tbuckley/cabot-search huggingface dataset:
Hemodialysis and Peritoneal Dialysis
Authors: Fabian Termorshuizen, Johanna C. Korevaar, Friedo W. Dekker, Jeannette G. van Manen, Elisabeth W. Boeschoten, Raymond T. Krediet
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. Various studies indicate that fair comparisons of mortality rates between hemodialysis (HD) patients and peritoneal dialysis (PD) patients are difficult because of differences in patient characteristics, because of nonconstant relative risks of death (RR), and because the survival times of patients who switch treatment modalities can be censored in different ways. The differences in mortality rates between HD and PD patients were investigated in an analysis in which these potential sources of bias were taken into account. The Netherlands Cooperative Study on the Adequacy of Dialysis is a multicenter, prospective, observational, cohort study in which new patients with ESRD are monitored until transplantation or death. A multivariate Cox regression analysis was used to analyze the mortality data according to treatment modality (HD, n = 742; PD, n = 480). No statistically significant differences in adjusted mortality rates between HD and PD patients were observed during the first 2 yr of dialysis. In the years thereafter, increases in mortality rates for PD patients and resulting decreases in RR in favor of HD were observed ( e.g. , months 24 to 36, adjusted RR, 0.53; 95% confidence interval, 0.31 to 0.91). This tendency was observed especially among patients ≥60 yr of age and was not influenced by the censoring strategy. These results suggest that long-term use of PD, especially among elderly patients, is associated with increases in mortality rates. Further analyses are required to determine the potential role of dialysis adequacy in the observed long-term differences in mortality rates between HD and PD patients and to establish the possible survival benefits for PD patients who switch to HD in time. E-mail: FTermorshuizen@cs.com
Highly Purified Eicosapentaenoic Acid Increases Interleukin-10 Levels of Peripheral Blood Monocytes in Obese Patients With Dyslipidemia
Authors: Noriko Satoh-Asahara, Akira Shimatsu, Yousuke Sasaki, Hidenori Nakaoka, Akihiro Himeno, Mayu Tochiya, Shigeo Kono, Tomohide Takaya, Koh Ono, Hiromichi Wada, Takayoshi Suganami, Koji Hasegawa, Yoshihiro Ogawa
Journal: Diabetes Care (2012)

It has recently been highlighted that proinflammatory (M1) macrophages predominate over anti-inflammatory (M2) macrophages in obesity, thereby contributing to obesity-induced adipose inflammation and insulin resistance. A recent clinical trial revealed that highly purified eicosapentaenoic acid (EPA) reduces the incidence of major coronary events. In this study, we examined the effect of EPA on M1/M2-like phenotypes of peripheral blood monocytes in obese dyslipidemic patients.Peripheral blood monocytes were prepared from 26 obese patients without and 90 obese patients with dyslipidemia. Of the latter 90 obese patients with dyslipidemia, 82 patients were treated with or without EPA treatment (1.8 g daily) for 3 months.Monocytes in obese patients with dyslipidemia showed a significantly lower expression of interleukin-10 (IL-10), an M2 marker, than those without dyslipidemia. EPA significantly increased serum IL-10 and EPA levels, the EPA/arachidonic acid (AA) ratio, and monocyte IL-10 expression and decreased the pulse wave velocity (PWV), an index of arterial stiffness, compared with the control group. After EPA treatment, the serum EPA/AA ratio was significantly correlated with monocyte IL-10 expression. Only increases in monocyte IL-10 expression and serum adiponectin were independent determinants of a decreased PWV by EPA. Furthermore, EPA significantly increased the expression and secretion of IL-10 in human monocytic THP-1 cells through a peroxisome proliferator-activated receptor (PPAR)γ-dependent pathway.This study is the first to show that EPA increases the monocyte IL-10 expression in parallel with decrease of arterial stiffness, which may contribute to the antiatherogenic effect of EPA in obese dyslipidemic patients.
Cardiovascular Comorbidity and Late Referral Impact Arteriovenous Fistula Survival
Authors: Pietro Ravani, Giuliano Brunori, Salvatore Mandolfo, Giovanni Cancarini, Enrico Imbasciati, Daniele Marcelli, Fabio Malberti
Journal: Journal of the American Society of Nephrology (2004)

