob, Norman H Lee
Journal: Nature Genetics (2006)
Role of Serial Plasma C.E.A. Assays in Detection of Recurrent and Metastatic Colorectal Carcinomas
Authors: A. M. Mackay, S. Patel, S. Carter, U. Stevens, D. J. R. Laurence, E. H. Cooper, A. M. Neville
Journal: BMJ (1974)

Serial estimations of plasma carcinoembryonic antigen (C.E.A.) levels have been carried out in 220 patients with colorectal carcinomas who had potentially and apparently curative surgery. In a two-year follow-up period 53 patients developed recurrences or metastases. In 36 of these patients sustained rises in plasma C.E.A. titres occurred synchronously with or between three and 18 months before the clinical detection of recurrences or metastases. The use of serial plasma C.E.A. assays is therefore recommended as an additional diagnostic aid for the earlier detection of recurrent or metastatic colorectal carcinomas.
Effect of Breast Milk Lead on Infant Blood Lead Levels at 1 Month of Age
Authors: Adrienne S. Ettinger, Martha María Téllez-Rojo, Chitra Amarasiriwardena, David Bellinger, Karen Peterson, Joel Schwartz, Howard Hu, Mauricio Hernández-Avila
Journal: Environmental Health Perspectives (2004)

Nursing infants may be exposed to lead from breast milk, but relatively few data exist with which to evaluate and quantify this relationship. This route of exposure constitutes a potential infant hazard from mothers with current ongoing exposure to lead as well as from mothers who have been exposed previously due to the redistribution of cumulative maternal bone lead stores. We studied the relationship between maternal breast milk lead and infant blood lead levels among 255 mother–infant pairs exclusively or partially breast-feeding through 1 month of age in Mexico City. A rigorous, well-validated technique was used to collect, prepare, and analyze the samples of breast milk to minimize the potential for environmental contamination and maximize the percent recovery of lead. Umbilical cord and maternal blood lead were measured at delivery; 1 month after delivery (± 5 days) maternal blood, bone, and breast milk and infant blood lead levels were obtained. Levels of lead at 1 month postpartum were, for breast milk, 0.3–8.0 μg/L (mean ± SD, 1.5 ± 1.2); maternal blood lead, 2.9–29.9 μg/dL (mean ± SD, 9.4 ± 4.5); and infant blood lead, 1.0–23.1 μg/dL (mean ± SD, 5.5 ± 3.0). Infant blood lead at 1 month postpartum was significantly correlated with umbilical cord (Spearman correlation coefficient rS = 0.40, p < 0.0001) and maternal (rS = 0.42, p < 0.0001) blood lead at delivery and with maternal blood (rS = 0.67, p < 0.0001), patella (rS = 0.19, p = 0.004), and breast milk (rS = 0.32, p < 0.0001) lead at 1 month postpartum. Adjusting for cord blood lead, infant weight change, and reported breast-feeding status, a difference of approximately 2 μg/L (ppb; from the midpoint of the lowest quartile to the midpoint of the highest quartile) breast milk lead was associated with a 0.82 μg/dL increase in blood lead for breast-feeding infants at 1 month of age. Breast milk lead accounted for 12% of the variance of infant blood lead levels, whereas maternal blood lead accounted for 30%. Although these levels of lead in breast milk were low, they clearly have a strong influence on infant blood lead levels over and above the influence of maternal blood lead. Additional information on the lead content of dietary alternatives and interactions with other nutritional factors should be considered. However, because human milk is the best and most complete nutritional source for young infants, breast-feeding should be encouraged because the absolute values of the effects are small within this range of lead concentrations.
Brain Infarction and Blood Pressure
Authors: Zenonas Danilevicius
Journal: JAMA (1976)

The Framingham Study taught us much about cardiovascular disease in man. Another interesting aspect of this study was recently brought to the attention of physicians by Kannel et al.<sup>1</sup>They studied the evolution of atherothrombotic brain infarction in a cohort of 5,209 men and women over a period of 18 years. The results ascertained that hypertension was the most common and most powerful precursor of brain infarction. The authors also compared the influence of the various components of blood pressure on the development of brain infarction. They evaluated the influence of systolic and diastolic pulse, mean arterial pressure, tension-time index, and lability or stability of pressure. In fact, all of these components were associated with the incidence of brain infarction; however, systolic pressure alone emerged as the best indicator of brain infarction risk. Of 105 infarctions diagnosed during the follow-up of 18 years, only ten occurred in normotensive persons.
Treatment of the Antiphospholipid Syndrome
Authors: Michael D. Lockshin, Doruk Erkan
Journal: New England Journal of Medicine (2003)

