http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Srivastav, (검색결과 10 건)
- 무료
- 기관 내 무료
- 유료
-
-
Akash Srivastav,Sanjeev Kumar Raghuwanshi 보안공학연구지원센터 2016 International Journal of Signal Processing, Image Vol.9 No.7
A novel technique to generate an arbitrary chirped waveform by harnessing features of Lithium Niobate Mach-Zehnder analog intensity Modulator is suggested and verified by mathematical analysis. The most important application of chirped microwave waveform is that, it improves the range- resolution of radar. In the proposed approach, two electrical drive signal of opposite gain is used to modulate light coming out from the continuous-wave (CW) laser in LiNb Mach-Zehnder modulator (MZM). The output of the MZM is chirped optical waveform due to the dependence of the mach-zehnder modulators chirp on the form of signals applied to the drive electrode. In our simple and straight forward method of producing chirped waveform, is basically based on the concept of change in phase at the two arms of Lithium Niobate Mach-Zehnder modulator due to change in refractive index at the respective arms when electric drive voltage is applied. The chirping phenomenon is expressed in terms of an intrinsic chirp parameter of the MZM. The proposed design is simple, easy to implement and cost effective than the previously proposed model of chirped waveform generation uses the MZM and chirped fiber Bragg grating.
-
Enhanced neuroinflammatory responses after systemic LPS injection in IL-32β transgenic mice
Neupane, Sabita,Srivastav, Sunil,Bhurtel, Sunil,Katila, Nikita,Shadfar, Sina,Park, Pil-Hoon,Hong, Jin Tae,Choi, Dong-Young Elsevier 2018 Journal of chemical neuroanatomy Vol.94 No.-
<P><B>Abstract</B></P> <P>IL-32 is a proinflammatory cytokine, and involved in various diseases including infection, inflammation, and cancer. However, effects of IL-32 on neuroinflammation remain obscure. Herein, we examined the effects of IL-32β on systemic LPS-induced neuroinflammation using IL-32β transgenic (Tg) mice. IL-32β wild type (WT) and Tg mice received LPS injection (5 mg/kg, i.p.), and then neuroinflammatory responses were evaluated. Systemic LPS caused remarkable gliosis in the brain at 12 h regardless of genotypes. The gliosis in WT mice was sustained by 24 h, whereas it became more severe in Tg mice by 24 h. Proinflammatory cytokines and proteins were increased at 12 h both in WT and Tg brains. The elevated levels of TNFα and VCAM-1were not altered over time, while levels of IL-6, IL-1β and iNOS were dropped in WT mice. In contrast, elevated levels IL-6, IL-1β, iNOS and VCAM-1 were sustained, and level of TNFα was augmented in Tg brains by 24 h. Interestingly, level of IL-10 mRNA in Tg mice was remarkably higher than in WT mice at 0 h, which was decreased at 12 h and maintained by 24 h. In WT brain, mRNA level of IL-10 was raised at 12 h after LPS injection, and further increased at 24 h. Activation of NF-κB signaling pathway was detected in glia cells after LPS injection which was exaggerated at 24 h in Tg mice in comparison to WT mice. These results indicate that IL-32β enhances neuroinflammatory responses caused by systemic LPS, and this might be attributable to prolonged activation of NF-κB signaling pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Effects of IL-32β on neuroinflammation were evaluated. </LI> <LI> Enhanced neuroinflammation was observed in IL-32β transgenic mice. </LI> <LI> Prolonged activation of NF-κB might be related to extended neuroinflammation. </LI> </UL> </P>
-
-
APPROXIMATION BY MODIFIED POST-WIDDER OPERATORS
( Sheetal Deshwal ),( Rupesh K. Srivastav ),( Gopi Prasad ) 한국수학교육학회 2023 純粹 및 應用數學 Vol.30 No.1
The current article manages with new generalization of Post-Widder operators preserving constant function and other test functions in Bohmann-Korovkin sense and studies the approximation properties via different estimation tools like modulus of continuity and approximation in weighted spaces. The viability of the recently modified operators as per classical Post-Widder operators is introduced in specific faculties also. Numerical examples are additionally introduced to verify our theortical results. In second last section we introduce Grüss-Voronovskaya results and in last section, we show the better approximation our new modified operators via graphical exmaples using Mathematica.