ABSTRACT. Autologous arteriovenous fistulas (AVF) have the best 5-yr patency and the lowest complication rate among hemodialysis vascular accesses. However, maturation requirements to optimize survival are unknown. A longitudinal cohort study was conducted to ascertain risk factors for failure, maturation time, and survival of the first AVF. All patients who initiated hemodialysis between January 1, 1997, and December 31, 2002, in three centers were included in this study. Analysis was restricted to patients who received an AVF. Cox regression was used to estimate the association between predictors of interest and primary and secondary AVF survival. Of the 535 patients enrolled (mean age, 66.5 yr; 57.8% male; 26.7% diabetic), 513 (96%) received an AVF. Patients who initiated with catheters (47%) cannulated their AVF earlier (median maturation period, 0.78 versus 1.80 mo; P < 0.001). Median primary and secondary survivals were longer than 50 and 72 mo, respectively. After adjustment for confounding factors, cardiovascular disease (hazard ratio [HR], 1.84; 95% confidence interval [CI], 1.26 to 2.67), utilization earlier than 1 mo after placement (HR, 1.94; 95% CI, 1.34 to 2.82), and referral within 3 mo of dialysis start (HR, 1.55; 95% CI, 1.04 to 2.32) were associated with a reduction in primary AVF survival. Presence of cardiovascular disease (HR, 2.21; 95% CI, 1.38 to 3.55), maturation time <15 d (HR, 2.12; 95% CI, 1.20 to 3.73), and presence of catheters at hemodialysis initiation (HR, 1.79; 95% CI, 1.13 to 2.84) were associated with lower secondary AVF survival. It is concluded that cardiovascular disease, late referral, temporary catheters, and early cannulation are associated with impaired AVF survival. It is recommended that AVF be allowed to mature at least 1 mo before cannulation. E-mail: [email protected]
Mandatory wearing of helmets for elite cyclists: new perspectives in prevention of head injuries
Authors: G Lippi, C Mattiuzzi
Journal: British Journal of Sports Medicine (2004)

If you have a burning desire to respond to a paper published in BJSM, why not make use of our ''rapid response'' option?Log onto our website (www.bjsportmed.com), find the paper that interests you, and send your response via email by clicking on the ''eLetters'' option in the box at the top right hand corner.Providing it isn't libellous or obscene, it will be posted within seven days.You can retrieve it by clicking on ''read eLetters'' on our homepage. Mandatory wearing of helmets for elite cyclists: new perspectives in prevention of head injuriesCycling related injuries, especially those to the head, are common causes of morbidity, death, and disability and could largely be prevented by the proper use of hard shell helmets. 1 2 Unfortunately, obvious evidence is often not acknowledged, and the use of such a valuable preventive measure has been too long ignored.Media coverage of elite competitions, showing most athletes racing without helmets, has unfavourably influenced amateur and young cyclists for a long time.However, owing to the progressive increase in severe and fatal injuries, especially involving elite cyclists, and the evidence that the outcome of most of these tragedies might have been prevented, 1 2 the International Cycling Union announced that, from 5 May 2003, it is mandatory to wear a hard shell helmet in elite men's events for classes 4 and above.This decision was taken in agreement with the Professional Riders Association, who supported the initiative despite some internal differences of opinion.Images transmitted world wide during the 2003 Tour de France, a sporting event second in popularity only to the Olympics, are encouraging, showing all athletes wearing helmets throughout most of the race.This is a valuable message for both amateur cyclists and adolescents, as awareness is often more productive than restrictive measures.In addition, individual persuasion to wear helmets does not have the side effect of reducing the incentive to do cycling.Less cycling, in reaction to restrictive legislation, may counterbalance the beneficial effects on head injury prevention, as regular recreational aerobic activity, such as cycling, has manifest benefits on health, preventing the development of chronic disorders, including atherosclerosis, diabetes, osteoporosis, obesity, depression, and cancer.
Foxo3 is required for the regulation of oxidative stress in erythropoiesis
Authors: Dragan Marinkovic, Xin Zhang, Safak Yalcin, Julia P. Luciano, Carlo Brugnara, Tara Huber, Saghi Ghaffari
Journal: Journal of Clinical Investigation (2007)

