Wideband chaotic tri-mode microlasers with optical feedback.

A tri-mode micro-square laser under optical feedback is proposed and demonstrated to generate chaos with the broadband flat microwave spectrum. By adjusting lasing mode intensities, frequency intervals, and optical feedback strength, we can enhance the chaotic bandwidth significantly. The existence of two mode-beating peaks makes the flat bandwidth much larger than the relaxation oscillation frequency. Effective bandwidth of 35.3 GHz is experimentally achieved with the flatness of 8.3 dB from the chaotic output spectrum of the tri-mode mode laser under optical feedback.

Optical frequency comb and picosecond pulse generation based on a directly modulated microcavity laser.

Optical frequency comb (OFC) and picosecond pulse generation are demonstrated experimentally based on a directly modulated AlGaInAs/InP square microcavity laser. With the merit of a high electro-optics modulation response of the microcavity laser, power-efficient OFCs with good flatness are produced. Ten 8-GHz-spaced optical tones with power fluctuation less than 3 dB are obtained based on the laser modulated by a sinusoidal signal. Moreover, the comb line number is enhanced to 20 by eliminating the nonlinear dynamics through optical injection locking. Owing to the high coherence of the OFC originating from the directly modulated microcavity laser, a 6.8 ps transform-limited pulse is obtained through dispersion compensation. The optical pulse is further compressed to 1.3 ps through the self-phase modulation effect in high nonlinear fiber.

Wideband multiwavelength Brillouin fiber laser based on dual-mode AlGaInAs/InP microcavity lasers.

A multiwavelength Brillouin fiber laser (BFL) is demonstrated using a 1.55-µm AlGaInAs/InP microcavity laser as a seed source. The combination of a nonlinear fiber cavity and a feedback loop leads to multiwavelength generation with a channel spacing of double-Brillouin-frequency assisted by cavity-enhanced four-wave mixing. The amplified output of a dual-mode lasing square microcavity laser with a wavelength interval of 1.5 nm is applied as the pump source for the broadband multiwavelength generation. A wideband multiwavelength BFL covering from 1490 nm to 1590 nm is successfully generated at an optimized pump power of 25 dBm and a feedback power of -17.2dBm. The power stability of 0.82 dB over a 60 min duration of the multiwavelength BFL can satisfy the demands for the optical fiber sensing and microwave photonic systems.

Low-phase-noise microwave generation using dual-mode microsquare laser phase locking by modulated sidebands.

An effective method for millimeter-wave (mmW) carrier generation from a dual-transverse-mode microsquare laser is experimentally demonstrated. By directly modulating the dual-mode microsquare laser at 6.7 GHz, multiple sidebands are generated due to enhanced modulation nonlinearity, and the lasing modes with an interval of 40 GHz are phase-locked. MmW carriers up to 47 GHz, corresponding to seven times that of the modulation frequency, are achieved with a linewidth below 10 Hz. The single-sideband phase noises of the signals keep the same level after transmission over 2.5 km of optical fiber.

[Risk assessment of lead exposure from different intake pathways for children in Wuhan City].

70 sampling points were set in Wuhan City to collect soil, dust, air and food samples. According to the U. S. EPA recommended childhood lead exposure parameters, U. S. EPA human exposure risk assessment method was used to assess the potential health risk of different pathway exposures of children in Wuhan City to lead. The results of calculation show: Wuhan urban children's daily lead exposure is 1.20 x 10(-3) mg x (kg x d)(-1). The digestive tract is the main way for children's exposure to lead, with the exposure of 1.04 x 10(-3) mg x (kg x d)(-1), followed by the respiratory route and dermal absorption route, the exposures were 0.153 x 10(-3) mg x (kg x d)(-1) and 8.56 x 10(-7) mg x (kg x d)(-1) respectively. Pathways of the digestive tract, ingestion of soil or dust lead exposure accounted for 52.0% of the total exposure, through the digestive tract of soil or dust ingestion is the main route of exposure. Monte-Carlo method was used to simulate the pathway in the digestive tract, the amount of lead exposure through ingestion of soil was 2. 48 x 10(-2) mg x d(-1). The probability that exceeded the PTDI (Provisional Tolerable Daily Intake) specified by JECFA (The Joint FAO/WHO Expert Committee on Food Additives) was 2.1%. The results of the risk assessment indicate that lead exposure risks from the digestive tract, respiratory tract, skin absorption are less than the maximum acceptable risk level 5.0 x 10(-5) respectively and the risk associated with skin absorption of lead is less than the negligible risk level 1 x 10(-8). Application of Kriging interpolation method, Wuhan City children lead exposure value on spatial distribution were obtained, and Qingshan district and Jiangan district have a high level of children lead exposure. The aggregate risk index of Wuhan City children lead exposure was yield by using the indicator Kriging.