-
Mechanistic comparison between MPTP and rotenone neurotoxicity in mice
Bhurtel, Sunil,Katila, Nikita,Srivastav, Sunil,Neupane, Sabita,Choi, Dong-Young Elsevier BV 2019 NeuroToxicology Vol.71 No.-
<P><B>Abstract</B></P> <P>Animal models for Parkinson’s disease (PD) are very useful in understanding the pathogenesis of PD and screening for new therapeutic approaches. 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) and rotenone are common neurotoxins used for the development of experimental PD models, and both inhibit complex I of mitochondria; this is thought to be an instrumental mechanism for dopaminergic neurodegeneration in PD. In this study, we treated mice with MPTP (30 mg/kg/day) or rotenone (2.5 mg/kg/day) for 1 week and compared the neurotoxic effects of these toxins. MPTP clearly produced dopaminergic lesions in both the substantia nigra and the striatum as shown by loss of dopaminergic neurons, depletion of striatal dopamine, activation of glial cells in the nigrostriatal pathway and behavioral impairment. In contrast, rotenone treatment did not show any significant neuronal injury in the nigrostriatal pathway, but it caused neurodegeneration and glial activation only in the hippocampus. MPTP showed no such deleterious effects in the hippocampus suggesting the higher susceptibility of the hippocampus to rotenone than to MPTP. Interestingly, rotenone caused upregulation of the neurotrophic factors and their downstream PI3K-Akt pathway along with adenosine monophosphate-activated protein kinase (AMPK) activation. These results suggest that MPTP-induced dopaminergic neurotoxicity is more acute and specific in comparison to rotenone toxicity, and compensatory brain-derived neurotrophic factor (BDNF) induction and AMPK activation in the rotenone-treated brain might suppress the neuronal injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Neurotoxic property of MPTP and rotenone was compared. </LI> <LI> Neurotoxicity of MPTP was acute and selective to the dopaminergic neurons. </LI> <LI> Rotenone caused glial activation and neuronal loss in the hippocampus. </LI> </UL> </P>
-
Tewari, Shikha,Khan, Kainat,Husain, Nuzhat,Rastogi, Madhup,Mishra, Surendra P,Srivastav, Anoop K Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.4
Diagnostic and therapeutic radiation fields are planned so as to reduce side-effects while maximising the dose to site but effects on healthy tissues are inevitable. Radiation causes strand breaks in DNA of exposed cells which can lead to chromosomal aberrations and cause malfunction and cell death. Several researchers have highlighted the damaging effects of high dose radiation but still there is a lacuna in identifying damage due to low dose radiation used for diagnostic purposes. Blood is an easy resource to study genotoxicity and to estimate the effects of radiation. The micronucleus assay and chromosomal aberration can indicate genetic damage and our present aim was to establish these with lymphocytes in an in vitro model to predict the immediate effects low dose radiation. Blood was collected from healthy individuals and divided into 6 groups with increasing radiation dose i.e., 0Gy, 0.10Gy, 0.25Gy, 0.50Gy, 1Gy and 2Gy. The samples were irradiated in duplicates using a LINAC in the radiation oncology department. Standard protocols were applied for chromosomal aberration and micronucleus assays. Metaphases were stained in Giemsa and 200 were scored per sample for the detection of dicentric or acentric forms. For micronuclei detection, 200 metaphases. Giemsa stained binucleate cells per sample were analysed for any abnormality. The micronuclei (MN) frequency was increased in cells exposed to the entire range of doses (0.1-2Gy) delivered. Controls showed minimal MN formation ($2.0%{\pm}0.05$) with triple MN ($5.6%{\pm}2.0$) frequency at the lowest dose. MN formation increased exponentially with the radiation dose thereafter with a maximum at 2Gy. Significantly elevated numbers of dicentric chromosomes were also observed, even at doses of 0.1-0.5Gy, compared to controls, and acentric chromosomes were apparent at 2Gy. In conclusion we can state that lymphocytes can be effectively used to study direct effect of low dose radiation.
-
Synthesis of monodisperse In2O3 nanoparticles and their d0 ferromagnetism
S.K.S. Patel,Khemchand Dewangan,Simant Kumar Srivastav,N.S. Gajbhiye 한국물리학회 2014 Current Applied Physics Vol.14 No.6
Monodisperse indium oxide (In2O3) nanoparticles (NPs) with the average diameter of 11nmwere prepared by a solvothermal method. The In2O3 NPs were characterized by X-ray diffraction, Raman and transmission electron microscopy. The intrinsic nature of ferromagnetism in In2O3 NPs has been established with the experimental observation of magnetic hysteresis loop. Photoluminescence and UVevisible studies were employed to evidence the presence of oxygen vacancies and revealed that the oxygen vacancies contribute to the ferromagnetism. The origin of ferromagnetism in In2O3 NPs may be due to exchange interactions among localized electron spin moments resulting from oxygen vacancies.
-
Shadfar, S.,Kim, Y. G.,Katila, N.,Neupane, S.,Ojha, U.,Bhurtel, S.,Srivastav, S.,Jeong, G. S.,Park, P. H.,Hong, J. T. HUMANA PRESS INC 2018 Molecular Neurobiology Vol.55 No.1
<P>Neurotrophic factors are essential for neuronal survival, plasticity, and development and have been implicated in the action mechanism of antidepressants. In this study, we assessed the neurotrophic factor-inducing and neuroprotective properties of antidepressants. In the first part of the study, we found that fluoxetine, imipramine, and milnacipran (i.p., 20 mg/kg/day for 1 week or 3 weeks) upregulated brain-derived neurotrophic factor in the striatum and substantia nigra both at 1 week and 3 weeks. In contrast, an increase in the glial-derived neurotrophic factor was more obvious at 3 weeks after the antidepressants treatment. Specifically, it was found that fluoxetine and imipramine are more potent in raising the levels of neurotrophic factors than milnacipran. Furthermore, antidepressants elevated the phosphorylation of extracellular signal-regulated-protein kinase (ERK1/2) and the serine/threonine kinase Akt. In the second part of the study, we compared the neuroprotective effects of fluoxetine, imipramine, and milnacipran in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. Pretreament with fluoxetine, imipramine or milnacipran for 3 weeks reduced MPTP-induced dopaminergic neurodegeneration and microglial activation in the nigrostriatal pathway. Neurochemical analysis by HPLC exhibited that antidepressants attenuated the depletion of striatal dopamine. In consistent, beam test showed that behavioral impairment was ameliorated by antidepressants. Neuroprotective effects were more prominent in the fluoxetine or imipramine treatment group than in milnacipran treatment group. Finally, we found that neuroprotection of the antidepressants against 1-methyl-4-phenylpyridinium neurotoxicity in SH-SY5Y cells was attenuated by ERK or Akt inhibitor. These results indicate that neuroprotection by antidepressants might be associated with the induction of neurotrophic factors, and antidepressant could be a potential therapeutic intervention for treatment of Parkinson's disease.</P>
-
KISS연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
