Alternaria yunnanensis sp. nov., a New Alternaria Species Causing Foliage Spot of Rubber Tree in China

A new species of Alternaria causing leaf spots on the rubber tree (Hevea brasiliensis) in Yunnan, China, was isolated, examined, and illustrated. Morphologically, it belongs to the section Porri of Alternaria, which produces relatively large conidia and a simple or branched, filamentous long beak. It is, however, characterized by conidiophores gradually enlarging near the apex into a clavate conidiogenous cell and long ellipsoid to obclavate, smooth-walled conidia with a long filamentous beak. Molecular phylogenetic analyses based on ITS rDNA, GAPDH, and TEF1-alpha sequences demonstrate that the phytopathogen falls in the clade of the section Porri, being most closely related to A. sidae, A. sennae, A. deseriticola, A. cyamopsidis, A. rostellata, A. nitrimali, A. crassa, and A. thunbergiae.

Designation and evaluation of antisense oligodeoxynucleotides targeted to glial glutamate transporter-1a / 中国应用生理学杂志

<p><b>OBJECTIVE</b>The present study was undertaken to design antisense oligodeoxynucleotides (AS-ODNs) of glial glutamate transporter-la (GLT-1a) and to evaluate the effectiveness of the designed AS-ODNs on the expression of GLT-1a.</p><p><b>METHODS</b>Five sequences of GLT-1a AS-ODNs were designed according to the C terminus specific sequences of GLT-1a mRNA using antisense design software of IDT Com- pany. Western blot analysis was used to evaluate the inhibition effects of the five GLT-1a AS-ODNs on the expression of GLT-la.</p><p><b>RESULTS</b>The sequence of GLT-1a AS-ODNs with sequence of 5'-GGTTCTTCCTCAACACTGCA-3' could specifically inhibit the expression of GLT-1a in the hippocampal CA1 subfield of rats, while it had no effect on the expression of GLT-1b. This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. It could also significantly inhibit the cerebral ischemic preconditioning (CIP)-induced up-regulation in the expression of GLT-1a. The magnitude of the inhibition in sham, Cef- or CIP-treated rats was similar by more than 60%.</p><p><b>CONCLUSION</b>From the designed five sequences of GLT-1a AS-ODNs, we obtained an effective sequence which can specifically inhibit the expression of GLT-1a.</p>

Hydrogen sulfide facilitates carotid sinus baroreceptor activity in anesthetized male rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>It has been reported that hydrogen sulfide (H(2)S) could relax vascular smooth muscle by direct activation of K(ATP) channels and hyperpolarization of the membrane potential. Recently, our study has shown that H(2)S facilitated carotid baroreflex. This study was conducted to investigate the effect of H(2)S on carotid baroreceptor activity (CBA).</p><p><b>METHODS</b>The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus.</p><p><b>RESULTS</b>H(2)S (derived from NaHS) 25, 50 and 100 micromol/L facilitated CBA, which shifted FCCB to the left and upward. There was a marked increase in peak slope (PS) and peak integral value of carotid sinus nerve charge (PIV) in a concentration-dependent manner. Pretreatment with glibenclamide (20 micromol/L), a K(ATP) channel blocker, the above effects of H(2)S on CBA were abolished. Pretreatment with Bay K8644 (an agonist of calcium channels, 500 nmol/L) eliminated the role of H(2)S on CBA. An inhibitor of cystathionine gamma-lyase (CSE), DL-propargylglycine (PPG, 200 micromol/L) inhibited CBA in male rats and shifted FCCB to the right and downward.</p><p><b>CONCLUSIONS</b>Our results suggest that exogenous H(2)S exerts a facilitatory role on isolated CBA through opening K(ATP) channels and further closing the calcium channels in vascular smooth muscle. Endogenous H(2)S may activate CBA in vivo.</p>

Injection of adenosine into the renal artery activates spontaneous activity of renal afferent nerve fibers / 生理学报

The effects of injection of adenosine into the renal artery on multi- and single-unit spontaneous discharges of renal afferent nerve fibers were investigated in anesthetized rabbits. The results obtained are as follows: (1) injection of 50, 100, and 200 nmol/kg adenosine into the renal artery increased the renal afferent nerve activity (ARNA) in a dose-dependent manner with unchanged arterial pressure; (2) pretreatment with 8-cyclopenthl-1,3-dipropylxanthine (DPCPX, 160 nmol/kg), an adenosine A1 receptor antagonist, partly abolished the effect of adenosine; and (3) pretreatment with a nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methylester (L-NAME, 0.1 mmol/kg) significantly enhanced the ARNA response to adenosine. The results suggest that injection of adenosine into the renal artery activates ARNA via adenosine receptors in anesthetized rabbits and that nitric oxide may be involved in regulating the activity of renal sensory nerve fibers as an inhibitory neurotransmitter.