5-Hydroxytryptamine directly inhibits neuronal nicotinic acetylcholine receptors in rat trigeminal ganglion neurons.

In the present study, whole-cell patch clamp recording technique was used to investigate the action of 5-hydroxytryptamine (5-HT) on the function of native neuronal nicotinic acetylcholine receptors expressed in the rat trigeminal ganglion neurons. Inward currents (I(nic)) caused by externally-applied nicotine were observed in majority of the examined neurons, which were mediated by alpha-bungarotoxin-insensitive nicotinic acetylcholine receptors. We found that 5-HT could reversibly inhibit I(nic) in a concentration-dependent manner, and the inhibition did not involve 5-HT receptors. Other serotonergic agents, such as 2-methyl-5-HT, alpha-methyl-5-HT, sumatriptan and ICS-205,930, also had similar inhibitory effects on I(nic). 5-HT inhibited nicotinic acetylcholine receptors in a non-competitive manner, as 5-HT decreased the maximal current response to nicotine but had no effect on the threshold and EC(50). The inhibition of I(nic) by 5-HT was voltage-dependent and became stronger at hyperpolarized potentials. These results indicated that 5-HT directly inhibited nicotinic acetylcholine receptors in the trigeminal ganglion neurons. As a local modulator of the nicotinic acetylcholine receptor, 5-HT might play a role in the modulation of sensory information.

Endothelial nitric oxide synthase-dependent tyrosine nitration of prostacyclin synthase in diabetes in vivo.

There is evidence that reactive nitrogen species are implicated in diabetic vascular complications, but their sources and targets remain largely unidentified. In the present study, we aimed to study the roles of endothelial nitric oxide synthase (eNOS) in diabetes. Exposure of isolated bovine coronary arteries to high glucose (30 mmol/l d-glucose) but not to osmotic control mannitol (30 mmol/l) switched angiotensin II-stimulated prostacyclin (PGI(2))-dependent relaxation into a persistent vasoconstriction that was sensitive to either indomethacin, a cyclooxygenase inhibitor, or SQ29548, a selective thromboxane receptor antagonist. In parallel, high glucose, but not mannitol, significantly increased superoxide and 3-nitrotyrosine in PGI(2) synthase (PGIS). Concurrent administration of polyethylene-glycolated superoxide dismutase (SOD), l-nitroarginine methyl ester, or sepiapterin not only reversed the effects of high glucose on both angiotensin II-induced relaxation and PGI(2) release but also abolished high-glucose-enhanced PGIS nitration, as well as its association with eNOS. Furthermore, diabetes significantly suppressed PGIS activity in parallel with increased superoxide and PGIS nitration in the aortas of diabetic C57BL6 mice but had less effect in diabetic mice either lacking eNOS or overexpressing human SOD (hSOD(+/+)), suggesting an eNOS-dependent PGIS nitration in vivo. We conclude that diabetes increases PGIS nitration in vivo, likely via dysfunctional eNOS.

Theaflavin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-inflammatory effect and modulation of STAT-1.

Theaflavin, a major constituent of black tea, possesses biological functions such as the antioxidative, antiviral, and anti-inflammatory ones. The purpose of this study was to verify whether theaflavin reduces focal cerebral ischemia injury in a rat model of middle cerebral artery occlusion (MCAO). Male Sprague-Dawley rats were anesthetized and subjected to 2 hours of MCAO followed 24 hours reperfusion. Theaflavin administration (5, 10, and 20 mg/kg, i.v.) ameliorated infarct and edema volume. Theaflavin inhibited leukocyte infiltration and expression of ICAM-1, COX-2, and iNOS in injured brain. Phosphorylation of STAT-1, a protein which mediates intracellular signaling to the nucleus, was enhanced 2-fold over that of sham group and was inhibited by theaflavin. Our study demonstrated that theaflavin significantly protected neurons from cerebral ischemia-reperfusion injury by limiting leukocyte infiltration and expression of ICAM-1, and suppressing upregulation of inflammatory-related prooxidative enzymes (iNOS and COX-2) in ischemic brain via, at least in part, reducing the phosphorylation of STAT-1.