Two decades after the presence of anticardiolipin antibodies and a syndrome of spontaneous thrombosis and fetal death were linked,1 and after the publication of approximately 3500 reports in which the term "antiphospholipid syndrome" has been used, we still lack scientifically robust, evidence-based rules for the treatment of the antiphospholipid syndrome. This failure is due in part to a lack of well-designed prospective studies and in part to the clinical complexity of the syndrome. The complexity stems in part from the fact that the antiphospholipid syndrome actually comprises two syndromes, one that is not associated with another illness (primary antiphospholipid syndrome), . . .
Bacterial translocation in acute liver injury induced byD- galactosamine
Authors: F B Kasravi, L Wang, X Wang, G Molin, S Bengmark, B Jeppsson
Journal: Hepatology (1996)

Acute liver injury is associated with a high rate of infectious and septic complications. Most of these infections are produced by gram negative enteric bacteria. We evaluated bacterial translocation, intestinal permeability, blood flow, portal pressure, and intestinal microflora after induction of liver injury and 70% liver resection in the rat. The rate of translocation to both portal and arterial blood was 100% at 24 hours and 50% at 48 hours after liver resection compared with 83% to portal vein and 50% to aortic blood at both time points after acute liver injury. Translocation to intraabdominal organs (liver, spleen, and mesenteric lymph nodes) was 100% in both groups at both 24 and 48 hours. The rate of translocation increased after liver injury at 48 hours with progression of the liver injury but was decreased in the 70% liver resection group with improvement of liver function. “Total aerobic” and “total anaerobic” bacterial counts in small intestine and cecum were not affected. Pulmonary, distal small intestine, and cecal blood flow were decreased in both groups, whereas blood flow in the proximal small intestine was unaffected. Portal pressure and flow were increased after 70% liver resection, but they were decreased in acute liver injury. After acute liver injury, permeability of both distal small intestine and cecum increased, but after liver resection only cecal permeability increased. The results of this experiment show that bacterial translocation occurs in experimental acute liver injury and that its dynamic, pattern and fate are different from that observed after liver resection, which is a reversible surgical model of liver insufficiency.
Prevention of Cyclical Attacks of Acute Intermittent Porphyria with a Long-Acting Agonist of Luteinizing Hormone–Releasing Hormone
Authors: Karl E. Anderson, Irving M. Spitz, Shigeru Sassa, C. Wayne Bardin, Attallah Kappas
Journal: New England Journal of Medicine (1984)

THE genetic disease acute intermittent porphyria may be exacerbated by a number of factors that are distinct from the inherited deficiency of the heme pathway enzyme, porphobilinogen deaminase (also known as uroporphyrinogen I synthase). These factors include endogenous steroid hormones and their metabolites, drugs, and nutrition.1 2 3 4 5 In some women with acute intermittent porphyria, exacerbations of symptoms occur in relation to the menstrual cycle, and in a minority, disabling premenstrual attacks occur regularly with every cycle.1 , 2 , 5 6 7 8 9 We report on a patient in whom premenstrual exacerbations of acute intermittent porphyria, which had previously occurred every month for at least two years, were . . .
Milk Has Something for Every Body?
Authors: Laurence M. Hursh
Journal: JAMA (1975)

GENERALLY speaking, milk is an exemplary food, one that offers a wide variety of needed nutrients. Moreover, milk offers them at a reasonable calorie level, with pleasing taste and convenience. But! "Milk has something for<i>every</i>body"? One can really quarrel with the implication that<i>milk</i>is<i>good</i>for<i>every</i>one of us. An earlier milk advertising slogan was even worse: "Every Body Needs Milk!" This simply isn't so—although it is true that all of us need certain amounts of most of the nutrients in milk. However, we do not require the cholesterol in milk since we synthesize cholesterol, and many other foods in our diet contain more cholesterol than milk does. Nor do we need the specific kind of fat in milk, because we eat many foods with similar fat components. Yet milk contains a more versatile array of nutrients than most single foods. Thus, milk is one of
Guggulipid for the Treatment of Hypercholesterolemia
Authors: Philippe O. Szapary, Megan L. Wolfe, LeAnne T. Bloedon, Andrew J. Cucchiara, Ara H. DerMarderosian, Michael D. Cirigliano, Daniel J. Rader
Journal: JAMA (2003)

