tbuckley/cabot-search huggingface dataset:
Carbon Dioxide–Rich Water Bathing Enhances Collateral Blood Flow in Ischemic Hindlimb via Mobilization of Endothelial Progenitor Cells and Activation of NO-cGMP System
Authors: Hidekazu Irie, Tetsuya Tatsumi, Mitsutaka Takamiya, Kan Zen, Tomosaburo Takahashi, Akihiro Azuma, Kento Tateishi, Tetsuya Nomura, Hironori Hayashi, Norio Nakajima, Mitsuhiko Okigaki, Hiroaki Matsubara
Journal: Circulation (2005)

Background— Carbon dioxide–rich water bathing has the effect of vasodilatation, whereas it remains undetermined whether this therapy exerts an angiogenic action associated with new vessel formation. Methods and Results— Unilateral hindlimb ischemia was induced by resecting the femoral arteries of C57BL/J mice. Lower limbs were immersed in CO 2 -enriched water (CO 2 concentration, 1000 to 1200 mg/L) or freshwater (control) at 37°C for 10 minutes once a day. Laser Doppler imaging revealed increased blood perfusion in ischemic limbs of CO 2 bathing (38% increase at day 28, P &lt;0.001), whereas N G -nitro- l -arginine methyl ester treatment abolished this effect. Angiography or immunohistochemistry revealed that collateral vessel formation and capillary densities were increased (4.1-fold and 3.7-fold, P &lt;0.001, respectively). Plasma vascular endothelial growth factor (VEGF) levels were elevated at day 14 (18%, P &lt;0.05). VEGF mRNA levels, phosphorylation of NO synthase, and cGMP accumulation in the CO 2 -bathed hindlimb muscles were increased (2.7-fold, 2.4-fold, and 3.4-fold, respectively) but not in forelimb muscles. The number of circulating Lin−/Flk-1+/CD34− endothelial-lineage progenitor cells was markedly increased by CO 2 bathing (24-fold at day 14, P &lt;0.001). The Lin−/Flk-1+/CD34− cells express other endothelial antigens (endoglin and VE-cadherin) and incorporated acetylated LDL. Conclusions— Our present study demonstrates that CO 2 bathing of ischemic hindlimb causes the induction of local VEGF synthesis, resulting in an NO-dependent neocapillary formation associated with mobilization of endothelial progenitor cells.
Sphingosine 1-phosphate promotes endothelial cell barrier integrity by Edg-dependent cytoskeletal rearrangement
Authors: Joe G.N. Garcia, Feng Liu, Alexander D. Verin, Anna Birukova, Melissa A. Dechert, William T. Gerthoffer, James R. Bamberg, Denis English
Journal: Journal of Clinical Investigation (2001)

Substances released by platelets during blood clotting are essential participants in events that link hemostasis and angiogenesis and ensure adequate wound healing and tissue injury repair. We assessed the participation of sphingosine 1-phosphate (Sph-1-P), a biologically active phosphorylated lipid growth factor released from activated platelets, in the regulation of endothelial monolayer barrier integrity, which is key to both angiogenesis and vascular homeostasis. Sph-1-P produced rapid, sustained, and dose-dependent increases in transmonolayer electrical resistance (TER) across both human and bovine pulmonary artery and lung microvascular endothelial cells. This substance also reversed barrier dysfunction elicited by the edemagenic agent thrombin. Sph-1-P–mediated barrier enhancement was dependent upon Giα-receptor coupling to specific members of the endothelial differentiation gene (Edg) family of receptors (Edg-1 and Edg-3), Rho kinase and tyrosine kinase-dependent activation, and actin filament rearrangement. Sph-1-P–enhanced TER occurred in conjunction with Rac GTPase- and p21-associated kinase–dependent endothelial cortical actin assembly with recruitment of the actin filament regulatory protein, cofilin. Platelet-released Sph-1-P, linked to Rac- and Rho-dependent cytoskeletal rearrangement, may act late in angiogenesis to stabilize newly formed vessels, which often display abnormally increased vascular permeability.
Ocular blunt trauma: loss of sight from an ice hockey injury * Commentary * Commentary
Authors: D S Morris
Journal: British Journal of Sports Medicine (2006)

A case of ocular blunt trauma is described in which a 17 year old male ice hockey player collided with an opponent during a game. The opponent’s stick travelled under the patient’s half face visor and struck his left eye causing hyphema, angle recession, lens subluxation, and choroidal rupture over the macula, permanently reducing his vision to counting fingers. Sequelae of ocular blunt trauma are discussed along with methods of injury prevention by addressing players’ behaviour and safety equipment. This injury is unlikely to have occurred with properly used full face protection.
Proliferation and glycosaminoglycans secretion in fibroblasts from psoriatic skin: differential responses to retinoids
Authors: G.C. PRIESTLEY
Journal: British Journal of Dermatology (1987)

