A new multi-channel EEG signal acquisition system,which adopts Cypress's EZ-USB FX2 series USB as its micro-controller,is presented in this paper.The system employs AD620 and OP07 at the pre-amplifying stage and the following two amplifying stages respectively.Universal Series Bus(USB) technology is used to realize the real-time recording,displaying and tele-monitoring of EEG signal,which can also be stored in CF card after compression.The USB software developing tool is WinDriver.

AIM: To demonstrate the effects of telmisartan on the proliferation and apoptosis of U937 cells.METHODS: The proliferation ability of the U937 cells was assessed by CCK-8 assay and colony formation test with methylcellulose.The CD11b expression rate of the U937 cells was identified by flow cytometry.The apoptotic rate was analyzed by flow cytometry with Annexin V-PI double staining and Hoechst 33342 staining.The protein levels of cleaved PARP and cleaved caspase-3 were determined by Western blot.RESULTS: The results of CCK-8 assay confirmed that the viability of U937 cells was inhibited by telmisartan.The colony formation capacity of U937 cells was also significantly inhibited by telmisartan.The differentiation of U937 cells was induced by telmisartan with the expression of CD11b.The results of flow cytometry analysis with Annexin V-PI double staining and Hoechst 33342 staining identified that the apoptosis of U937 cells was induced by telmisartan in dose-dependent and time-dependent manners with the up-regulation of cleaved PARP and cleaved caspase-3 proteins.CONCLUSION: Telmisartan inhibits the proliferation and induces the differentiation of U937 cells.Telmisartan also induces the apoptosis of U937 cells through the caspase pathway.

AIM:To investigate the activity change of voltage-dependent delayed rectifier potassium channel(Kv) on human airway smooth muscle cells(HASMCs) after transfection of Kv1.5 antisense oligonucleotides(AsOND),and to discuss the regulating mechanism of Kv1.5.METHODS: The mRNA and protein expressions of Kv1.5 in liposome-mediated Kv1.5 AsOND transfected HASMCs were measured with techniques of reverse transcriptase-polymerase chain reaction(RT-PCR) and Western blotting.Kv activities in transfected HASMCs were investigated with whole-cell patch clamp.RESULTS: After HASMC were transfected by liposome-mediated Kv1.5 AsOND,the mRNA and protein expressions of Kv1.5 were decreased,and Kv activity was inhibited,which made the cell membrane potential(Em) inclined to depolarization.CONCLUSION: Transfection of Kv1.5 AsOND made the function of Kv in HASMCs decreased.Kv1.5 may play a critical role in the regulation of Kv activity.

The effects of protein kinase C (PKC) on the tension and the activity of voltage-dependent delayed rectifier potassium channel (K(y)) were examined in normal and passively sensitized human airway smooth muscle (HASM), by measuring tones and whole-cell patch clamp techniques, and the K(v) activities and membrane potential (E (m)) were also detected. The results showed that phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group (P<0.05), and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. K(v) activities of HASM cells were significantly inhibited by PMA, and the E (m) became more positive, as compared with the DMSO (a PMA menstruum)-treated group (P<0.01). This effect could be blocked by Ro31-8220 (P<0.01). It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced K(v) activity. In passively sensitized HASM rings, this effect was more notable.

Objective To investigate the apoptosis inducing effects of oridonin on leukemic THP-1 cells and its mechanisms of action. Methods THP-1 cells in culture medium in vitro were given different concentrations of oridonin (16～56 μmol/L) for 24, 48 and 72 h. The inhibitory rate of the cells were measured by MTT assay, apoptotic morphology was observed by Hoechst 33258 staining, and Annexin V/PI staining was used to detect cell apoptosis by flow cytometry (FCM). Caspase-3 and poly (ADP-ribose) polymerase (PARP) expression were detected by Western blotting. Results Oridonin (over 32 μmol/L) could inhibit the growth of THP-1 cells and cause apoptosis remarkably, the suppression was both in time-and dose-dependentmanner. Marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Hoechst 33258 staining, and Annexin V/PI staining showed that apoptotic cells gradually increased after the cells treated with oridinon. Western blotting showed cleavage of the caspase-3 zymogen protein (32×103), with the appearance of its 20×103 subunit, and a cleaved 89×103 fragment of 116×103 PARP was also found. Conclusion Oridonin can inhibit cell growth and induce apoptosis in THP-1 cells via activation of caspase-3. The results indicated that oridonin might be an important potential anti-leukemia reagent.

Objective To investigate the apoptosis inducing effect of peroxisome proliferator-activated receptor r(PPARr)agomst on leukemic K562 cells and its mechanisms of action.Methods K562 cells in culture medium in vitro were given different concentrations of PPARragonist rosiglitazone(RGZ)(20-80 umol/L)for O,24,48 and 72h The inhibitory rate of the cells were measured by MTT assay,cell apoptosis was detected by Annexin V/PI staining,and the expression of P53 protein as well as the activity of caspase-3 were also detected.Results RGZ(over 40umoL/L)could inhibit the growth of K562 cells and cause apopto-sis remarkably,the suppression Was both in time-and dose-dependent manner.The expression of P53 pmtein was upregulated and the activity of caspase-3 Was increased concomitantly after the cells werle treated by RGZ.Conclusion PPARr agonist RGZ(over 40 umol/L)can induce apoptosis on K562 cells signifieantly,upregu-lation the expression of P53 protein as well as increasing caspase-3 activity may be one of its most important mechamisms.

