BÁO CÁO Y HỌC: "COCCIDIOIDES POSADASII INFECTION ALTERS THE EXPRESSION OF PULMONARY SURFACTANT PROTEINS (SP)-A AND SP-D" PPS

acute HCV infection persists and 4% to 20% of patients with chronic hepatitis C will develop liver cirrhosis within 20 years. In patients with liver cirrhosis, the risk to develop HCC is 1-5% per year. Current standard therapy is the combination of pegylated interferon-α (PEG-IFN-α) and ribavirin. D[r]

change in muscle strength (r=0.73, P=0.001). Group assignment was be the only independent predictor of hSGLT3 transcript levels, explaining 68% of its variability (P=0.01). Our data show that hSGLT3, but not GLTU4, expression was enhanced in skeletal muscle after 16 weeks of resistance training. Thi[r]

20. Hwang SJ, Luo JC, Chu CW, et al. Hepatic steatosis in chronic hepatitis C virus infection: Prevalence and clinical correlation. J Gastroenterol Hepatol 2001;16:190-5. 21. Lonardo A, Adinolfi LE, Loria P, et al. Steatopsis and hepatitis C virus: Mechanisms and significance for hepatic and[r]

such as poorly controlled hypertension or diabetes, obstructive pulmonary disease, or significant heart disease. Patients with autoimmune hepatitis or other conditions known to be exacerbated by interferon and ribavirin or known to have hypersensitivity to these drugs should not receive treatment. T[r]

date the mechanism of this network. However, a poor correlation between mRNA and protein abundance has also been reported [9]. Furthermore, a single gene can encode for more than one mRNA species through differential splicing, and proteins can undergo as many as 200 posttranslational m[r]

Corresponding address: Jin Zhong Li, D.V.M. Ph.D., Department of Neurological Surgery, University of Virginia Health System, P. O. Box 800212, Charlottesville, Virginia 22908, USA Received: 2006.05.02; Accepted: 2006.05.31; Published: 2006.06.01 Osteogenic potentials of some recombinan[r]

PPARγ, and PPARδ. While PPARα is mainly expressed in liver, muscle, kidney and heart, PPARγ is most abundant in adipocytes, intestinal cells and macrophages and PPARδ is expressed in many tissues [2-4]. Each subgroup is activated by a certain variety of fatty acids and their derivatives and b[r]

of general populations [8, 9], and as high as 30% of the population aged 65 and older in the Framingham Heart Study (tHcy > 14 nmol/ml) [10]. Increasing tHcy concentrations accelerate cardiovascular diseases by promoting vascular inflammation, endothelial dys-function, and hypercoagulability[r]

CagA protein. Science 2002; 295: 683-6. 5. Higashi H, Nakaya A, Tsutsumi R, et al. Helicobacter pylori CagA induces Ras-independent morphogenetic response through SHP-2 recruitment and activation. J Biol Chem 2004; 279: 17205-16. 6. Hatakeyama M. Helicobacter pylori CagA--a potential b[r]

non-responders to peginterferon alpha 2b and ribavirin. In: AASLD (Abstract 413); Oct 29- Nov 2 2004; Boston, MA. 36. Gross JB et al. Renew Trial- High dose re-treatment with peginterferon alpha 2b plus ribavirin for non responders in chronic HCV patients. In: AASLD 2003 (Abstract 321); Oct 24-28 20[r]

4. Serfaty L, Aumaitre H, Chazouilleres O, Bonnand AM, Rosmorduc O, Poupon RE, et al. Determinants of outcome of compensated hepatitis C virus-related cirrhosis. Hepatology 1998;27:1435-1440. 5. Kasahara A, Hayashi N, Mochizuki K, Takayanagi M, Yoshioka K, Kakumu S, Iijima A, Urushihar[r]

protein degradation. Metabolism 1997; 46: 673-9. 25. Baulieu EE, Robel P. Dehydroepiandrosterone (DHEA) and de-hydroepiandrosterone sulfate (DHEAS) as neuroactive neuros-teroids. Proc. Natl Acad Sci USA. 1998; 95: 4089-91. 26. Yorek MA, Coppey LJ, Gellett JS, et al. Effect of treatment of diabetic r[r]

FBW7, FBXW7) has recently emerged as a potent new potential tumor suppressor gene [1, 2]. The highly conserved protein consists of an NH2 terminal F-box and seven WD40 repeats in the COOH terminal region and acts as an adaptor protein providing substrate specificity for SCF (Skp–Cullin–F-box)[r]

C. Persistence of hepatitis B and hepatitis C viral genomes in primary liver cancers from HBsAg-negative patients: a study of a low-endemic area. Hepatology 1993;17:20-29. 33. Koike K, Kobayashi M, Gondo M, Hayashi I, Osuga T, Takada S. Hepatitis B virus DNA is frequently found in live[r]

severe with occasional lymphoid aggregates (Figure 2) [4,11]. Actively proliferating bile ductiles are often seen. Risk factors for severe recurrent HCV include advanced donor age, HCV genotype 1, high HCV RNA levels before and after transplant, early histological recurrence of HCV, concomitant cyto[r]

118mouse embryonic stem (ES) cells carrying targeted mutations of BRCA1 (homozygous deletion of exons 22-24, referred to as BRCA1-/-) or BRCA2 (trEx11/ΔEx27, referred to as BRCA2-/-), Farmer et al. (2005) revealed similar sensitivity of these cells to PARP-1 inhibitors in vitro [25]. Will this work[r]

association between hepatitis C infection and survival after orthotopic liver transplantation. Gastroenterology 2002;122:889-96. 10. Berenguer M, Prieto M, San Juan F, Rayon JM, Martinez F, Carrasco D, Moya A, Orbis F, Mir J, Berenguer J. Contribution of donor age to the recent decreas[r]

outstandingly favorable against H. pylori infections for not interfering the normal bacterial flora in the intestine of humans. Moreover, it should also be advantageous that the compounds of Rice-fluid failed to affect the survival of S. aureus, S. epidermidis, and P. aeruginosa, demonstrating that[r]

antibiotic resistance on the eradication rate of Helicobacter pylori infection by a 1-week regimen of proton pump inhibitor, amoxicillin and clarithromycin. Aliment Pharmacol Ther. 2003; 17: 259-65. 17. Miki I, Aoyama N, Sakai T, et al. Impact of clarithromycin resistence and CYP2C19 genetic[r]

4. Serfaty L, Aumaitre H, Chazouilleres O, Bonnand AM, Rosmorduc O, Poupon RE, et al. Determinants of outcome of compensated hepatitis C virus-related cirrhosis. Hepatology 1998;27:1435-1440. 5. Kasahara A, Hayashi N, Mochizuki K, Takayanagi M, Yoshioka K, Kakumu S, Iijima A, Urushihar[r]