The effects of four retinoids, all-trans-retinoic acid (tretinoin), 13-cis-retinoic acid (isotretinoin), Ro 10–1670 (etrctin) and the arotinoid, Ro 15–0778, on fibroblast proliferation and glycosaminoglycans (GAG) secretion in vitro were studied. Fibroblast lines cultured from normal skin (HSF) were compared with those from lesional (PSA) and non-lesional (PSB) psoriatic skin. In general, the retinoids inhibited proliferation; the action was cytostatic, in rank order tretinoin > isotretinoin > etretin > arotinoid. The psoriatic cells tended to be more sensitive than the HSF lines, overall mean proliferation values (± SEM), as a percentage of untreated controls being: HSF 72 ± 3, PSA 61 ± 3 and PSB 54 ± 3. Stimulation of GAG secretion at low concentrations (IO-7M) of all four retinoids, declined as concentrations increased, and secretion was inhibited at IO-7M) in PSB fibroblasts. Calculation of effects on GAG secretion due to changes in cell density confirmed the rank order for direct stimulation of secretion as arotinoid > etretin > isotretinoin > tretinoin. Electrophoresis of [3H]-labelled glycosaminoglycans secreted in the presence of 10-7M arotinoid showed that it was predominantly hyaluronic acid, as in untreated cells. These data confirm that different retinoids have contrasting levels of effects on mesenchymal cells and suggest a greater sensitivity to drugs in fibroblasts from psoriatic skin.
Ferrokinetic study of splenic erythropoiesis: Relationships among clinical diagnosis, myelofibrosis, splenomegaly, and extramedullary erythropoiesis
Authors: Yves Beguin, Georges Fillet, Jean Bury, Yvette Fairon
Journal: American Journal of Hematology (1989)

Splenic erythropoiesis was demonstrated by surface counting of 59Fe in 129 of 1,350 ferrokinetic studies performed over a 15 year period. These 129 studies were carried out in 108 patients, including 40 with chronic myelogenous leukemia (CML), 24 with agnogenic myeloid metaplasia (AMM), 18 with polycythemia vera (PV), six with a myelodysplastic syndrome, five with acute leukemia, three with prostate or breast carcinoma, two each with aplastic anemia or Hodgkin's disease, and one each with idiopathic thrombocythemia, multiple myeloma, chronic renal failure, or treated hypopituitarism. Splenomegaly was present in 83% of the studies and hepatomegaly in 72%. Grade II-III myelofibrosis was demonstrated in 62% of the cases. Hepatic erythropoiesis was present in 77% of the studies (only 38% in PV), and marrow erythropoiesis was undetectable in 33%. Total erythropoiesis was about twice normal (range 0.2 to 8 times normal) but was ineffective to varying degrees in 86% of the studies. Relationships between organomegaly, myelofibrosis, and extramedullary erythropoiesis, as well as differences among clinical disorders, are discussed. Differences observed between CML in chronic or blastic phase suggested that the erythroid cell line was involved in the proliferative process. It is concluded that splenic erythropoiesis 1) is encountered in a variety of clinical conditions; 2) is not necessarily associated with splenomegaly or myelofibrosis, even in the myeloproliferative disorders; 3) is part of a predominantly extramedullary (in the liver as well as in the spleen), expanded, and largely inefficient total erythropoiesis; and 4) can be evaluated in a semiquantitative manner by surface counting.
Stem cell factor stimulates neurogenesis in vitro and in vivo
Authors: Kunlin Jin, Xiao Ou Mao, Yunjuan Sun, Lin Xie, David A. Greenberg
Journal: Journal of Clinical Investigation (2002)

