Minocycline Attenuates Microglial Response and Reduces Neuronal Death after Cardiac Arrest and Cardiopulmonary Resuscitation in Mice

The possible role of minocycline in microglial activation and neuronal death after cardiac arrest（CA） and cardiopulmonary resuscitation（CPR） in mice was investigated in this study. The mice were given potassium chloride to stop the heart beating for 8 min to achieve CA, and they were subsequently resuscitated with epinephrine and chest compressions. Forty adult C57BL/6 male mice were divided into 4 groups（n=10 each）： sham-operated group, CA/CPR group, CA/CPR＋minocycline group, and CA/CPR＋vehicle group. Animals in the latter two groups were intraperitoneally injected with minocycline（50 mg/kg） or vehicle（normal saline） 30 min after recovery of spontaneous circulation（ROSC）. Twenty-four h after CA/CPR, the brains were removed for histological evaluation of the hippocampus. Microglial activation was evaluated by detecting the expression of ionized calcium-binding adapter molecule-1（Iba1） by immunohistochemistry. Neuronal death was analyzed by hematoxylin and eosin（H＆E） staining and the levels of tumor necrosis factor-alpha（TNF-α） in the hippocampus were measured by enzyme-linked immunosorbent assay（ELISA）. The results showed that the neuronal death was aggravated, most microglia were activated and TNF-α levels were enhanced in the hippocampus CA1 region of mice subjected to CA/CPR as compared with those in the sham-operated group（P〈0.05）. Administration with minocycline 30 min after ROSC could significantly decrease the microglial response, TNF-α levels and neuronal death（P〈0.05）. It was concluded that early administration with minocycline has a strong therapeutic potential for CA/CPR-induced brain injury.

A Stream Control Transmission Protocol Based OAM System of 3G Cellular Network

OAM (Operations, Administration and Maintenance) system is a very impo rtant component of 3G cellular network. In order to acquire overall managemen t, fast response and steady operation, an SCTP (Stream Control Transmission Prot ocol) based OAM, i.e., SOAM system was proposed. SOAM implements new characters of SCTP such as multi-stream, enforced SACK and heartbeat mechanism on its tran sport layer. These characters help SOAM decrease the message transmission delay and accelerate the link failure detection. Besides, a new component named SOAM agent was introduced to improve the operation efficiency of SOAM. The experim ental results prove the proposed SOAM system achieves better performance on sign aling transmission compared with conventional TCP based OAM system.