Erythroid cells accumulate hemoglobin as they mature and as a result are highly prone to oxidative damage. However, mechanisms of transcriptional control of antioxidant defense in erythroid cells have thus far been poorly characterized. We observed that animals deficient in the forkhead box O3 (Foxo3) transcription factor died rapidly when exposed to erythroid oxidative stress–induced conditions, while wild-type mice showed no decreased viability. In view of this striking finding, we investigated the potential role of Foxo3 in the regulation of ROS in erythropoiesis. Foxo3 expression, nuclear localization, and transcriptional activity were all enhanced during normal erythroid cell maturation. Foxo3-deficient erythrocytes exhibited decreased expression of ROS scavenging enzymes and had a ROS-mediated shortened lifespan and evidence of oxidative damage. Furthermore, loss of Foxo3 induced mitotic arrest in erythroid precursor cells, leading to a significant decrease in the rate of in vivo erythroid maturation. We identified ROS-mediated upregulation of p21CIP1/WAF1/Sdi1 (also known as Cdkn1a) as a major contributor to the interference with cell cycle progression in Foxo3-deficient erythroid precursor cells. These findings establish an essential nonredundant function for Foxo3 in the regulation of oxidative stress, cell cycle, maturation, and lifespan of erythroid cells. These results may have an impact on the understanding of human disorders in which ROS play a role.
Peripheral Serum Thyroxine, Triiodothyronine and Reverse Triiodothyronine Kinetics in the Low Thyroxine State of Acute Nonthyroidal Illnesses
Authors: Elaine M. Kaptein, William J. Robinson, Deborah A. Grieb, John T. Nicoloff
Journal: Journal of Clinical Investigation (1982)

The low thyroxine (T4) state of acute critical nonthyroidal illnesses is characterized by marked decreases in serum total T4 and triiodothyronine (T3) with elevated reverse T3 (rT3) values. To better define the mechanisms responsible for these alterations, serum kinetic disappearance studies of labeled T4, T3, or rT3 were determined in 16 patients with the low T4 state and compared with 27 euthyroid controls and a single subject with near absence of thyroxine-binding globulin. Marked increases in the serum free fractions of T4 (0.070±0.007%, normal [nl] 0.0315±0.0014, P < 0.001), T3 (0.696±0.065%, nl 0.310±0.034, P < 0.001), and rT3 (0.404±0.051%, nl 0.133±0.007, P < 0.001) by equilibrium dialysis were observed indicating impaired serum binding. Noncompartmental analysis of the kinetic data revealed an increased metabolic clearance rate (MCR) of T4 (1.69±0.22 liter/d per m2, nl 0.73±0.05, P < 0.001) and fractional catabolic rate (FCR) (32.8±2.6%, nl 12.0±0.8, P < 0.001), analogous to the euthyroid subject with low thyroxine-binding globulin. However, the reduced rate of T4 exit from the serum (Kii) (15.2±4.6 d−1, nl 28.4±3.9, P < 0.001) indicated an impairment of extravascular T4 binding that exceeded the serum binding defect. This defect did not apparently reduce the availability of T4 to sites of disposal as reflected by the increased fractional disposal rate of T4 (0.101±0.018 d−1, nl 0.021±0.003, P < 0.001). The decreased serum T3 binding was associated with the expected increases in MCR (18.80±2.22 liter/d per m2, nl 13.74±1.30, P < 0.05) and total volume of distribution (26.55±4.80 liter/m2, nl 13.10±2.54, P < 0.01). However, the unaltered Kii suggested an extravascular binding impairment comparable to that found in serum. The decreased T3 production rate (6.34±0.53 μg/d per m2, nl 23.47±2.12, P < 0.005) appeared to result from reduced peripheral T4 to T3 conversion because of decreased 5′-deiodination rather than from a decreased T4 availability. This view was supported by the normality of the rT3 production rate. The normal Kii values for rT3 indicated a comparable defect in serum and extravascular rT3 binding. The reduced MCR (25.05±6.03 liter/d per m2, nl 59.96±8.56, P < 0.005) and FCR (191.0±41.19%, nl 628.0±199.0, P < 0.02) for rT3 are compatible with an impairment of the rT3 deiodination rate.
Effects of divalent cations on the conversion of fibrinogen to fibrin and fibrin polymerization
Authors: Hideo Kanaide, Takako Uranishi, Motoomi Nakamura
Journal: American Journal of Hematology (1982)