Objective To investigate the effects of anti-adhesion treatment and high-strength suture technique on the treatment of extensor tendon rupture by animal experiments and clinical application.Methods Twenty-eight leg-born chickens were randomly divided into four groups(7 each).Double cross suture was applied in group A,while double cross suture combined with sodium hyaluronate spraying in group B,cross-finger-like micro-braided suture in group C,and cross-finger-like micro-braided suture combined with sodium hyaluronate spraying in group D.The animals were sacrificed 6 weeks after operation,morphological,histological and biomechanics were observed and compared among the groups.One hundred and sixteen patients were treated with the surgical method in group D(89 males,27 females,aged 20-55 with an average of 36 years;73 with extensor tendon rupture,38 with strain/chalasis,5 with firearm injuries;56 on back of hand,48 on central slip,12 on lateral fixing chorda;82 with one-stage operation,and 34 with second-stage operation),and then followed-up for 2-5 years to observe the therapeutic effects.Results The repaired tendons in group D was in good contour,most tendon cells arranged regularly in bunches.The maximum load was significantly higher in group D(70.9?5.7N) than in group A(48.4?5.7N),Group B(51.3?3.2N) and Group C(68.3?2.8N,P

AIM: To investigate the regulatory effects of voltage-dependent delayed rectifier potassium channel (Kv) on the tension of normal and passively sensitized human airway smooth muscle (HASM). METHODS: By using blockers of potassium channels as tools, the tension of HASM and Kv gene mRNA and protein expressions in normal and asthmatics serum sensitized HASM cells were measured with techniques of reverse transcriptase/polymerase chain reaction (RT-PCR) and immunocytochemistry. RESULTS: (1) 4-aminopyridine (4-AP), the blocker of Kv, caused a concentration dependent constriction in normal HASM rings. The negative logarithm of the drug concentration causing 50% of maximal effect (pD_2) in normal group (2.09?0.09) was significantly different from that in the sensitized group (2.44?0.16, P0.05). (2) There were Kv1.2, Kv1.3 and Kv1.5 mRNA expressions in cultured HASM cells, but only Kv1.5 mRNA (P

OBJECTIVETo investigate the apoptosis inducing effects of ponicidin (PON) on leukemic K562 cells and its mechanisms of action.

METHODK562 cells in culture medium in vitro were given different concentrations of PON (10-50 micromol x L(-1)) for 24, 48 and 72 h. The inhibitory rate of the cells was measured by MTT assay, cell apoptotic rates were detected by flow cytometry (FCM) using Annexin V staining after K562 cells were treated with different concentrations of PON for 72 hours, and cell morphology was observed by Wright-Giemsa staining. Western blot was used to detect caspase-3 and poly(ADP-ribose) polymerase (PARP) expression, and the protein levels in mitogen-activated protein kinase signaling pathways (MAPKs, p-P38, p-ERK and p-JNK) as well as p-AKT and p-P85 in PI3K/AKT signaling pathways were also detected.

RESULTPON (over 30 micromol x L(-1)) could inhibit the growth of K562 cells in both time- and dose-dependent manner. FCM analysis revealed that apoptotic cells were gradually increased in a dose-dependent manner after treatment for 72 hours, and that marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Wright-Giemsa staining after treatment by 50 micromol x L(-1) PON. Western blot showed cleavage of the caspase-3 zymogen protein (32 kD), with the appearance of its 17 kD subunit, and a cleaved 89 kD fragment of 116 kD PARP was also found. Furthermore, Western blotting also showed that expression of p-AKT and p-P85 in PI3K/AKT signaling pathways was downregulated dramatically whereas the expression of p-P38 as well as p-ERK and p-JNK remained unchanged after the cells were treated by PON for 48 h.

CONCLUSIONThe results demonstrate that PON exhibits in vitro anti-leukemia effect by induction of apoptosis in K562 cells, and that PON induced apoptosis in K562 cells mainly related to activation of caspase-3 as well as inactivation of PI3K/AKT signaling pathway via down regulation of the expression of p-AKT and p-P85 protein levels. These results provide strong laboratory evidence for further anti-leukemia trials of PON.

Apoptosis ; drug effects ; Blotting, Western ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Diterpenes ; pharmacology ; Humans ; Poly(ADP-ribose) Polymerases ; metabolism ; Signal Transduction ; drug effects

The effects of protein kinase C (PKC) on the tension and the activity of voltage-dependent delayed rectifier potassium channel (Kv) were examined in normal and passively sensitized human airway smooth muscle (HASM), by measuring tones and whole-cell patch clamp techniques, and the Kv activities and membrane potential (Em) were also detected. The results showed that phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group (P＜0.05), and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. Kv activities of HASM cells were significantly inhibited by PMA, and the Em became more positive, as compared with the DMSO (a PMA menstruum)-treated group (P＜0.01). This effect could be blocked by Ro31-8220 (P＜0.01). It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced Kv activity. In passively sensitized HASM rings, this effect was more notable.