ContextHerbal extracts from Commiphora mukul (guggul) have been widely used in Asia as cholesterol-lowering agents, and their popularity is increasing in the United States. Recently, guggulsterones, the purported bioactive compounds of guggul, have been shown to be potent antagonists of 2 nuclear hormone receptors involved in cholesterol metabolism, establishing a plausible mechanism of action for the hypolipidemic effects of these extracts. However, there are currently no published safety or efficacy data on the use of guggul extracts in Western populations.ObjectiveTo study the short-term safety and efficacy of 2 doses of a standardized guggul extract (guggulipid, containing 2.5% guggulsterones) in healthy adults with hyperlipidemia eating a typical Western diet.DesignDouble-blind, randomized, placebo-controlled trial using a parallel design, conducted March 2000-August 2001.Participants and SettingA total of 103 ambulatory, community-dwelling, healthy adults with hypercholesterolemia in the Philadelphia, Pa, metropolitan area.InterventionOral, 3 times daily doses of standard-dose guggulipid (1000 mg), high-dose guggulipid (2000 mg), or matching placebo.Main Outcome MeasuresPercentage change in levels of directly measured low-density lipoprotein cholesterol (LDL-C) after 8 weeks of therapy. Secondary outcome measures included levels of total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglycerides, and directly measured very low-density lipoprotein cholesterol (VLDL-C), as well as adverse events reports and laboratory safety measures including electrolyte levels and hepatic and renal function.ResultsCompared with participants randomized to placebo (n = 36), in whom levels of LDL-C decreased by 5%, both standard-dose guggulipid (n = 33) and high-dose guggulipid (n = 34) raised levels of LDL-C by 4% (P = .01 vs placebo) and 5% (P = .006 vs placebo), respectively, at 8 weeks, for a net positive change of 9% to 10%. There were no significant changes in levels of total cholesterol, HDL-C, triglycerides, or VLDL-C in response to treatment with guggulipid in the intention-to-treat analysis. While guggulipid was generally well tolerated, 6 participants treated with guggulipid developed a hypersensitivity rash compared with none in the placebo group.ConclusionsDespite plausible mechanisms of action, guggulipid did not appear to improve levels of serum cholesterol over the short term in this population of adults with hypercholesterolemia, and might in fact raise levels of LDL-C. Guggulipid also appeared to cause a dermatologic hypersensitivity reaction in some patients.
Abstract 397: Increased Rho GTPase and reduced glycolysis activity in metastatic cancer cells.
Authors: Pei-Fen Su, Shu-Hao Chang, Chia-Hsin Ho, Wei-Li Huang
Journal: Cancer Research (2013)

Abstract Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer in the world. Metastases are resistant to conventional therapies and are responsible for 90% of tumour-related death. Better understanding on the molecular mechanism of metastasis may shed light on prevention and treatment of disease. We have established a systemic cellular model for metastases investigation. The parental SAS cells, a low tumorigenic HNSCC cell line; SASVO3 (VO3) cells, a highly tumorigenic cells derived from SAS; and SASVO3M-1 (M1) and SASVO3M-5 (M5) cells, two lines of pulmonary metastatic cells derived from SASVO3 cells using mice model. Transcriptome analysis revealed that M1 and M5 shared the most similar transcription signature and their common genes were designated common M. The profiles of VO3 and common M were distinct from that of parental SAS. Biological pathway analyses showed the signaling of cell movement such as integrin, RhoA, Cdc42, Rac, and actin polymerization were identified in metastatic cells. Of oncogenic properties, metastatic cells possess increased activities of foci formation, filopodia formation, wound healing, and in vivo pulmonary metastases. Interestingly, metabolism assay revealed that the glycolysis activity was increased in highly tumorigenic VO3 cells compare to parental SAS. Yet it was decreased in metastatic M5 cells compared to VO3 cells. “Reverse Warburg effect," which indicating a lowered glycolysis in tumor cells, has been demonstrated by others in metastatic breast cancer by in situ immunohistochemistry stain. The correlation of metabolism and metastasis of HNSCC cells will be discussed. Citation Format: Pei-Fen Su, Shu-Hao Chang, Chia-Hsin Ho, Wei-Li Huang. Increased Rho GTPase and reduced glycolysis activity in metastatic cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 397. doi:10.1158/1538-7445.AM2013-397
Abstract A37: Mechanistic study involving antiproliferative effect of Etoricoxib, a highly selective COX-2 inhibitor on human cancer cell lines
Authors: Shweta Tripathi, Sudhir Chandna, B.S. Dwarkanath, Daman Saluja, Madhu Chopra
Journal: Cancer Research (2009)