Abstract Effects of divalent cations on fibrinogen and its reaction with thrombin were re‐examined and correlated to improve definition of mechanisms underlying the acceleration of clot formation by the ions. The rate of release of fibrinopeptides from fibrinogen was not affected by any of the specific ions studied, but increased rates of fibrin monomer polymerization were obtained with all but magnesium ions. Maximal acceleration of monomer polymerization was observed with the divalent ions at concentration of 2.5–5 mM, and no added specific ion effects were observed with much higher levels. The acceleratory ions were found to have a corresponding effect on the solubility of fibrinogen, as judged from acceleration of its precipitation at low temperature. Although magnesium ions had no effect on fibrin monomer polymerization, they did have a low ranking effect on cryoprecipitation. These data confirm that the principal effect of divalent cations in the fibrinogen‐fibrin transformation is to accelerate fibrin monomer polymerization, and suggest that the acceleration is associated with effects on the solubility of fibrinogen.
THE ROLE OF THE GOLGI COMPLEX IN FAT ABSORPTION AS STUDIED WITH THE ELECTRON MICROSCOPE WITH OBSERVATIONS ON THE CYTOLOGY OF DUODENAL ABSORPTIVE CELLS
Authors: Jules M. Weiss
Journal: The Journal of Experimental Medicine (1955)

An electron microscopic study of the morphology of fat absorption in the duodenum of normal and fat-fed mice supports the view that all absorbed fat passes through the cytoplasm of absorptive cells. The Golgi complex plays an important role in the transport of fat across these cells.
A Negative Confirmatory Biopsy Among Men on Active Surveillance for Prostate Cancer Does Not Protect Them from Histologic Grade Progression
Authors: Lih-Ming Wong, Shabbir M.H. Alibhai, Greg Trottier, Narhari Timilshina, Theodorus Van der Kwast, Alexandre Zlotta, Nathan Lawrentschuk, Girish Kulkarni, Robert Hamilton, Sarah Ferrara, David Margel, John Trachtenberg, Michael A. Jewett, Ants Toi, Andrew Evans, Neil E. Fleshner, Antonio Finelli
Journal: European Urology (2013)
Developmental coronary maturation is disturbed by aberrant cardiac vascular endothelial growth factor expression and Notch signalling
Authors: Nynke M.S. van den Akker, Vincenza Caolo, Lambertus J. Wisse, Patricia P.W.M. Peters, Robert E. Poelmann, Peter Carmeliet, Daniël G.M. Molin, Adriana C. Gittenberger-de Groot
Journal: Cardiovascular Research (2007)

Currently, many potential cardiac revascularization therapies target the vascular endothelial growth factor (VEGF) pathway, with variable success. Knowledge regarding the role of the VEGF/Notch/ephrinB2 cascade in (ab)normal coronary development will provide information on the subtle balance of VEGF signalling in coronary maturation and might enhance our therapeutic possibilities. The effect of VEGF isoforms on coronary development was explored in vivo using immunohistochemistry and RT–qPCR on Vegf120/120 mouse embryos solely expressing VEGF120. In vitro, human arterial coronary endothelial cells were treated with VEGF121 or VEGF165 upon which RT–qPCR was performed. In vivo, mutant coronary arterial endothelium showed a decrease in protein expression of arterial markers such as cleaved Notch1, Delta-like4, and ephrinB2 concomitant with an increase of venous markers such as chicken ovalbumin upstream promoter transcription factor II. The venous endothelium showed the opposite effect, which was confirmed on the mRNA level. In vitro, mRNA expression of arterial markers highly depended on the VEGF isoform used, with VEGF165 having the strongest effect. Also, coronary arteriogenesis was anomalous in the mouse embryos with decreased arterial and increased venous medial development as shown by staining for smooth muscle α-actin, Delta-like1, and Notch3. We demonstrate that VEGF isoform-related spatiotemporal cardiac alterations in the VEGF/Notch/ephrinB2 cascade lead to disturbed coronary development. This knowledge can contribute to optimizing therapies targeting VEGF signalling by enabling balancing between angiogenesis and vascular maturation.
Autophagy Regulates TGF-β Expression and Suppresses Kidney Fibrosis Induced by Unilateral Ureteral Obstruction
Authors: Yan Ding, Sung ll Kim, So-Young Lee, Ja Kun Koo, Zhibo Wang, Mary E. Choi
Journal: Journal of the American Society of Nephrology (2014)

