Accumulation and infiltration of polymorphonuclear leukocytes are pivotal factors in accelerating cell apoptosis and death in ischemia/reperfusion(I/R) injury, however, adhesion molecules play an important role in its rolling，latching and infiltrating. The goal of the review is to explore the effect and significance of intercellular adhesion molecule-1(ICAM-1) in ischemia/reperfusion.

Joint -Up Community is crucial to the community health services. Joint - Up is an kind of co -operation, but it is neither the co - operation of bureaucracy nor that of the market model. The new relationship of Joint - Up is based neither on responsibility nor on contract, but on equal partnership. It is vital to solve the ethical plight of health services in country.

Dystonia is common in children with cerebral palsy. It can cause motor dysfunction, and is frequently associated with altered speech articulation, abnormal swallowing, and excessive drooling. Although trihexyphenidyl (Artane) is an anticholinergic agent with a long history of use in the management of dystonia in adults, information is limited regarding the use of trihexyphenidyl in children. This study reviewed the clinical experience of the use of trihexyphenidyl in children with cerebral palsy for dystonia, with special emphasis on benefits and tolerability.

BACKGROUND:Nitric oxide can interfere with the function of mitochondria, and accelerate the intervertebral disc damage and degeneration by interfering with the release of inflammatory cytokines. Nitric oxide is an important inflammatory cel medium leading to degeneration of intervertebral disc induced by pressure and other external factors.
OBJECTIVE:To investigate the regulatory effect of nitric oxide and nitric oxide synthase inhibitor niacinamide on mitochondrial function and its association with biological behavior of rabbit nucleus pulposus.
METHODS:Cultured nucleus pulposus cel s of rabbit lumbar intervertebral disc were randomly divided into six groups:normal blank control group, 10μmol/L sodium nitroprusside group, 100μmol/L sodium nitroprusside group, 200μmol/L sodium nitroprusside group, 0.05 g/L nicotinamide group (100μmol/L sodium nitroprusside+0.05g/L nicotinamide), and 0.5 g/L nicotinamide group (100μmol/L sodium nitroprusside and 0.5 g/L nicotinamide). Different doses of nitric oxide donor sodium nitroprusside and nicotinamide were added in the medium of each group. Three days after intervention, cel proliferation activity, intracel ular ATP concentration, cel nitric oxide synthase activity, cel ular reactive oxygen species level, and mitochondrial membrane potential were detected respectively.
RESULTS AND CONCLUSION:(1) After 3 days of rabbit nucleus pulposus cel s intervened by different concentrations of sodium nitroprusside, intracel ular nitric oxide synthase content increased with sodium nitroprusside volume increase, and ATP concentration decreased along with sodium nitroprusside volume increase;there were significantly differences between the normal control group and sodium nitroprusside groups (P<0.01). (2) Reactive oxygen species could be increased in the sodium nitroprusside group. Niacinamide groups indicated a dose-dependent manner to improve the increase of cel ular reactive oxygen species levels with sodium nitroprusside intervention (P<0.01). (3) In the sodium nitroprusside groups, nucleus pulposus cel membrane potential decreased. In the niacinamide groups, sodium nitroprusside-induced decline in mitochondrial membrane potential was reduced (P<0.01). (4) Niacinamide groups also indicated a dose-dependent manner to improve the proliferative activity of nucleus pulposus cel s as compared with sodium nitroprusside groups (P<0.01). Significant differences were determined between the two groups (P<0.01). (5) Results suggest that the excess nitric oxide can damage mitochondrial metabolic function of rabbit nucleus pulposus cel s and cause cel energy metabolism. Niacinamide can reverse these damages by inhibiting nitric oxide synthesis, thereby contributing to the prevention against intervertebral disc degeneration.

Objective To investigate the pefinatal infant brain damage in the blcod of neuron specific enolase and long-term changes in the development of nervous system disordem related to the neonatal brain injury prognosis timely predictions for the early intervention and provide a theoretical basis.Methods 40 cases of periatal brain injury in newborns were selected for the study.20 patients over the same period of normal newborns assigned to the control groups.both groups in the 72 hours after birth within the collected blood samples submitted preservation of the neuronspecific enolase enzyme,and rely follow-up of the two groups,so as to cover Gesell development scale statistical analysis of neuron specific enolase and perinatal brain damage in children with long-term development of nervous system disorder relevant.Results Brain injury group blood neurompeeifie enolase concentrations were higher:15-month-old brain-injury group scale evaluation of sale to group health suspicious after three clays of Mood neuronspecific enolase concentrations significantly higher to the development of the normal group.Conclusion Neuronspecific enolase may change as early diagnosis of perinatal brain injury,as well aft the main indicators of the long-term prognosis.

AIM To investigate the poteintation of adriamycin induced apoptosis by neferine in resistant human breast cancer cell line MCF 7/Adr. METHODS Apoptosis was detected by PI stain flow cytometry and Tunel assay. The intracellular adriamycin (ADR) accumulation was assayed by HPLC and the expression of P gp was determined by flow cytometry. RESULTS (1)MCF 7/Adr cells resisted the apoptosis induced by ADR while Nef augmented ADR medidated apoptosis; (2) Nef (10 ?mol?L -1 ) increased the accumulation of ADR up to 2 88 fold in MCF 7/Adr cells but not in sensitive cells MCF 7/S; (3) Nef(10 ?mol?L -1 ) reduced the expression of P gp in MCF 7/Adr cells. CONCLUSIONS Nef can overcome apoptosis resistance in MCF 7/Adr cells and its mechanisms are involved in the augment of ADR accumulation and the down-modulation of P gp expression in MCF 7/Adr cells.