Endogenous nitric oxide mediates lipoteichoic acid induced preconditioning on reoxygenation injury of cultured human coronary artery endothelial cells.

AIM: To explore the effects of lipoteichoic acid (LTA) induced delayed preconditioning (PC) on hypoxia-reoxygenation (H/R) injury of cultured human coronary artery endothelial cells (HCAECs), and to investigate the potential role of endogenous nitric oxide (NO) participated in the protective mechanism. METHODS: HCAECs were incubated for 2 h in a hypoxic atmosphere and reoxygenated for 4 h in a normoxic atmosphere. The delayed PC was induced by pretreatment with LTA (30 or 300 microg x L(-1)) for 4 h before 24 h recovery. The extent of cellular injury after reoxygenation was assessed by the percentage of cellular injury with Trypan blue exclusion and by the amount of lactate dehydrogenase (LDH) in culture media. The NO level of the culture media was measured spectrophotometrically. Furthermore, HCAECs were exposed to 300 microg x L(-1) of LTA for 4 h, and to detect the expression of eNOS mRNA by RT-PCR method after cells were recovered from different points. RESULTS: LTA pretreatment significantly decreased the percentage of the killed cell and the concentration of LDH in media. Also, LTA pretreatment obviously raised the concentrations of NO in culture media. The protective effects of LTA were abrogated by pretreatment with N-monomethyl-L-arginine (L-NMMA). Moreover, the expression of eNOS mRNA was significantly upregulated after HCAECs exposure to LTA for 4 h following 2 h or 4 h recovery. CONCLUSION: LTA could induce the delayed protection against H/R induced endothelial injury and dysfunction of cultured HCAECs. NO produced by eNOS acts initially as a trigger and subsequently as a mediator of delayed PC.

Bradykinin potentiates 5-HT3 receptor-mediated current in rat trigeminal ganglion neurons.

AIM: To explore the modulatory effect of bradykinin (BK) on 5-HT(3 )receptor-mediated current in trigeminal ganglion (TG) neurons in rats. METHODS: The whole-cell patch-clamp technique was used to record 5-HT-activated currents (I(5-HT)) in neurons freshly dissociated from rat TG. Drugs were applied by rapid solution exchange. RESULTS: The majority of the neurons examined responded to 5-HT applied externally with an inward current (76.3%, 74/97) that could be blocked by the 5-HT(3 )receptor antagonist, ICS-205,930 (10(-6) mol/L). In 66 of the 74 cells sensitive to 5-HT (89.2%), pretreatment for 30 s with BK (10(-6)-10(-10) mol/L) could potentiate I(5-HT) with the maximal modulatory effect occurring at 10(-7) mol/L BK (71.6%+/-4.9%). BK shifted the 5-HT concentration-response curve upwards with an increase of 68.9%+/-7.2% in the maximal current response, but with no significant change in the EC(50) value (19.1+/-3.2 mumol/L vs 20.9+/-3.5 micromol/L; t-test, P>0.05; n=8). BK potentiated I(5-HT) in a holding potential-independent manner and did not alter the reverse potential of I(5-HT). This BK-induced potentiation of I(5-HT) was almost completely blocked by Hoe 140 (5*10(-7) mol/L), a selective B2 BK receptor antagonist, and was removed after intracellular dialysis of GF-109203X (2 micromol/L), a selective protein kinase C (PKC) inhibitor, with the re-patch clamp. CONCLUSION: Pre-application of BK exerts an enhancing effect on I(5-HT) via a PKC-dependent pathway in rat TG neurons, which may explain the peripheral mechanism of pain and hyperalgesia caused by, for example, tissue damage and inflammation.