Cerebral ischemia stimulates neurogenesis in proliferative zones of the rodent forebrain. To identify the signaling factors involved, cerebral cortical cultures prepared from embryonic mouse brains were deprived of oxygen. Hypoxia increased bromodeoxyuridine (BrdU) incorporation into cells that expressed proliferation markers and immature neuronal markers and that lacked evidence of DNA damage or caspase-3 activation. Hypoxia-conditioned medium and stem cell factor (SCF), which was present in hypoxia-conditioned medium at increased levels, also stimulated BrdU incorporation into normoxic cultures. The SCF receptor, c-kit, was expressed in neuronal cultures and in neuroproliferative zones of the adult rat brain, and in vivo administration of SCF increased BrdU labeling of immature neurons in these regions. Cerebral hypoxia and ischemia may stimulate neurogenesis through trophic factors, including SCF.
Apoptosis and colorectal cancer
Authors: A J M Watson
Journal: Gut (2004)

c Important effector mechanism in the immune system c Activated by the binding of ligands to ''death receptors'' such as FasR c Type 1 cells (for example, thymocytes) not regulated by Bcl-2 c Type 2 cells (for example, hepatocytes) regulated by Bcl-2 c Initiator caspase-caspase 8 1702
Immunotherapy response assessment in neuro-oncology: a report of the RANO working group
Authors: Hideho Okada, Michael Weller, Raymond Huang, Gaetano Finocchiaro, Mark R Gilbert, Wolfgang Wick, Benjamin M Ellingson, Naoya Hashimoto, Ian F Pollack, Alba A Brandes, Enrico Franceschi, Christel Herold-Mende, Lakshmi Nayak, Ashok Panigrahy, Whitney B Pope, Robert Prins, John H Sampson, Patrick Y Wen, David A Reardon
Journal: The Lancet Oncology (2015)
Serum myoglobin and creatine kinase concentrations in patients with polymyositis or dermatomyositis.
Authors: J C Borleffs, R H Derksen, D P Bar
Journal: Annals of the Rheumatic Diseases (1987)

Serum myoglobin and creatine kinase concentrations in patients with polymyositis or dermatomyositis SIR, Measurement of serum creatine kinase is an accepted procedure in the follow up of patients with polymyositis or dermatomyositis.This parameter is nearly always raised at some point in the illness, and serves as a useful guide in making decisions regarding therapy.There are preliminary reports on the importance of determination of serum myoglobin levels in such patients, however, suggesting that changes of myoglobin levels may precede alterations of creatine kinase and clinical features.'Since the assay for measuring myoglobin is time consuming and expensive and requires the use of radioactive isotopes, it was of interest to perform a prospective study dealing with the possible differences of myoglobin and creatine kinase levels in patients with polymyositis or dermatomyositis and their relevance to the clinical situation.Eight patients (one male, seven female) entered this study and were followed up for a mean period of 80 weeks (range 23-121 weeks).Five of them had definite poly- myositis group I, the others definite dermatomyositis group II, according to the classification of Bohan and Peter.2In all patients the diagnosis was confirmed by
Calcium-Sensing Receptor Expression and Parathyroid Hormone Secretion in Hyperplastic Parathyroid Glands from Humans
Authors: Sagrario Can[Combining Tilde]adillas, Antonio Canalejo, Rafael Santamaría, Maria E. Rodríguez, Jose C. Estepa, Alejandro Martín-Malo, Juan Bravo, Blanca Ramos, Escolastico Aguilera-Tejero, Mariano Rodríguez, Yolanda Almadén
Journal: Journal of the American Society of Nephrology (2005)

In uremic patients, severe parathyroid hyperplasia is associated with reduced parathyroid calcium-sensing receptor (CaR) expression. Thus, in these patients, a high serum Ca concentration may be required to inhibit parathyroid hormone (PTH) secretion. This study compares the magnitude of reduction in CaR expression and the degree of the abnormality in Ca-regulated PTH release in vitro. A total of 50 glands from 23 hemodialysis patients with refractory hyperparathyroidism were studied. Tissue slices were incubated in vitro to evaluate (1) the PTH secretory output in a normal Ca concentration (1.25 mM) and (2) the PTH secretory response to high (1.5 mM) and low (0.6 mM) Ca concentration. Tissue aliquots were processed for determination of CaRmRNA expression. The results showed that, corrected for DNA, parathyroid tissue with lowest CaR expression secreted more PTH than that with relatively high CaR expression (146 +/- 23 versus 60 +/- 2 pg/microg DNA; P < 0.01). Furthermore, glands with low CaR expression demonstrated a blunted PTH secretory response to both the inhibitory effect of high Ca and the stimulatory effect of low Ca. The study also showed that the larger the gland, the lower the CaRmRNA expression. Thus, large parathyroid glands produce a large amount of PTH not only as a result of the increased gland size but also because the parathyroid tissue secretory output is increased. These abnormalities in PTH regulation are related to low CaR expression.
Glioblastoma: Molecular Analysis and Clinical Implications
Authors: Jason T. Huse, Eric Holland, Lisa M. DeAngelis
Journal: Annual Review of Medicine (2012)

