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61.
Autologous bone marrow transplantation for acute myeloid leukemia using busulfan plus etoposide as a preparative regimen 总被引:1,自引:0,他引:1
We have studied the use of a new preparative regimen for the treatment of patients in remission of acute myeloid leukemia (AML) with autologous bone marrow transplantation. Chemotherapy consisted of busulfan 1 mg/kg every 6 hours for 4 days (total dose, 16 mg/kg) on days -7 through -4 followed by an intravenous infusion over 6 to 10 hours of etoposide 60 mg/kg on day -3. Autologous bone marrow, treated in vitro with 100 micrograms/mL of 4-hydroperoxycyclophosphamide, was infused on day 0. We have treated 58 patients up to the age of 60 years, 32 in first remission, 21 in second or third remission, and 5 with primary refractory AML unresponsive to high-dose Ara-C, but achieving remission with aggressive salvage regimens. Of the first remission patients, there has been 1 treatment related death and 5 relapses. With median follow-up of 22 months, the actuarial relapse rate is 22% +/- 9% and disease-free survival is 76% +/- 9% at 3 years. Patients with favorable French-American-British (FAB) subtypes (M3 or M4 EO) did especially well, with no relapses seen in 15 patients observed for a median of 30 months. Actuarial relapse rate at 3 years was 48% for first remission patients with less favorable FAB subtypes. Of patients in second or third remission, there were 5 treatment related deaths and 4 relapses. With median follow-up of 22 months, the actuarial relapse rate is 25% +/- 11% and disease-free survival is 56% +/- 11% at 3 years. Four of five primary refractory patients died during treatment and 1 remains in remission with short follow-up. These preliminary data are very encouraging and, if confirmed, support the use of autologous purged bone marrow transplantation using aggressive preparative regimens as one approach to improve the outcome of adults with AML. 相似文献
62.
Arunaloke Chakrabarti Prashant Sood Shivaprakash M. Rudramurthy Sharon Chen Harsimran Kaur Malini Capoor Deepinder Chhina Ratna Rao Vandana Kalwaje Eshwara Immaculata Xess Anupama J. Kindo P. Umabala Jayanthi Savio Atul Patel Ujjwayini Ray Sangeetha Mohan Ranganathan Iyer Jagdish Chander Anita Arora Raman Sardana Indranil Roy B. Appalaraju Ajanta Sharma Anjali Shetty Neelam Khanna Rungmei Marak Sanjay Biswas Shukla Das B. N. Harish Sangeeta Joshi Deepak Mendiratta 《Intensive care medicine》2015,41(2):285-295
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64.
Ram B. Singh Gurpreet S. Wander Amit Rastogi Pradeep K. Shukla Adarsh Mittal Jagdish P. Sharma Shiv K. Mehrotra Raj Kapoor Raj K. Chopra 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》1998,12(4):347-353
The effects of oral treatment with coenzyme Q10 (120 mg/d) were compared for 28 days in 73 (intervention group A) and 71 (placebo group B) patients with acute myocardial infarction (AMI). After treatment, angina pectoris (9.5 vs. 28.1), total arrhythmias (9.5% vs. 25.3%), and poor left ventricular function (8.2% vs. 22.5%) were significantly (P < 0.05) reduced in the coenzyme Q group than placebo group. Total cardiac events, including cardiac deaths and nonfatal infarction, were also significantly reduced in the coenzyme Q10 group compared with the placebo group (15.0% vs. 30.9%, P < 0.02). The extent of cardiac disease, elevation in cardiac enzymes, and oxidative stress at entry to the study were comparable between the two groups. Lipid peroxides, diene conjugates, and malondialdehyde, which are indicators of oxidative stress, showed a greater reduction in the treatment group than in the placebo group. The antioxidants vitamin A, E, and C and beta-carotene, which were lower initially after AMI, increased more in the coenzyme Q10 group than in the placebo group. These findings suggest that coenzyme Q10 can provide rapid protective effects in patients with AMI if administered within 3 days of the onset of symptoms. More studies in a larger number of patients and long-term follow-up are needed to confirm our results. 相似文献
65.
H. S. Chandel S. P. Pandey D. Shukla K. Lalsare S. K. Selvaraj M. K. Jha B. Saha 《Clinical and experimental immunology》2014,176(2):283-290
Toll‐like receptors (TLRs) recognize pathogen‐associated molecular patterns and results in innate immune system activation that results in elicitation of the adaptive immune response. One crucial modulator of the adaptive immune response is CD40. However, whether these molecules influence each other's expression and functions is not known. Therefore, we examined the effects of TLRs on CD40 expression on macrophages, the host cell for the protozoan parasite L eishmania major. While polyinosinic‐polycytidylic acid [poly (I:C)], a TLR‐3 ligand, lipopolysaccharide (LPS), a TLR‐4 ligand, imiquimod, a TLR‐7/8 ligand and cytosine–phosphate–guanosine (CpG), a TLR‐9 ligand, were shown to enhance CD40 expression, CD40 stimulation enhanced only TLR‐9 expression. Therefore, we tested the synergism between CD40 and CpG in anti‐leishmanial immune response. In L eishmania‐infected macrophages, CpG was found to reduce CD40‐induced extracellular stress‐regulated kinase (ERK)1/2 activation; with the exception of interleukin (IL)‐10, these ligands had differential effects on CD40‐induced IL‐1α, IL‐6 and IL‐12 production. CpG significantly enhanced the anti‐leishmanial function of CD40 with differential effects on IL‐4, IL‐10 and interferon (IFN)‐γ production in susceptible BALB/c mice. Thus, we report the first systematic study on CD40–TLR cross‐talk that regulated the experimental L . major infection. 相似文献
66.
