Tumor necrosis factor α in the pathogenesis of cerebral malaria

Physiologically in the brain, cytokines such as tumor necrosis factor-alpha (TNmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">) are released by the immune system and can modulate neurological responses. Conversely, the central nervous system (CNS) is also able to modulate cytokine production. In the case of CNS disorders, cytokine release may be modified. Cerebral malaria (CM) is a complication of Plasmodium falciparum infection in humans and is characterized by a reversible encephalopathy with seizures and loss of consciousness. Central clinical signs are partly due to sequestration of parasitized red blood cells in the brain microvasculature due to interactions between parasite proteins and adhesion molecules. TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> is produced and released by host cells following exposure to various malarial antigens. The increase of TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> release is responsible for the overexpression of adhesion molecules. This article reviews the involvement of TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> in cerebral malaria and the relation with all the processes involved in this pathology. It shows that (i) TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> levels are increased in plasma and brain but with no clear correlation between TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> levels and occurrence and severity of CM; (ii) TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> is responsible for intercellular adhesion molecule-1 upregulation in CM, the relation being less clear for other adhesion molecules; (iii) TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> receptors are upregulated in CM, with TNF receptor 2 (TNFR2) showing a higher upregulation than TNFR1 in vivo; (iv) in murine CM, low doses of TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> seem to protect from CM, whereas excess TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> induces CM and anti-TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> therapies (antibodies, pentoxifylline) did not show any efficiency in protection from CM. Moreover, the involvement of lymphotoxin a, which shares with TNFmg src="/content/1mg59111pgxrm61x/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0"> the same receptors with similar affinity, appears to be an interesting target for further investigation.Received 4 December 2002; received after revision 7 February 2003; accepted 14 February 2003     

添加镍粉球磨对Mg17Al12合金相结构及电化学储氢性能的影响

研究了Mg17A12铸态合金和Mg17Al12＋x％Ni（z=50～200）球磨复合物的相结构和电化学性能。结果表明，Mg17Al12-Ni复合物的相结构和放电容量主要取决于复合物中镍粉的加入量。加入的镍粉越多，越利于非晶结构的形成，其放电容量就越大。球磨120h的Mg17Al12＋200％Ni复合物在303K的放电容量高达658．2mAh·g^-1（除去镍粉的质量）。     

添加镍粉球磨对Mg_(17)Al_(12)合金相结构及电化学储氢性能的影响(英文)

研究了Mg17Al12铸态合金和Mg17Al12 x%Ni(x=50～200)球磨复合物的相结构和电化学性能。结果表明,Mg17Al12-Ni复合物的相结构和放电容量主要取决于复合物中镍粉的加入量。加入的镍粉越多,越利于非晶结构的形成,其放电容量就越大。球磨120h的MgAl 200%Ni复合物在303K的放电容量高达658.2mAh.g-1(除去镍粉的质量)。     

三硝基甲苯（TNT）废水连续光催化降解分析

在自制的列管式光催化器中,以纳米Ti O2P25为光催化剂,对三硝基甲苯（TNT）废水连续光催化降解条件进行实验研究。结果表明,反应管连接方式及列管数目、流体流量、催化剂用量、H2O2的添加以及光照条件等均对TNT废水的光降解存在不同程度的影响。4根管子采用串联方式,气体流量3 L/min,液体流量0.5 L/h,同时添加27 mmol/L H2O2时,TNT废液（20 mg/L）可彻底矿化。