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Nephrol Dial Transplant. 2000 Nov;15(11):1773-81.
An oral sorbent reduces overload of indoxyl sulphate and gene expression of TGF-beta1 in uraemic rat kidneys.
Miyazaki T, Aoyama I, Ise M, Seo H, Niwa T.
Nagoya University Daiko Medical Center, 1-1-20, Daiko-minami, Higashi-ku, Nagoya, Japan.
BACKGROUND: An oral adsorbent (AST-120) delays the progression of chronic renal failure (CRF). The aims of the present study are to determine the effects of AST-120 on the localization of indoxyl sulphate in uraemic rat kidneys, and to examine whether AST-120 reduces the renal cortical gene expression of transforming growth factor (TGF)-beta1, tissue inhibitor of metalloproteinase (TIMP)-1 and pro-alpha1(I)collagen, and ameliorates glomerular and tubulointerstitial injuries in uraemic rats. METHODS: Two weeks after 5/6-nephrectomy, 10 rats were divided into pairs such that both rats in each pair exhibited almost the same levels of serum creatinine, blood urea nitrogen and creatinine clearance. One rat from each pair was assigned to a control uraemic group, the other to a uraemic group which received AST-120 everyday for 11 weeks. The localization of indoxyl sulphate was studied by immunohistochemistry using a monoclonal anti-indoxyl sulphate antibody we had developed. The renal cortical gene expression was studied by using northern blotting. RESULTS: Rats treated with AST-120 showed decreased levels of serum creatinine, blood urea nitrogen and urinary protein as well as increased levels of creatinine clearance as compared with control uraemic rats. AST-120 markedly decreased indoxyl sulphate levels in both serum and urine. Immunohistochemistry demonstrated that indoxyl sulphate was localized in the renal proximal tubular epithelial cells, especially of dilated tubules, and that AST-120 markedly reduced the tubular staining of indoxyl sulphate. AST-120 attenuated interstitial fibrosis, tubular injury as well as glomerular sclerosis, and reduced the renal gene expression of TGF-beta1, TIMP-1 and pro-alpha1(I)collagen. CONCLUSIONS: AST-120 reduces the gene expression of TGF-beta1, TIMP-1 and pro-alpha1(I)collagen in the kidneys, and delays the progression of CRF, at least in part, by alleviating the overload of indoxyl sulphate on remnant proximal tubular epithelial cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11071964&dopt=Abstract
Stem Cells. 2000;18(6):428-34.
In vitro proliferation and differentiation of megakaryocytic progenitors in patients with aplastic anemia, paroxysmal nocturnal hemoglobinuria, and the myelodysplastic syndromes.
Cox CV, Killick SB, Patel S, Elebute MO, Marsh JC, Gordon-Smith EC, Gibson FM.
Department of Hematology, St. George's Hospital Medical School, London, UK.
It has previously been shown that patients with aplastic anemia (AA) have a stem cell defect both of proliferation and differentiation. This has been shown by long-term bone marrow (BM) culture, long-term initiating cell assays, and committed progenitor assays. We present, for the first time, data on megakaryocyte (Mk) colony formation from purified BM CD34(+) cells from patients with AA. The results are compared with those from normal controls and from patients with paroxysmal nocturnal hemoglobinuria (PNH) and the myelodysplastic syndromes (MDSs). Those treated for AA had previously received immunosuppression (antithymocyte globulin and/or cyclosporin). No patients had received bone marrow transplantation. A total of 13 AA patients (five untreated, eight treated), six PNH, six MDS, and 13 normal donors were studied. BM CD34(+) cells were purified by indirect labeling and then cultured in a collagen-based Mk assay kit (MegaCult-C, StemCell Technologies). The cultures were fixed on day 12, and the Mk colonies were identified by the alkaline phosphatase anti-alkaline phosphatase technique using the monoclonal antibody CD41 (GP IIb/IIIa). The slides were scored for Mk colony-forming units (CFU-Mks) (3-20 and >20 cells), Mk burst-forming units (BFU-Mks) (>50 cells), and mixed colonies. The results show that total Mk colony formation in AA was significantly lower than in normal donors (p<0.0001), both in untreated patients/nonresponders to treatment (p = 0.0001) and in complete/partial responders (p<0.002). There was no significant difference in Mk colony formation in treated and untreated patients (p = 0.05). Patients with AA had a lower total colony formation than PNH patients (p = 0.0002). PNH patients exhibited lower colony formation than normal controls (p = 0.03), as shown by MDS patients, although the considerable number of variables resulted in a lack of statistically significant difference from normal controls (p = 0.2). We have now shown that Mk colony formation from purified BM CD34(+) cells is significantly reduced, supporting previous evidence that AA results from a stem cell defect.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11072031&dopt=Abstract
Presse Med. 2000 Sep 30;29(28):1559-61.
[Arterial aneurysms associated with cystic hepato-renal disease]
[Article in French]
De Toma G, Plocco M, Nicolanti V, Cavallaro G, Amato D, Letizia C.