Abstract Introduction: Cyclooxygenase (COX), also known as prostaglandin endoperoxidase or prostaglandin G/H synthase, is a rate limiting enzyme involved in the conversion of arachidonic acid to prostaglandins. Two forms of cyclooxygenase, COX-1 and COX-2, have been identified. COX-1 is constitutively expressed in many tissues, while COX-2 is an inducible enzyme involved in inhibition of apoptosis, potentiation of cell growth and angiogenesis and as such is a target for drug development. Recently clinical, cellular and animal experimental studies have indicated its relevance to tumor invasion and metastasis. Etoricoxib is a novel non-steroidal anti-inflammatory drug (NSAIDs) that stops the production of inflammatory prostaglandins, without stopping the production of prostaglandins that protect the stomach and intestine. There is persuasive evidence that COX-2 inhibitors suppress tumor growth due to their ability to inhibit cell proliferation and induce apoptosis. The purpose of this study was to elucidate the mechanism of action by which Etoricoxib induces the arrest of Human cervical tumor cells growth. Methods: Cell viability was measured by MTT assay and trypan blue exclusion method. Apoptosis was examined by DNA fragmentation and Comet Assay and the distribution of cells in the cell cycle was estimated by flow cytometry. Western blotting was used to explore various mechanisms of Etoricoxib induced apoptosis. Results: Etoricoxib in the concentration range of 100–200 µM was 2–3 fold more cytotoxic (MTT assay) in the tumorigenic cell lines HeLa (cervical COX-2 positive), C-33A (cervical COX-2 negative), U-87, MCF-7, Hep3B, MiaPaCa-2 as compared to the non-tumorigenic cell lines (Cos-7, NIH3T3, HEK). These results correlated well with the observations on inhibition of cell growth and were comparable to the results reported for Celecoxib, another COX-2 selective inhibitor. Interestingly, Methotrexate widely used anticancer agent, showed 70–80% cytotoxicity in the non tumorigenic cell lines as compared to only 20% cytotoxicity with etoricoxib, suggesting thereby that it is selectively toxic to tumor cells unlike many other anticancer drugs. Comet assay results in HeLa cells showed a dose and time dependent increase in DNA damage suggestive of drug induced DNA damage at early times, followed by apoptotic DNA fragmentation and necrotic DNA degradation at later times. Western blotting results confirms the downregulation of the NF-κB pathway. In conclusion this study shows that in the human cervical cancer cell lines, HeLa &amp; C33A, Etoricoxib suppresses proliferation, induces apoptosis and causes cell death by DNA damage in both Cox-2 dependent as well as independent pathway. Citation Information: Cancer Res 2009;69(23 Suppl):A37.
Thrombolytic therapy causes an increase in vascular permeability that is reversed by 1-deamino-8-D-vasopressin.
Authors: M A Rudd, M T Johnstone, L E Rabbani, D George, J A Ware, J Loscalzo
Journal: Circulation (1991)

BACKGROUND To examine the effect of plasminogen activator therapy on vascular permeability, we used a modified rabbit mesenteric model of extravascular tissue accumulation of radiolabeled albumin. METHODS AND RESULTS Albumin deposition was measured after saline, tissue-type plasminogen activator (t-PA; 0.86 mg/kg for 1 hour followed by 0.29 mg/kg for 2 hours), or t-PA plus 1-deamino-8-D-arginine vasopressin (DDAVP; 0.6 mg/kg/hr for 30 minutes) infusion in animals with or without aspirin (ASA; 15-mg/kg bolus) pretreatment. In animals not given ASA, t-PA caused a 240% increase in tissue [125I]albumin accumulation over time (p less than 0.001). DDAVP prevented the rise in albumin accumulation normally seen with t-PA alone (p less than 0.05) in animals not given ASA. In animals pretreated with ASA, t-PA similarly caused an increase in tissue albumin accumulation, but this was significantly attenuated from that of animals not given ASA (p less than 0.03). Interestingly, DDAVP failed to block the response to t-PA in the animals given ASA. Because increases in vascular permeability correlated with increases in bleeding time (r = 0.37, p less than 0.03), these data suggest that the effect of plasmin generation on vascular permeability may contribute to the bleeding tendency seen with thrombolytic therapy. The ability of DDAVP to reverse the bleeding tendency and bleeding time may be due in part to its reversal of the increased vascular permeability induced by the administration of plasminogen activators. CONCLUSIONS These data show that plasminogen activation causes an increase in vascular permeability that is inhibited by DDAVP; ASA blunts this action of t-PA and prevents the DDAVP blockade of the increase in permeability induced by t-PA in this rabbit model.
LONG-TERM OUTCOME OF BARE METAL STENT VS. DRUG-ELUTING STENT IMPLANTATION IN OCTOGENARIANS
Authors: Junya Matsumi, Shigeru Saito, Junko Honne, Satoshi Takeshita, Shinji Tanaka, Saeko Takahashi, Yutaka Tanaka, Hidetaka Suenaga, Shingo Mizuno, Nobuhiro Okamura, Kazuya Sugitatsu, Takuya Izumikawa, Kouki Shishido
Journal: Journal of the American College of Cardiology (2010)