T-type calcium channels present in cardiovascular, neuronal and endocrine systems, and they are now receiving attention as novel therapeutic targets. It plays important roles in multiple cellular functions and genes those encode the T-type calcium channels have been recently reported. Many drugs and compounds non-specifically block T-type calcium channels. We review circumstances of the research of T- type calcium channels in the molecular structure, distribution, function, regulation and the related drugs.

Melatonin (MT) is secreted by the pineal gland and has obvious biological rhythmicity including circadian, season rhythm and life rhythm (aging clock). The reduction of MT secretion is related to body aging, particularly in close relation to brain aging. The hypothesis of aging is involved in pineal calcification, biological clock, neuro-en-docrinoimmunology, and free radical damage. MT is an endogenous free radical scavenger, may anto-gonize the attack of hydroxyl free radical ( ?OH)on organism and glutamate (Glu) excitotoxicity, and has a potent protective effect of central nervous system. In vivo studies showed that the food restriction and exogenous MT could obviously prolong life, postpone aging, and reduce the chances of age-related diseases. Investigating of MT anti-aging effect shows a vast prospect.

The mechanism of killer toxin is believed to relate to the inhibition of yeast cell wall ? glucan synthesis. Mannoprotein probably is one of the receptor for HM 1 killer toxin. The resistance is due to the decrease of N glycosylation of the sensitive yeast strain. HM 1 is a hydrophilic protein consisting of 88 amino acids. Two arginine residues located at positions 82 and 86 in the C terminal region of molecule are essential for the action of killer activity of HM 1 toxin. It is very useful to develop a novel anti fungal agent and prevent wild yeast contamination.

This article reviews the proteins and transduction pat hw ay in endotoxic action. Lipopolysaccharide-binding protein(LBP) binds and trans ports the LPS to its receptors, which include CD14 and CD11/CD18. Toll-like rec eptors(TLRs) is closely associated with transducting the signals into cytoplasm. Scavenger receptors are related to hepatic clearance on endotoxin .The intracel lular signal transduction is involved in several paths which finally leads to t he release of cytokines.

AIM To observe the effects of melatonin on acute and chronic injuries induced by oxygen and glucose deprivation (OGD) in co-cultured neuron and glia and to explore the probable mechanisms of melatonin in antagonizing the injuries. METHODS The injury model of cultured neuron and co-cultured neuron and glia was made by administration of sodium dithionite and glucose-deprived Earles solution. In neuron and glia co-culture, two different models, acute injury model at the phase of OGD and chronic injury model after 'reperfusion' were established. The levels of nitric oxide (NO) and the activity of lactate dehydrogenase (LDH) were measured by Griess reagent and LDH kits respectively. The content of malondialdehyde (MDA) was determined by TBA method. Cell viability was analyzed using colorimetric MTT assay. RESULTS Melatonin increased the level of NO at the concentration of 10 -6 , 10 -7 mol?L -1 and decreased the level of MDA content elevated by OGD at the concentration of 10 -6 , 10 -7 , 10 -8 mol?L -1 in vitro cultured cortical neurons. In the chronic injury model after 'reperfusion' melatonin (10 -6 , 10 -7 , 10 -8 mol?L -1 ) significantly decreased LDH activity and increased MTT value in neurons and glia co-cultured. But in the acute injury model, melatonin obviously increased LDH activity and decreased MTT value. CONCLUSION Melatonin protection for neuron from injuries induced by oxygen and glucose deprivation may be related to increase in the level of NO and decrease in the content of MDA. Melatonin can antagonize the injury in the chronic injury model after 'reperfusion', but exaggerate the injury in the acute injury model. These may be all related to its antioxidant action. Our results also suggest that melatonin may probably inhibit activation of microglia.

Objective To study the surgical effects of frontalis suspension for children blepharoptosis . Methods Frontal muscle suspensions using dacron mesh sling were performed on 164 cases (200 eyes) of children blepharoptosis with dacron mesh sling and home made needles. The follow up periods were 3 months to 2 years (average 5.24 months). Results After the operation, the excellently corrected eyes were 166 (83 %); Under corrected eyes were 32 (16 %); Over corrected eyes were 2 (1 %). Conclusion Frontal muscle suspension using dacron mesh sling is effective to treat children blepharoptosis, which is suitable for the treatments of all kinds of children blepharoptosis. [

Neuroinflammation may be one of the causes in the pathogenesis of Alzheimer's disease(AD).Epidemiological studies suggest that long-term use of nonsteroidal anti-inflammatory drugs(NSAIDs)can reduce the risk of AD.Laboratory evidence indicates that the protection of NSAIDs is mediated by inhibition of cyclooxygenase(COX)activity and the non-COX mechanisms.This review summarizes the possible underlying mechanisms in the action.

Objective: Our purpose was to observe the effect of epithelial scrape injury on corneal morphology. Methods: Twenty 4-week-old white rabbits were used. We scraped the corneal epithelia of the left eye of each rabbit (0.2 mm near the limbus of corneal were left in 10 eyes, in the remaining rabbits within 8 mm in the center). The right eyes were control group. We observed the healing of corneal protrusion with slit-lamp microscope, examined the corneal form with corneal topography, and measured the depth of anterior chamber and the corneal thickness with A-ultrasound. Results: The extensive epithelial scrape significantly increased the healing time. The corneal protrusion of experimental group and the depth of anterior chamber increased. The corneal thickness became thinner. Conclusion: The extensive epithelial injury can make cornea thinner, which results in the changes of corneal protrusion.

Aim To investigate the protective effects of LMWH-SOD(Low molecular weight heparin- Superoxide dismutase Conjugate)on the injuries induced by oxygen and glucose deprivation in cultured neurons. Methods The cortical neurons of fetal rat were cultured in vitro. The antioxidant and protective effects of LMWH-SOD were observed by treating neurons with oxygen and glucose deprivation. Results LMWH-SOD reduced the number of cell death and the efflux of LDH and the content of NO,MDA and increased the membrane fluidity after the injuries of cells. Conclusion LMWH-SOD has protective effects on cerebral cortical neurons through its action of scavenging free radicals.

AIM: To study the effects of cyproheptadine (Cyp) and anisodamine (Ani)on the changes of intracellular free Ca 2+ concentration ([Ca 2+ ] i) induced by tumor necrosis factor (TNF ?) in single endothelial cells, and to explore the mechanisms of TNF ?-mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains(ECV304) were seed in 35 mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca 2+ ] i in single endothelial cell was determined by laser scanning confocal microscopy(LSCM). RESULTS: [Ca 2+ ] i in single endothelial cell after stimulation of TNF ? rapidly increased in a dose-dependent manner and approached the peak value within 60 seconds, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca 2+ ] i elevation was more obvious in nuclear than in cytoplasma, and decreased slowly. Cyp (3?10 -5 , 6?10 -5 mol/L) and Ani (2?10 -5 , 4?10 -5 mol?L -1 ) markedly inhibited TNF ? (1.2?10 -9 mol?L -1 )-induced [Ca 2+ ] i elevation. CONCLUSIONS: TNF ? markedly induces elevation of [Ca 2+ ] i in single endothelial cell, it may be an important mechanism of TNF ?-induced shock and tissue injury. Cyp and Ani obviously suppress TNF ?-induced [Ca 2+ ] i elevation, which probably is one of the mechanisms of their antishock effects.