Autophagy is an evolutionarily conserved process that cells use to degrade and recycle cellular proteins and remove damaged organelles. During the past decade, there has been a growing interest in defining the basic cellular mechanism of autophagy and its roles in health and disease. However, the functional role of autophagy in kidney fibrosis remains poorly understood. Here, using GFP-LC3 transgenic mice, we show that autophagy is induced in renal tubular epithelial cells (RTECs) of obstructed kidneys after unilateral ureteral obstruction (UUO). Deletion of LC3B (LC3−/− mice) resulted in increased collagen deposition and increased mature profibrotic factor TGF-β levels in obstructed kidneys. Beclin 1 heterozygous (beclin 1+/−) mice also displayed increased collagen deposition in the obstructed kidneys after UUO. We also show that TGF-β1 induces autophagy in primary mouse RTECs and human renal proximal tubular epithelial (HK-2) cells. LC3 deficiency resulted in increased levels of mature TGF-β in primary RTECs. Under conditions of TGF-β1 stimulation and autoinduction, inhibition of autolysosomal protein degradation by bafilomycin A1 increased mature TGF-β protein levels without alterations in TGF-β1 mRNA. These data suggest a novel intracellular mechanism by which mature TGF-β1 protein levels may be regulated in RTECs through autophagic degradation, which suppresses kidney fibrosis induced by UUO. The dual functions of TGF-β1, as an inducer of TGF-β1 autoinduction and an inducer of autophagy and TGF-β degradation, underscore the multifunctionality of TGF-β1.
p53 in chronic myelogenous leukemia. Study of mechanisms of differential expression.
Authors: M Lübbert, C W Miller, L Crawford, H P Koeffler
Journal: The Journal of Experimental Medicine (1988)

The p53 is a nuclear protein that is associated with normal cellular proliferation and can cooperate with Ha-ras in causing cellular transformation in vitro. Lineage association is known to exist between p53 expression and normal lymphopoiesis, but not myelopoiesis. We studied the expression of p53 using chronic myelogenous leukemia (CML) cell lines, somatic hybrids of these cells, and leukemic cells from CML patients. Lymphoid CML lines expressed both p53 mRNA and protein. We also analyzed p53 synthesis by two B-lymphoid lines from the same CML patient; cells of one line were derived from the neoplastic clone, cells of the other were derived from the normal clone. Both synthesized equal amounts of a phosphorylated p53 protein. None of the myeloid CML lines expressed detectable p53 protein and two of four expressed negligible p53 mRNA. Two other myeloid CML lines and myeloid cells from three of four patients expressed p53 mRNA. These findings suggest that expression of the gene is not regulated normally in CML. Several approaches were pursued to explore the differential expression of p53. Southern blot analyses showed no gross alterations in the p53 gene from cells of either the expressing or the nonexpressing lines. No difference in the pattern of demethylated CpG sites was noted in the region of the p53 gene in cells from K562 (myeloid p53 nonexpressor) and in BV173 (lymphoid p53 expressor). The sites of demethylation clustered in and around the p53 promoter in both cell lines. Somatic hybrids formed between a p53 mRNA nonexpressor myeloid line (K562) and the parental p53 expressor lymphoid lines (Daudi, PUT) produced p53 mRNA and protein, suggesting that p53 is a dominantly expressed protein and that lack of expression in myeloid cells is not mediated by a trans-acting negative regulatory protein. DNA transfection experiments performed using the indicator gene chloramphenicol acetyltransferase attached to promoter sequences of p53 showed that these constructs were equally activated in BV173 (p53 expressor) and K562 (p53 mRNA nonexpressor). The mechanism of p53 regulation in CML remains unclear.
Prophylactic Antibiotics with Sigmoidoscopy?
Authors: WILLIAM C. TAYLOR
Journal: Annals of Internal Medicine (1977)

Comments1 January 1977Prophylactic Antibiotics with Sigmoidoscopy?WILLIAM C. TAYLOR, M.D.WILLIAM C. TAYLOR, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-1-116_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the recent Letter, "Bacteremia after Sigmoidoscopy: Another View" (Ann Intern Med 85:77-78, 1976), the recommendation made by Dr. Engeling and associates is not justified by their data.They found no positive blood cultures in 54 cirrhotic patients undergoing sigmoidoscopy. They compare their results to those of LeFrock and associates (1), who found 19 instances of bacteremia in 200 patients undergoing sigmoidoscopy. From statistical analysis showing that P = 0.05, the statement is made that the reported results are "significantly different" from those of LeFrock and co-workers. Other studies that found a low incidence of bacteremia with...Reference1. LEFROCKELLISTURCHIK JCJ: Transient bacteremia associated with sigmoidoscopy. N Engl J Med 289:467-469, 1973 CrossrefMedlineGoogle Scholar1. DICKMAN M: Colonoscopy associated bacteremia. Surg Gynecol Obstet 142:173, 1976 MedlineGoogle Scholar2. NORFLEET R: Does bacteremia follow colonoscopy? Gastroenterology 70:20, 1976 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1977Volume 86, Issue 1Page: 116-117KeywordsAntibioticsBacteremiaBlood Issue Published: 1 January 1977 PDF DownloadLoading ...