Suman Srivastava Neha Thakur Ashutosh Singh Poonam Shukla Vipin Kumar Maikhuri Neha Garg Ashok Prasad Rampal Pandey 《RSC advances》2019,9(51):29856
A new fluorescent sensor 5 based on a fused imidazopyridine scaffold has been designed and synthesized via cascade cyclization. The reaction features the formation of three different C–N bonds in sequence. Imidazopyridine based fluorescent probe 5 exhibits highly sensitive and selective fluorescent sensing for Fe3+(‘turn-on’) and Hg2+(‘turn-off’). The excellent selectivity of imidazopyridine for Fe3+/Hg2+ was not hampered in the presence of any of the competing cations. The limit of detection (LOD) of 5 toward Fe3+ and Hg2+ has been estimated to be 4.0 ppb and 1.0 ppb, respectively, with a good linear relationship (R2 = 0.99). Notably, 5 selectively detects Fe3+/Hg2+ through fluorescence enhancement signalling both in vitro and in HeLa cells.A new fluorescent sensor 5 having fused imidazopyridine scaffold has been synthesized via cascade cyclization. It exhibits highly sensitive and selective detection of Fe3+ (‘turn-on’) and Hg2+ (‘turn-off’) in vitro and in HeLa cells. 相似文献
67.
Aneesa Ansari Md.Shahed Zaman Shahriar Md.Mehedi Hassan Shukla Rani Das Begum Rokeya Md.Anwarul Haque Md.Enamul Haque Nirupam Biswas Tama Sarkar 《Asian Pacific journal of tropical medicine》2014,7(1):21-25
Objective:To evaluate the antidiabetic and antioxidant potential of Emblica officinalis(E.officinalis)fruit on normal and type 2 diabetic rats.Methods:Type 2 diabetes was induced into the male Long-Evans rats.The rats were divided into nine groups including control groups receiving water,type 2 diabetic controls,type 2 diabetic rats treated with glibenclamide(T2GT)and type 2diabetic rats treated with aqueous extract of fruit pulp of E.officinalis.They were fed orally for8 weeks with a single feeding.Blood was collected by cutting the tail tip on 0 and 28 days and by decapitation on 56 day.Packed red blood cells and serum were used for evaluating different biochemical parameters.Results:Four weeks administration of aqueous extract of E.officinalis improved oral glucose tolerance in type 2 rats and after 8 weeks it caused significant(P0.007)reduction in fasting serum glucose level compared to 0 day.Triglycerides decreased by 14%but there was no significant change in serum ALT,creatinine,cholesterol and insulin level in any group.Furthermore,reduced erythrocyte malondialdehyde level showed no significant change(P0.07)but reduced glutathione content was found to be increased significantly(P0.05).Conclusions:The aqueous extract of E.officinalis has a promising antidiabetic and antioxidant properties and may be considered for further clinical studies in drug development. 相似文献
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69.
Annayya R. Aroor Ricardo J. Restrepo Kusum K. Kharbanda Shivendra D. Shukla 《Hepatology International》2014,8(2):421-430
Purpose
Ethanol binge augments liver injury after chronic ethanol consumption in humans, but the mechanism behind the enhanced liver injury by ethanol binge is not known. In this study we used a clinically relevant rat model in which liver injury is amplified by binge after chronic ethanol treatment and investigated the importance of histone modifications.Methods
Eight-week-old Sprague-Dawley rats were fed ethanol in a liquid diet for 4 weeks. Control rats were fed an isocaloric liquid diet. This was followed by three binge administrations of ethanol (intragastric 5 g/kg body weight, 12 h apart). In the control, ethanol was replaced by water. Four hours after the last binge administration, liver samples were analyzed for histone modifications and parameters of liver injury.Results
Chronic ethanol administration alone caused an increase in histone H3 ser10 and ser28 (H3S10 or S28) phosphorylation, and binge ethanol reduced their levels. Levels of dually modified phosphoacetylated histone H3 (H3AcK9/PS10) increased after acute binge ethanol and remained same after chronic ethanol binge. In contrast, histone H3 lysine-9 acetylation (H3AcK9) was not increased after chronic ethanol but increased significantly after acute binge and chronic ethanol binge. Increase in histone acetylation was accompanied by increased phospho-ERK1/2 in the nuclear extracts. Increased acetylation after chronic ethanol binge was also accompanied by increased protein levels of GCN5 histone acetyl transferase and a modest increase in HDAC3 in the nucleus. Histone lysine-9 dimethylation was significantly increased after chronic ethanol binge. Chronic ethanol binge also resulted in a decrease in the SAM:SAH ratio with a relative decrease of SAM levels and a corresponding increase in SAH levels.Conclusions
Ethanol binge after chronic ethanol altered the profile of site-specific histone modifications and may underlie the mechanism of augmented liver injury by chronic-ethanol-binge-treated rats.70.