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Saxena, Amit,Sharma, Abha,Singh, Beer,Suryanarayana, Malladi Venkata Satya,Mahato, Timir Haran,Sharma, Mamta,Semwal, Rajendra Prasad,Gupta, Arvind Kumar,Sekhar, Krishnamurthy Korean Carbon Society 2005 Carbon Letters Vol.6 No.3
Room temperature kinetics of degradation of nerve agent simulants and sarin, an actual nerve agent at the surface of different carbon based adsorbent materials such as active carbon grade 80 CTC, modified whetlerite containing 2.0 and 4.0 % NaOH, active carbon with 4.0 % NaOH, active carbon with 10.0 % Cu (II) ethylenediamine and active carbon with 10.0 % Cu (II) 1,1,1,5,5,5-hexafluoroacetylacetonate were studied. The used adsorbent materials were characterized for surface area and micropore volume by $N_2$ BET. For degradation studies solution of simulants of nerve agent such as dimethyl methylphosphonate (DMMP), diethyl chlorophosphate (DEClP), diethyl cyanophosphate (DECnP) and nerve agent, i.e., sarin in chloroform were prepared and used for the uniform adsorption on the adsorbent systems using their incipient volume at room temperature. Degradation kinetics was monitored by GC/FID and was found to be following pseudo first order reaction. Kinetics parameters such as rate constant and half life were calculated. Half life of degradation with modified whetlerite (MWh/NaOH) system having 4.0 % NaOH was found to be 1.5, 7.9, 1206 and 20 minutes for DECnP, DEClP, DMMP and sarin respectively. MWh/NaOH system showed maximum degradation of simulants of nerve agents and sarin to their hydrolysis products. The reaction products were characterized using NMR technique. MWh/NaOH adsorbent was also found to be active against sulphur mustard.
BRIP1/FANCJ Mutation Analysis in a Family with History of Male and Female Breast Cancer in India
Ananthapur Venkateshwari,David Wayne Clark,Pratibha Nallari,Cingeetham Vinod,Thangaraj Kumarasamy,Goverdhan Reddy,Akka Jyothy,Malladi Vijay Kumar,Raghuraman Ramaiyer,Komaraiah Palle 한국유방암학회 2017 Journal of breast cancer Vol.20 No.1
Male breast cancer (MBC) is a rare and poorly studied disease that is a growing global health problem. Interestingly, both the molecular basis of MBC and its histological profile are often quite distinct from the far more prevalent female breast cancer, emphasizing the need for increased focus on MBC. Here, we present a case report of an MBC patient from India with a strong familial history of breast cancer. This patient was normal for BRCA1/2 and many other common breast cancer-associated genes. However, upon further analysis, the individual was found to possess two mutations in the DNA helicase and tumor suppressor gene BRIP1, including a silent mutation at residue 879 as well as a P919S variant. Other family members were also screened for these mutations. To the best of our knowledge, this is the first report of BRIP1 mutation in MBC in the Indian population.
Syn, Wing‐,Kin,Choi, Steve S.,Liaskou, Evaggelia,Karaca, Gamze F.,Agboola, Kolade M.,Oo, Ye Htun,Mi, Zhiyong,Pereira, Thiago A.,Zdanowicz, Marzena,Malladi, Padmini,Chen, Yuping,Moylan, Cynthia,J Wiley Subscription Services, Inc., A Wiley Company 2011 Hepatology Vol.53 No.1
<P><B>Abstract</B></P><P>Nonalcoholic steatohepatitis (NASH) is a leading cause of cirrhosis. Recently, we showed that NASH‐related cirrhosis is associated with Hedgehog (Hh) pathway activation. The gene encoding osteopontin (OPN), a profibrogenic extracellular matrix protein and cytokine, is a direct transcriptional target of the Hh pathway. Thus, we hypothesize that Hh signaling induces OPN to promote liver fibrosis in NASH. Hepatic OPN expression and liver fibrosis were analyzed in wild‐type (WT) mice, Patched‐deficient (Ptc<SUP>+/−</SUP>) (overly active Hh signaling) mice, and OPN‐deficient mice before and after feeding methionine and choline–deficient (MCD) diets to induce NASH‐related fibrosis. Hepatic OPN was also quantified in human NASH and nondiseased livers. Hh signaling was manipulated in cultured liver cells to assess direct effects on OPN expression, and hepatic stellate cells (HSCs) were cultured in medium with different OPN activities to determine effects on HSC phenotype. When fed MCD diets, Ptc<SUP>+/−</SUP> mice expressed more OPN and developed worse liver fibrosis (<I>P</I> < 0.05) than WT mice, whereas OPN‐deficient mice exhibited reduced fibrosis (<I>P</I> < 0.05). In NASH patients, OPN was significantly up‐regulated and correlated with Hh pathway activity and fibrosis stage. During NASH, ductular cells strongly expressed OPN. In cultured HSCs, SAG (an Hh agonist) up‐regulated, whereas cyclopamine (an Hh antagonist) repressed OPN expression (<I>P</I> < 0.005). Cholangiocyte‐derived OPN and recombinant OPN promoted fibrogenic responses in HSCs (<I>P</I> < 0.05); neutralizing OPN with RNA aptamers attenuated this (<I>P</I> < 0.05). <I>Conclusion:</I> OPN is Hh‐regulated and directly promotes profibrogenic responses. OPN induction correlates with Hh pathway activity and fibrosis stage. Therefore, OPN inhibition may be beneficial in NASH (H<SMALL>EPATOLOGY</SMALL> 2011)</P>