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osu.edu

BACKGROUND: Interleukin-8 (IL-8) is a potent neutrophil chemokine that has been implicated in the pathogenesis of renal inflammation in human glomerulonephritis. To explain inter-patient variations in renal inflammation during diseases such as systemic lupus erythematosus (SLE), it was postulated that the promoter region of the IL-8 gene contains polymorphic residues that influence the level of IL-8 expression in response to immune-complex deposition, and thereby affect the severity of renal injury. This study was undertaken to identify polymorphisms in the 5'-flanking region of the IL-8 gene that correlate with the severity of SLE nephritis. METHODS: A 1526 base pair segment of the IL-8 5'-flanking region was PCR amplified from the genomic DNA of 100 individuals and sequenced on an automated capillary electrophoresis system. Sequence data were compared with the published IL-8 sequence to identify polymorphisms. Allelic variations were verified by cloning and re-sequencing, and also by restriction enzyme analysis. Patients with SLE nephritis were genotyped for IL-8 polymorphisms, and associations between specific alleles and severity of SLE nephritis [based on the World Health Organization (WHO) classification] were determined. RESULTS: Three single nucleotide polymorphisms were identified in the IL-8 flanking region. Labeled relative to the IL-8 translational start site, these are T-845C, T-738A, and A-353T. T-845C and T-738A are novel, and found primarily in African Americans. The C for T change at position -845 was found to be 3.6 to 7.5 times more frequent in African Americans with severe (WHO Class IV) SLE nephritis, than in African American controls, or patients with less severe forms of SLE nephritis, respectively. CONCLUSIONS: IL-8-845C might predispose African Americans with SLE nephritis to more severe renal injury, perhaps by influencing IL-8 expression. Genotyping patients with glomerulonephritis for IL-8 polymorphisms may be useful in predicting disease outcome and individualizing immunosuppressive therapy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12081586&dopt=Abstract

Kidney Int. 2002 Jul;62(1):339-45.
Left ventricular hypertrophy, cardiac remodeling and asymmetric dimethylarginine (ADMA) in hemodialysis patients.

Zoccali C, Mallamaci F, Maas R, Benedetto FA, Tripepi G, Malatino LS, Cataliotti A, Bellanuova I, Boger R; CREED Investigators.

CNR, Division of Nephrology, Centre of Clinical Physiology and Renal Unit, Via Sbarre Inferiori 39, 89131 Reggio Calabria, Italy. carmine.zoccalin.it

BACKGROUND: The endogenous inhibitor of nitric oxide (NO), asymmetric dimethylarginine (ADMA), is a strong predictor of adverse cardiovascular outcomes in patients with end-stage renal disease (ESRD). METHODS: Since arterial and cardiac remodeling is associated with altered endothelial microcirculatory responses to forearm ischemia (a NO-dependent response), interference of ADMA with the NO system may be important for the pathogenesis of left ventricular hypertrophy (LVH) in these patients. This study sought to identify the relationship between plasma ADMA and LV geometry and function in a cohort of 198 hemodialysis patients. RESULTS: Plasma ADMA was significantly higher (P = 0.008) in patients with LVH (median 3.00 micromol/L, inter-quartile range 1.73 to 3.97 micromol/L) than in those without this alteration (1.88 micromol/L, 1.15 to 3.56 micromol/L) and was significantly related to left ventricular (LV) mass (r = 0.26, P < 0.001). Interestingly, ADMA was much higher (P < 0.001) in patients with concentric LVH (3.60 micromol/L, 2.90 to 4.33 micromol/L) than in patients with eccentric LVH (2.17 micromol/L, 1.47 to 3.24 micromol/L) or normal LV mass (1.76 micromol/L, 1.13 to 2.65 micromol/L). Furthermore, plasma ADMA was higher (P = 0.02) in patients with systolic dysfunction (3.52 micromol/L, 2.08 to 5.87 micromol/L) than in those with normal LV function (2.58 micromol/L, 1.53 to 3.84 micromol/L) and inversely related to ejection fraction (EF; r = -0.25, P < 0.001). The link between ADMA and LV mass and EF was confirmed by multivariate analysis (ADMA vs. LVMI, beta = 0.17, P = 0.006; ADMA vs. EF, beta = -0.24, P < 0.001). CONCLUSIONS: Overall, this study indicates that raised plasma concentration of ADMA is associated to concentric LVH and LV dysfunction. Intervention studies are needed to see whether the link between ADMA and concentric LVH remodeling and LV dysfunction is a causal one.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12081596&dopt=Abstract

J Vet Pharmacol Ther. 2002 Jun;25(3):161-74.
Pharmacokinetics and pharmacokinetic/pharmacodynamic integration of marbofloxacin in calf serum, exudate and transudate.

Aliabadi FS, Lees P.

Department of Veterinary Basic Sciences, The Royal Veterinary College, Hawkshead Campus, North Mymms, Hatfield, Hertfordshire, AL9 7TA UK.