Istituto di Clinica Chirurgica, Universita degli studi di Roma La Sapienza, Italia. detomniroma1.it
BACKGROUND: Ehlers Danlos syndrome (type IV) and kidney and liver cyst disease can present a common factor: anomalous biosynthesis of structural collagen and elastic tissue. We present an exceptional case. CASE REPORT: A 62-year-old man complained of pain in the upper left quadrant of the abdomen. Ultrasonography, magnetic resonance imaging and arteriography evidenced an aneurysm of the splenic artery, an aneurysm of the hypogastric artery, multiple cysts in the kidney and liver, and mitral valvulopathy. Treatment was splenectomy with resection of the splenic aneurysm and resection of the iliac aneurysm and iliac-iliac bypass. DISCUSSION: The association of kidney and liver cyst disease with venous gastrointestinal and cardiovascular complications is well known. The simultaneous presence of cysts and peripheral and visceral aneurysms with anomalies of the arterial wall resembling Ehlers Danlos syndrome (type IV) would suggest that these two diseases might result from a common connective tissue anomaly. The underlying mechanism(s) remain unknown.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11072372&dopt=Abstract
Clin Exp Rheumatol. 2000 Sep-Oct;18(5):547-52.
The effect of promoter strength in adenoviral vectors in hyperplastic synovium.
Goossens PH, Schouten GJ, Heemskerk B, 't Hart BA, Bout A, Kluin PM, Breedveld FC, Valerio D, Huizinga TW.
Department of Rheumatology, Leiden University Medical Center, The Netherlands.
OBJECTIVES: To compare the activity of the CytoMegaloVirus promoter (CMV) and the Major Late promoter (MLP) in synoviocytes in vitro and in vivo. To determine the phenotype of infected cells and the induction of inflammation. To investigate the effects of the cytomegalovirus (CMV) or major late (MLP) promoter on adenovirus-mediated reporter gene transduction of synoviocytes in vitro and in vivo. METHODS: After infection with adenoviral vectors harboring CMV- and MLP-driven luciferase and lacZ genes, gene expression was examined in cultured synoviocytes and in the synovium of rhesus monkeys with collagen-induced arthritis. Immunohistochemical staining for the macrophage-marker CD68 and lacZ expression was performed. Inflammation was scored in the synovial membrane of injected and non-injected joints. RESULTS: CMV-driven reporter gene expression was found to be 6 to 10 times higher than MLP-driven gene expression in both cultured synoviocytes and monkey synovium. Both CD68 positive and CD68 negative cells were lacZ positive. Inflammation in joints injected with CMV-driven adenoviral vectors was not higher than that in MLP-driven adenoviral vectors- or non-injected joints. CONCLUSION: These experiments show that the CMV promoter induces higher gene expression in synoviocytes than the MLP promoter. Both fibroblast-like and macrophage-like synoviocytes can be infected with adenoviral vectors. No deleterious effects of the CMV-promoter driven adenoviral vectors were observed.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11072592&dopt=Abstract
Clin Exp Rheumatol. 2000 Sep-Oct;18(5):625-8.
Axial osteomalacia with sacroiliitis and moderate phosphate diabetes: report of a case.
Cortet B, Berniere L, Solau-Gervais E, Hacene A, Cotten A, Delcambre B.
Department of Rheumatology, University Hospital of Lille, France. bcortehru-lille.fr
We report a new case of axial osteomalacia diagnosed in a 51-year-old white Caucasian male, made particular by its association with sacroiliitis, positive HLA-B27 antigen, and also moderate phosphate diabetes responsible for a decreased appendicular bone mass. The diagnosis was suspected when X-ray evaluation showed increased density and coarse trabeculation mainly involving the pelvis and spine. Dual energy X-ray absorptiometry confirmed the elevated bone density at the lumbar spine (T score: +1.92) contrasting with a decreased bone mass at the femoral neck (T score: -2.33). The diagnosis was confirmed by histomorphometry of the iliac crest showing marked thickening of the cortices (2190 microns +/- 0.574, N = 780 +/- 40) and an increased trabecular bone volume (33.24%, N = 14 +/- 3). Osteoid parameters were also markedly increased with an osteoid volume of 2.1% (N = 1.2 +/- 0.5) and a mean osteoid thickness of 28.7 microns (N = 13 +/- 2.5), with a normal bone fluoride content (0.082%, N < 0.10). Bone resorption as assessed on bone biopsy and by the measurement of markers of bone remodeling (serum procollagen type I C-terminal telopeptide and 24 hr urinary cross-laps to creatinine ratio) was increased. This latter finding was not necessarily due to axial osteomalacia and could be the consequence of moderate phosphate diabetes. The patient was treated with calcitriol which was promptly discontinued due to gastrointestinal symptoms and replaced by calcidiol without any significant effect on the low back pain.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11072608&dopt=Abstract
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