|1.||Ukomadu, Chinweike: 2 articles (10/2003 - 02/2003)|
|2.||Dutta, Anindya: 2 articles (10/2003 - 02/2003)|
|3.||Stanton, M E: 2 articles (11/2001 - 03/2000)|
|4.||Ivkovich, D: 2 articles (11/2001 - 03/2000)|
|5.||Konac, E: 1 article (04/2014)|
|6.||Alp, E: 1 article (04/2014)|
|7.||Yilmaz, A: 1 article (04/2014)|
|8.||Menevse, S: 1 article (04/2014)|
|9.||Inokuchi, Junichi: 1 article (02/2011)|
|10.||Takeuchi, Ario: 1 article (02/2011)|
|1.||Hyperlipoproteinemia Type II (Familial Hypercholesterolemia)
03/17/1983 - "If long-term safety can be demonstrated, the compactin-cholestyramine regimen may prove useful in heterozygous familial hypercholesterolemia. "
09/01/1984 - "Combined drug therapy with cholestyramine and compactin was found to be extremely effective against heterozygous cases of familial hypercholesterolemia. "
09/01/1984 - "Combined drug therapy--cholestyramine and compactin--for familial hypercholesterolemia."
09/01/1984 - "With a single drug regimen, compactin at a dosage of 15 mg/day produced a cholesterol reduction of 23% (70 mg/dl) in cases of combined hyperlipidemia, while twice the dosage (30 mg/day) was needed to produce a comparable effect with heterozygous familial hypercholesterolemia. "
09/01/1984 - "When compaction was combined with cholestyramine (in a 4 g dose three times a day), the cholesterol-lowering effect of compactin was strongly improved with heterozygous familial hypercholesterolemia; half the dosage of compactin was enough to produce the additive effect compared with the effect produced by each single drug regimen."
01/01/2010 - "Complete eradication of infection has been seen by immunofluorescent staining at 40 microM mevastatin concentration, when expression level of chlamydial 16S rRNA and euo was undetectable. "
12/01/2002 - "Rho family GTPase activity was essential for invasion, since the pan-Rho GTPase inhibitor, compactin, blocked infection of HEp2 cells. "
04/01/2004 - "Pharmacokinetic and pharmacodynamic (PK/PD) parameters, which are important indices of the therapeutic efficacy of antimicrobials, and the minimum inhibitory concentration (MIC) predictive of clinical efficacy at common clinical doses, were examined for biapenem (BIPM; 300 mg b.i.d.), imipenem/cilastatin (IPM/CS; 500 mg/500 mg b.i.d.), meropenem (MEPM; 500 mg b.i.d.), and ceftazidime (CAZ; 1000 mg b.i.d.), using a mouse model of thigh infection caused by Pseudomonas aeruginosa. "
02/01/2007 - "As for the pneumococcal infection in patient with good immunological response, good clinical effect might be obtained by panipenem/betamipron (PAPM/BP) 500 mg, imipenem/cilastatin (IPM/CS) 500 mg, meropenem (MEPM) 500 mg and biapenem (BIPM) 300 mg, b.i.d., while for immunocompromised hosts or infections by penicillin-resistant Streptococcus pneumoniae (PRSP), PAPM/BP, 500 mg, b.i.d., or IPM/CS 500 mg, MEPM 500 mg, t.i.d. "
10/01/2003 - "Using a murine lung alveolar carcinoma cell line (Line 1), we report a dose-dependent inhibition of tumor cell proliferation, adhesion and invasiveness, in response to alendronate (3-30 micromol/L) and mevastatin (1-10 micromol/L). "
01/01/1992 - "[Study on the effects of the hypocholesteremic agents, cholestyramine and compactin on the induction of renal tumors in rats by N-ethyl-N-hydroxyethyl nitrosamine]."
01/01/2003 - "Therefore, depletion of mevalonate can block both the processing and the transforming activities of Ras, indicating that drugs such as lovastatin and compactin, which had previously been exploited for lowering cholesterol levels, may be useful chemotherapeutic agents for treating tumors harboring oncogenic Ras mutation. "
11/01/2009 - "Moreover, several MRLs inhibit the metabolic activity of L1210 tumor cells in vitro to a greater degree than fluvastatin, lovastatin, mevastatin and simvastatin, whereas pravastatin is inactive. "
06/01/2004 - "In order to investigate the anti-tumor activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and the mechanism underlying the cell proliferation and apoptosis modulated in myeloma cells, the effects of mevastatin, an HMG-CoA reductase inhibitor, on cell growth, cell cycle progression and apoptosis in U266 human multiple myeloma (MM) cell line in vitro were explored by MTT colorimetric assay, morphologic observation, flow cytometry, DNA gel electrophoresis, and RT-PCR. "
01/01/2010 - "Taken together, we report for the first time a role of NO in neurite outgrowth of neuroblastoma cells triggered by mevastatin or serum reduction."
07/01/2009 - "We found that mevastatin triggered neurite outgrowth of neuroblastoma cells and examined the responsible signaling pathways. "
07/01/2009 - "Mevastatin-induced neurite outgrowth of neuroblastoma cells via activation of EGFR."
01/01/2010 - "In Neuro2a neuroblastoma cells, we found that mevastatin and serum withdrawal triggered the production of nitric oxide (NO). "
01/01/2010 - "Neuroblastoma cells differentiate in response to serum reduction or addition of the cholesterol synthesis inhibitor mevastatin. "
|5.||Colorectal Neoplasms (Colorectal Cancer)
07/01/2001 - "The aim of our study was to determine the effect of mevastatin, alone or in combination with butyrate, on proliferation, the cell cycle and apoptosis in the human colorectal carcinoma cell line Caco-2. "
07/01/2001 - "HMG-CoA reductase inhibitor mevastatin enhances the growth inhibitory effect of butyrate in the colorectal carcinoma cell line Caco-2."
|1.||Cholestyramine Resin (Questran)
|3.||biapenem (L 627)
|5.||imipenem drug combination cilastatin (Primaxin)
|1.||Drug Therapy (Chemotherapy)
|2.||Hormone Replacement Therapy (Therapy, Hormone Replacement)
|3.||Blood Component Removal (Apheresis)