Marbofloxacin is a fluoroquinolone antimicrobial drug used in cattle for the treatment of respiratory infections. In this investigation the pharmacokinetics (PK) of marbofloxacin were determined after intravenous and intramuscular dosing at a dosage of 2 mg/kg. In addition the ex vivo pharmacodynamics (PD) of the drug were determined in serum and three types of tissue cage fluid (transudate, inflammatory exudate generated by carrageenan and exudate generated by lipopolysaccharide). Marbofloxacin PK was characterized by a high volume of distribution after dosing by both routes (1.28 L/kg intravenous and 1.25 L/kg intramuscular). Corresponding area under the concentration-time curve (AUC) and elimination half-life (t(1/2)el) values were 9.99 and 10.11 microg h/mL and 4.23 and 4.33 h, respectively. Values of AUC for carrageenan-induced exudate, lipopolysaccharide-induced exudate and transudate were, respectively, 8.28, 7.83 and 7.75 microg h/mL after intravenous and 8.84, 8.53 and 8.52 microg h/mL after intramuscular dosing. Maximum concentration (Cmax) values were similar for the three tissue cage fluids after intravenous and intramuscular dosing. For in vivo PK data values of AUC: minimum inhibitory concentration (MIC) (AUIC) ratio for serum were 250 and 253, respectively, after intravenous and intramuscular dosing of marbofloxacin against a pathogenic strain of Mannheimia haemolytica (MIC=0.04 microg/mL). For all tissue cage fluids AUIC values were >194 and >213 after intravenous and intramuscular dosing, and Cmax/MIC ratios were 9 or greater, indicating a likely high level of effectiveness in clinical infections caused by M. haemolytica of MIC 0.04 microg/mL or less. This was confirmed by both in vitro (serum) and ex vivo (serum, exudate and transudate) measurements, which demonstrated a concentration-dependent killing profile for marbofloxacin against M. haemolytica. Ex vivo, after 24-h incubation, virtually all bacteria were killed (<10 cfu/mL) in all samples collected up to 9 h (serum), 24 h (carrageenan-induced exudate and transudate) and 36 h (lipopolysaccharide-induced exudate). Application of the sigmoid Emax equation to the ex vivo antibacterial data provided, for serum, AUIC24 h values of 37.1 for bacteriostasis, 46.3 for bactericidal activity and 119.6 for elimination of bacteria. These data may be used as a rational basis for setting dosing schedules which optimize clinical efficacy and minimize the opportunities for emergence of resistant organisms.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12081611&dopt=Abstract

Gastroenterology. 2002 Dec;123(6):1962-71.
Helicobacter pylori CagA protein activates serum response element-driven transcription independently of tyrosine phosphorylation.

Hirata Y, Maeda S, Mitsuno Y, Tateishi K, Yanai A, Akanuma M, Yoshida H, Kawabe T, Shiratori Y, Omata M.

Department of Gastroenterology, University of Tokyo, Japan. HIRATAY-IN.u-tokyo.ac.jp

BACKGROUND & AIMS: Infection with Helicobacter pylori possessing the cag pathogenicity island (PAI) is associated with severe gastritis and gastric cancer. CagA protein, one of the products of cag PAI, is translocated into epithelial cells, where cytoskeletal rearrangements occur as a result of CagA tyrosine (Tyr) phosphorylation. Here we identify a new role for CagA protein as an activator of host cell signaling. METHODS: We transfected CagA into epithelial cells and analyzed its effect on transcription by reporter assays. The mechanism of reporter activation was assessed by electrophoretic mobility shift assays (EMSA) and immunoblots. Responsible regions of CagA for reporter activation were determined by truncation and mutagenesis of cagA gene. RESULTS: In HeLa cells, expression of CagA increased serum response element (SRE)-driven and serum response factor (SRF)-driven transcription by 40-fold and 3.3-fold, respectively, but did not affect nuclear factor kappaB- or AP-1-driven transcription. CagA-mediated SRE activation was also observed in gastric cell lines. Immunoblotting and EMSA revealed that transfection of CagA enhanced phosphorylation of and DNA binding by Elk1. Furthermore, involvement of Ras and MEK in CagA-mediated Elk1 phosphorylation was observed. SRE activation was dependent on several regions within the C-terminal portion of CagA (CagA(873-1002)), and independent of Tyr phosphorylation. CONCLUSIONS: The C-terminal portion of CagA enhances SRE-driven transcription by activating an upstream signaling cascade without requiring CagA Tyr phosphorylation. This result suggests that translocated CagA regulates 2 distinct cellular responses: phosphorylation-dependent cytoskeletal rearrangement and phosphorylation-independent transcriptional activation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12454853&dopt=Abstract

leicester.ac.uk

BACKGROUND: Chronic renal allograft nephropathy is characterized by an abnormal accumulation of extracellular matrix proteins in the glomeruli and tubulo-interstitium. The aim of this study was to determine the relationship between intragraft expression of the genes controlling the accumulation of extracellular matrix and the development of chronic renal allograft nephropathy in human renal transplants. METHODS: Forty renal allografts with stable renal function were biopsied 6 months after transplantation. Single glomeruli were plucked from the surface of these protocol biopsies and total messenger RNA (mRNA) was extracted. Reverse transcriptase-polymerase chain reaction was used to study the intragraft expression of several fibrosis-associated genes (collagen III, collagen IValpha2, matrix metalloproteinase (MMP) 2, tissue inhibitors of metalloproteinases (TIMPs) 1 and 2, tenascin and transforming growth factor (TGF) beta1). The level of tubulo-interstitial fibrosis was measured by quantitative immunostaining of collagen III. RESULTS: There were positive correlations between the level of tubulo-interstitial collagen III immunostaining and intragraft expression of the genes for TIMP-1 (rs= 0.70, P < 0.02) and TIMP-2 (rs = 0.59, P < 0.02). Interstitial fibrosis was also strongly correlated with the levels of TGF-beta mRNA (rs = 0.67, P < 0.002). Finally, TIMP-1 expression increased with TGF-beta expression (rs = 0.77, P < 0.002). CONCLUSION: Failure of extracellular matrix degradation may be an important molecular mechanism in the pathogenesis of chronic renal allograft damage.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12081746&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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