Glioblastoma, the most common malignant primary brain tumor, carries an invariably poor prognosis. Targeting underlying biological foundations of the disease will be crucial to developing more effective treatment strategies. Although increasing evidence clearly indicates that glioblastoma is a molecularly heterogeneous disorder, recent large-scale expression profiling has provided a framework for categorizing the tumor into 3 to 4 distinct subclasses, each with its own characteristic genomic alterations. As such, there remains the enticing possibility that glioblastoma subclasses themselves might represent predictive biomarkers, particularly in the context of specific targeted agents. This review focuses on how best to ascertain the functional relevance of molecular subclass in glioblastoma through both preclinical and clinical investigations. The availability of appropriate mouse modeling systems along with expanded molecular profiling capabilities in the clinical setting should aid such efforts. However, significant systematic challenges remain, particularly in the setting of clinical trials.
Global Impairment of CD4<sup>+</sup>CD25<sup>+</sup>FOXP3<sup>+</sup>Regulatory T Cells in Idiopathic Pulmonary Fibrosis
Authors: Ioannis Kotsianidis, Evangelia Nakou, Irene Bouchliou, Argyrios Tzouvelekis, Emmanouil Spanoudakis, Paschalis Steiropoulos, Ioannis Sotiriou, Vassilis Aidinis, Dimitrios Margaritis, Costas Tsatalas, Demosthenes Bouros
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

The implication of T cells in the pathogenesis of idiopathic pulmonary fibrosis (IPF) is controversial. CD4(+)CD25(+)FOXP3(+) regulatory T cells (Tregs) are pivotal in maintaining immune homeostasis, but their role in IPF pathophysiology has not yet been studied.To explore Treg dynamics and function in IPF.Treg levels and dynamics were analyzed by flow cytometry in the peripheral blood (PB) and bronchoalveolar lavage (BAL) of 21 patients with IPF, 35 patients with lung diseases other than IPF (patients without IPF), 20 patients with collagen vascular diseases with pulmonary parenchymal involvement (CVD-IP), and 28 healthy volunteers. The suppression of autologous CD4(+)CD25(-) cell-proliferative responses and cytokine release by magnetic bead-isolated Tregs was evaluated by proliferation assays and cytometric bead array. Correlations of Treg function and levels with lung function parameters were also performed.In patients with IPF, both BAL and PB Tregs were reduced compared with those of healthy volunteers and patients without IPF, although not always significantly. Treg levels were not affected by the administration of low-dose prednisone in four nonresponding patients. The suppressor potential of BAL and PB Tregs was compromised in patients with IPF and patients with CVD-IP, compared with healthy volunteers and patients without IPF. Similarly, the Treg-induced suppression of helper T-cell type 1 and 2 cytokine secretion was impaired in the BAL of patients with IPF and patients with CVD-IP. Moreover, the defective function of BAL Tregs correlated highly with parameters of disease severity.This study provides the first evidence of global Treg impairment in IPF that strongly correlates with disease severity, suggesting a role for Tregs in the fibrotic process.
Venous Thromboembolism and Cancer: Risks and Outcomes
Authors: Agnes Y.Y. Lee, Mark N. Levine
Journal: Circulation (2003)

Cancer and its treatments are well-recognized risk factors for venous thromboembolism (VTE). Evidence suggests that the absolute risk depends on the tumor type, the stage or extent of the cancer, and treatment with antineoplastic agents. Furthermore, age, surgery, immobilization, and other comorbid features will also influence the overall likelihood of thrombotic complications, as they do in patients without cancer. The role of hereditary thrombophilia in patients with cancer and thrombosis is still unclear, and screening for this condition in cancer patients is not indicated. The most common malignancies associated with thrombosis are those of the breast, colon, and lung, reflecting the prevalence of these malignancies in the general population. When adjusted for disease prevalence, the cancers most strongly associated with thrombotic complications are those of the pancreas, ovary, and brain. Idiopathic thrombosis can be the first manifestation of an occult malignancy. However, intensive screening for cancer in patients with VTE often does not improve survival and is not generally warranted. Independently of the timing of cancer diagnosis (before or after the VTE), the life expectancy of cancer patients with VTE is relatively short, because of both deaths from recurrent VTE and the cancer itself. Patients with cancer and acute VTE who take anticoagulants for an extended period are at increased risk of recurrent VTE and bleeding. A recent randomized trial, the Randomized Comparison of Low Molecular Weight Heparin versus Oral Anticoagulant Therapy for Long-Term Anticoagulation in Cancer Patients with Venous Thromboembolism (CLOT) study, showed that low molecular weight heparin may be a better treatment option for this group of patients. The antineoplastic effects of anticoagulants are being actively investigated with promising preliminary results.
Post-cataract Prevention of Inflammation and Macular Edema by Steroid and Nonsteroidal Anti-inflammatory Eye Drops
Authors: Line Kessel, Britta Tendal, Karsten Juhl Jørgensen, Ditte Erngaard, Per Flesner, Jens Lundgaard Andresen, Jesper Hjortdal
Journal: Ophthalmology (2014)