Aim To investigate the effect of 8-bromo-7-methoxychrysin(BrMChR) on apoptosis of human gastric carcinoma SGC-7901 cell line.Methods SGC-7901 cells were cultured and the inhibitory effect of BrMChR on the proliferation of SGC-7901 cell line was measured by MTT assay.The apoptosis of SGC-7901 cells induced by BrMChR was analyzed using flow cytometry (FCM) with PI staining.DNA ladder bands were observed by DNA agarose gel electrophoresis.Results MTT assay suggested that BrMChR markedly inhibited the proliferation of SGC-7901 cells in a concentration-dependent manner,its IC50 was 2.6 ?mol?L-1,the potency of BrMChR was 8 times more than that of lead compound,chrysin (ChR,IC50 was 16.5 ?mol?L-1),and was 3 times more than that of 5-fluorouracil (5-FU,IC50 was 7.7 ?mol?L-1). FCM with PI staining indicated the apoptotic rate of SGC-7901 cell line treated with BrMChR (1.25,5.00,20.00 ?mol?L-1) for 48 h was (19.8%?0.2%),(36.8%?1.9%) and (45.5%?3.5%) respectively and the rate treated with BrMChR (1.25 ?mol?L-1) was higher than that treated with ChR (20.00 ?mol?L-1,12.9%?1.5%). DNA agarose gel electrophoresis showed that when treated with BrMChR(20.00 ?mol?L-1) for 48 h,the gene DNA of SGC-7901 cells presented typical DNA ladder bands which could attenuated by the effect of pre-incubation of GW9662(10.00 ?mol?L-1),a blocker of PPAR?.Conclusion BrMChR might induce apoptosis of SGC-7901 cell line partially by activating PPAR?.

The distribution of serotonin(5-HT), phenylethanolamine-N-methyltransferase (PNMT), substance P(SP) and leu-enkephalin(L-ENK) immunoreactive neurons in the rostral ventrolateral medulla (RVL) of the cat was studied with the immunohistochemical ABC technique, and the projection of 5-HT, SP and L-ENK positive neurons of the RVL into the thoracic cord was preliminarily investigated by a combined fluorescent retrograde transport and immunofluorescence method. The results indicate that 5-HT, PNMT, SP and L-ENK immunoreactive neurons mentioned above were localized primarily in the caudal part of nucleus paragigantocellularis lateralis and the rostral part of nucleus lateralis reticularis. SP positive cell bodies in the reticular formation close ventrolateral to nucleus ambiguus were also found. Some 5-HT, SP and L-ENK positive cells were situated in the area near the pia mater. In the most area of the RVL, 5-HT, PNMT, SP and L-ENK immunoreactive cell bodies had an overlapping distribution. 5-HT or PNMT or L-ENK positive neurons crowded, intertwined each other with their processes in the region at the levels 1.0-3.5mm caudal to trapezoid body, about 3.3mm lateral to the midline and about 0.8mm from the ventral surface of the medulla, and formed a longer or shorter continuous cell column which ran in the rostrocaudal direction. These three columns nearly coincided with each other at the level 1.5-2.5mm caudal to trapezoid body. Part of 5-HT, SP and L-ENK positive neurons in the RVL projected into the thoracic cord. The functional significance of these substances in the RVL was also discussed.

AIM To study the effects of neferine on gastric car cinoma apoptosis induced by vincristine in vitro. METHODS Cytotoxicity assay was tested by MTT method. The influence of neferine to affect vincristine to induce gastric carcinoma apoptosis was detected by PI staining flow cytometry, AO/EB double fluorescence stain and terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). RESULTS 2 5, 5,10 ?mol?L -1 neferine enhanced vincristine to inhibit the proliferation of SGC7901 cells; 10 ?mol?L -1 neferine enhanced vincristine (0 1, 0 5, 2, 4 mg?L -1 ) to induce SGC7901 cells apoptosis. CONCLUSIONS Neferine enhanced vincristine to induce gastric carcinoma cells apoptosis. It is inferred a kind of low poisonous and high effective chemosenstizers.

1.15). Rosiglitazone at the concentration of 1.25 ?mol?L -1 augme nted the induction apoptosis of A549 cells by treatment with Cisplatin at variou s concentrations of 1.98 mg?L -1, 2.8 mg?L -1 and 4.0 mg?L -1 . A549 cells treated with Rosiglitazone at concentration of 1.25 ?mol?L -1 domostrated nuclear traslocations of PPAR? protein and down-regulation of Bcl-2 protein. Conclusion The ligand of PPAR? Rosiglitazone enhanc ed the inhibition of proliferation and induction of apoptosis by treatment with Cisplatin in A549 cells cultured in vitro. Activation of PPAR? protein and the down-regulation of Bcl-2 possiblely play an improtant role in chemosenstiz eic mechanism of Rosiglitazone in vitro.