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991.
992.
Kodam Sujatha Naidu Babu Ommi Anwita Mudiraj Phanithi Prakash Babu Rajeswar Rao Vedula 《Archiv der Pharmazie》2019,352(12)
Novel thiazolyl hydrazonothiazolamines and 1,3,4‐thiadiazinyl hydrazonothiazolamines were synthesized by a facile one‐pot multicomponent approach by the reaction of 2‐amino‐4‐methyl‐5‐acetylthiazole, thiosemicarbazide or thiocarbohydrazide and phenacyl bromides or 3‐(2‐bromoacetyl)‐2H‐chromen‐2‐ones in acetic acid with good to excellent yields. These new compounds were screened in vitro for their antimalarial activity; among them, four compounds, 4h, 4i, 4k, 4l , showed moderate activity with half‐maximal inhibitory concentration (IC50) values of 3.2, 2.7, 2.7, and 2.8 and 3.2, 3.2, 3.1, and 3.5 μM against chloroquine‐sensitive and ‐resistant strains of Plasmodium falciparum, respectively. Compound 4l inhibited the ring stage growth of P. falciparum 3D7 at an IC90 concentration of 12.5 µM in a stage‐specific assay method, where the culture is incubated with specific stages of P. falciparum for 12 hr, and no activity was found against the trophozoite and schizont stages, confirming that 4l may have potent action against the ring stage of P. falciparum. 相似文献
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Hypertriglyceridemia is common in children with systemic lupus erythematosus (SLE). A retrospective analysis of the baseline clinical–pathological presentation and treatment outcome (status of lipid profiles) was performed in two children with SLE, who presented with extreme hypertriglyceridemia over a follow-up period of four weeks. The children were treated with prednisolone, mycophenolate mofetil (MMF), hydroxychloroquine and hypolipidemic agents, depending on their disease status. On serial follow-up, the first child showed a significantly raised serum triglyceride level after receiving one week of oral prednisolone therapy. Anti-lipoprotein-lipase (LPL) autoantibody was absent. Lipid profile levels of this child gradually improved after replacing oral prednisolone with another immunosuppressant, namely MMF. The second child presented with extreme hypertriglyceridemia with positive anti-LPL autoantibody. She responded to plasmapheresis followed by increasing the dose of immunosuppressant. So, extreme hypertriglyceridemia in children with SLE may be steroid induced or due to presence of anti-LPL auto antibody. Management should be individualized depending on the etiology. 相似文献
995.
Ponnusankar S Pandit S Babu R Bandyopadhyay A Mukherjee PK 《Journal of ethnopharmacology》2011,133(1):120-125
Ethnopharmacological relevance
‘Triphala’ is one of the age-old, most commonly used polyherbal preparation from Ayurveda as Rasayana drug.Aim of the study
This study was aimed at evaluating the effect of ‘Triphala’ on drug modulating enzymes to assess its safety through its potential to interact with co-administered drugs.Materials and methods
The cytochrome P450 inhibitory effect of ‘triphala’ formulation was investigated on rat liver microsomes using CYP450-CO complex assay and on individual isoform such as CYP3A4 and 2D6 using fluorescence screening. RP-HPLC method was developed to standardize ‘triphala’ and its individual components using gallic acid as analytical marker compound.Results
RP-HPLC analysis demonstrated the presence of gallic acid (4.30 ± 2.09 mg/g) in the formulation. The formulation showed 23% inhibition of the rat liver microsomes through CYP450-CO complex assay which is comparatively less when compared with the individual components. Further, the effect of standardized formulation dissolved in ethanol showed CYP3A4 and CYP2D6 inhibitory activity at the IC50 values of 119.65 ± 1.91 μg/ml and 105.03 ± 0.98 μg/ml respectively. Gallic acid was also found to inhibit both the isoforms at the IC50 values of 87.24 ± 1.11 μg/ml and 92.03 ± 0.38 μg/ml respectively.Conclusions
Various concentrations of the formulation and its individual components showed significantly less inhibitory activity (p < 0.001) on individual isoforms when compared with the positive control. Assessment on the in vitro effect of ‘triphala’ on drug modulating enzymes has important implications for predicting the likelihood of herb-drug interactions if these are administered concomitantly. 相似文献996.
997.
Expression of p53 in leukoplakia and squamous cell carcinoma of the oral mucosa: correlation with expression of Ki67 下载免费PDF全文
S Kannan G Jagadeesh Chandran K Raveendran Pillai Babu Mathew K Sujathan K R Nalinakumary M Krishnan Nair 《Journal of clinical pathology》1996,49(3):M170-M175
Aim—To study p53 expression in relation to proliferative status in normal and nondysplastic, dysplastic and malignant lesions of the oral mucosa. 相似文献
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999.
Perivascular drainage of amyloid-beta peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease. 总被引:1,自引:0,他引:1
Roy O Weller Malavika Subash Stephen D Preston Ingrid Mazanti Roxana O Carare 《Brain pathology (Zurich, Switzerland)》2008,18(2):253-266
Alzheimer's disease is the commonest dementia. One major characteristic of its pathology is accumulation of amyloid-beta (Abeta) as insoluble deposits in brain parenchyma and in blood vessel walls [cerebral amyloid angiopathy (CAA)]. The distribution of Abeta deposits in the basement membranes of cerebral capillaries and arteries corresponds to the perivascular drainage pathways by which interstitial fluid (ISF) and solutes are eliminated from the brain--effectively the lymphatic drainage of the brain. Theoretical models suggest that vessel pulsations supply the motive force for perivascular drainage of ISF and solutes. As arteries stiffen with age, the amplitude of pulsations is reduced and insoluble Abeta is deposited in ISF drainage pathways as CAA, thus, further impeding the drainage of soluble Abeta. Failure of perivascular drainage of Abeta and deposition of Abeta in the walls of arteries has two major consequences: (i) intracerebral hemorrhage associated with rupture of Abeta-laden arteries in CAA; and (ii) Alzheimer's disease in which failure of elimination of ISF, Abeta and other soluble metabolites from the brain alters homeostasis and the neuronal environment resulting in cognitive decline and dementia. Therapeutic strategies that improve elimination of Abeta and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease. 相似文献
1000.