Favorable outcome after cataract surgery depends on proper control of the inflammatory response induced by cataract surgery. Pseudophakic cystoid macular edema is an important cause of visual decline after uncomplicated cataract surgery.We compared the efficacy of topical steroids with topical nonsteroidal anti-inflammatory drugs (NSAIDs) in controlling inflammation and preventing pseudophakic cystoid macular edema (PCME) after uncomplicated cataract surgery.Patients undergoing uncomplicated surgery for age-related cataract.We performed a systematic literature search in Medline, CINAHL, Cochrane, and EMBASE databases to identify randomized trials published from 1996 onward comparing topical steroids with topical NSAIDs in controlling inflammation and preventing PCME in patients undergoing phacoemulsification with posterior chamber intraocular lens implantation for age-related cataract.Postoperative inflammation and pseudophakic cystoid macular edema.Fifteen randomized trials were identified. Postoperative inflammation was less in patients randomized to NSAIDs. The prevalence of PCME was significantly higher in the steroid group than in the NSAID group: 3.8% versus 25.3% of patients, risk ratio 5.35 (95% confidence interval, 2.94-9.76). There was no statistically significant difference in the number of adverse events in the 2 treatment groups.We found low to moderate quality of evidence that topical NSAIDs are more effective in controlling postoperative inflammation after cataract surgery. We found high-quality evidence that topical NSAIDs are more effective than topical steroids in preventing PCME. The use of topical NSAIDs was not associated with an increased events. We recommend using topical NSAIDs to prevent inflammation and PCME after routine cataract surgery.
Phase II trial of a paclitaxel and carboplatin combination in Asian patients with metastatic nasopharyngeal carcinoma
Authors: E.-H. Tan, K.S. Khoo, J. Wee, K.W. Fong, K.S. Lee, K.M. Lee, E.T. Chua, T. Tan, H.S. Khoo-Tan, T.L. Yang, E. Au, M. Tao, Y.K. Ong, E.J. Chua
Journal: Annals of Oncology (1999)
Changes in Subcutaneous Fat Cell Volume and Insulin Sensitivity After Weight Loss
Authors: Daniel P. Andersson, Daniel Eriksson Hogling, Anders Thorell, Eva Toft, Veronica Qvisth, Erik Näslund, Anders Thörne, Mikael Wirén, Patrik Löfgren, Johan Hoffstedt, Ingrid Dahlman, Niklas Mejhert, Mikael Rydén, Erik Arner, Peter Arner
Journal: Diabetes Care (2014)

OBJECTIVE Large subcutaneous fat cells associate with insulin resistance and high risk of developing type 2 diabetes. We investigated if changes in fat cell volume and fat mass correlate with improvements in the metabolic risk profile after bariatric surgery in obese patients. RESEARCH DESIGN AND METHODS Fat cell volume and number were measured in abdominal subcutaneous adipose tissue in 62 obese women before and 2 years after Roux-en-Y gastric bypass (RYGB). Regional body fat mass by dual-energy X-ray absorptiometry; insulin sensitivity by hyperinsulinemic-euglycemic clamp; and plasma glucose, insulin, and lipid profile were assessed. RESULTS RYGB decreased body weight by 33%, which was accompanied by decreased adipocyte volume but not number. Fat mass in the measured regions decreased and all metabolic parameters were improved after RYGB (P &amp;lt; 0.0001). Whereas reduced subcutaneous fat cell size correlated strongly with improved insulin sensitivity (P = 0.0057), regional changes in fat mass did not, except for a weak correlation between changes in visceral fat mass and insulin sensitivity and triglycerides. The curve-linear relationship between fat cell size and fat mass was altered after weight loss (P = 0.03). CONCLUSIONS After bariatric surgery in obese women, a reduction in subcutaneous fat cell volume associates more strongly with improvement of insulin sensitivity than fat mass reduction per se. An altered relationship between adipocyte size and fat mass may be important for improving insulin sensitivity after weight loss. Fat cell size reduction could constitute a target to improve insulin sensitivity.