Capsaicin facilitates carotid sinus baroreflex in anesthetized rats / 生理学报

The effects of capsaicin (CAP) on the carotid sinus baroreflex were studied in 30 anaesthetized rats with perfused isolated carotid sinus. The results are as follows. (1) By perfusing the isolated carotid sinus with CAP (1 micromol/L), the functional curve of the baroreflex was shifted to the left and downward, with a peak slope (PS) increasing from 0.34+/-0.01 to 0.42+/-0.01 (P<0.01), whereas the reflex decrease (RD) in mean arterial pressure was enhanced from 36.51+/-1.26 to 45.01+/-0.71 mmHg (P<0.01). Meanwhile, the threshold pressure, equilibrium pressure and saturation pressure were all significantly decreased from 70.43 +/-2.09 to 52.86 +/-2.80 mmHg (P<0.01), 95.5+/-1.71 to 87.00+/-1.58 mmHg (P<0.01) and 177.60+/-1.37 to 163.55+/-2.12 mmHg (P<0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in PS and RD induced by capsaicin were dose-dependent. (2) By pretreatment with ruthenium red (RR, 100 micromol/L), an antagonist of vanilloid receptor subtype 1 (VR(1)), the above effects of CAP on carotid baroreflex were abolished. (3) The CAP-induced change in the baroreflex was also eliminated by pretreatment with glibenclamide (20 microm ol/L), a K(ATP) channel blocker. On the basis of the results, it is concluded that CAP facilitates the carotid baroreflex, an effect of which may be resulted from the opening of K(ATP) channels mediated by VR(1).

High-frequency electrical stimulation of femoral nerve reduces infarct size following myocardial ischemia-reperfusion in rats / 生理学报

The effects of femoral nerve electrostimulation (FNES) on ischemia-reperfused myocardium were examined in the urethane- anesthetized rats to determine whether FNES may provide cardioprotection and to observe the possible mechanism. The area at risk (AR) and infarct area (IA) were determined using Evans blue and nitro-blue tetrazolium staining, respectively. Infarct size (IS) was defined as 100xIA/AR (%). The results are as follows: (1) During 30 min myocardial ischemia and subsequent 120 min reperfusion, the myocardial infarct size occupied (54.96+/-0.82)% of the area at risk. (2) FNES of high frequency (10 V, 100 Hz, 1 ms) significantly reduced myocardial infarct size to (36.94+/-1.34)% (P<0.01), indicating the cardioprotective effect FNES of high frequency on myocardial ischemia-reperfusion, while FNES of low frequency (10 V, 10 Hz, 1 ms) had no effect on myocardial infarct size. (3) Pretreatment with either naloxone (5 mg /kg, i.v), a nonselective opioid receptor antagonist, or glibenclamide (5 mg /kg, i.v), a K(ATP) channel antagonist, completely abolished the cardioprotection of FNES (100 Hz) from myocardial ischemia-reperfusion. It is suggested that FNES of high frequency can protect myocardium from ischemia-reperfusion injury. The possible mechanism is that FNES of high frequency may induce the release of opioids from the central nervous system, and the activation of opioid receptors in the heart results in an opening of myocardial K(ATP) channels which can protect myocardium.

Cholecystokinin octapeptide inhibits carotid sinus baroreflex in anesthetized rats / 生理学报

The purpose of this study was to determine the effect of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreflex in 36 anesthetized male rats by isolated carotid sinus perfusion in vivo. The results obtained are as follows. (1) By perfusion with CCK-8 (0.1, 0.5, 1.0 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a decrease in peak slope (PS) (p<0.001) and a reflex decrease (RD) in mean arterial pressure, while the threshold pressure (TP) and saturation pressure (SP) were significantly increased. Among the functional parameters of carotid sinus baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with proglumide (100 micromol/L), a nonselective CCK receptor antagonist, the inhibitory effect of CCK-8 (0.5 micromol/L) on the baroreflex was significantly attenuated. (3) Pretreatment with L-NAME (100 micromol/L), an inhibitor of nitric oxide (NO) synthase, did not affect the inhibitory action of CCK-8 (0.5 micromol/L). (4) Preperfusion with Bay K 8644 (500 nmol/L), an agonist of calcium channel, could attenuate the effect of CCK-8 (0.5 micromol/L). It is suggested that the inhibitory action of CCK-8 on the baroreflex may be mediated by the activation of its receptors in the carotid sinus baroreceptor, leading to an inhibition of stretch-sensitive channels and a decrease in Ca(2+) influx. However, NO released from the endothelium seems not to be involved in the mechanism of this effect.

Limb ischemic preconditioning reduces infarct size following myocardial ischemia-reperfusion in rats / 生理学报

The effect of limb ischemic preconditioning (LIP) on ischemia-reperfused myocardium was examined in the urethane-anesthetized rats to determine whether LIP produces cardioprotection and to observe the roles of adenosine and neural reflex in this effect. The area at risk (AR) and infarct area (IA) were determined using Evans blue and nitro-blue tetrazolium staining respectively. Infarct size (IS) was defined as 100xIA/AR (%). The results obtained are as follows: (1) During 30 min myocardial ischemia and subsequent 120 min reperfusion, the myocardial infarct size occupied 51.48+/-0.82% of the area at risk. (2) LIP significantly reduced the myocardial infarct size to 35.14+/-0.88% (p<0.01 ), indicating the cardioprotective effect of such an intervention. (3) Femoral nerve section (FNS) completely abolished the cardioprotection afforded by LIP. (4) Intrafemoral artery injection of adenosine (10 nmol/kg) produced a similar effect to that of LIP, reducing the myocardial infarct size to 37.28+/-1.68%, while intrafemoral vein injection of the same dose of adenosine showed no effect. (5) Pretreatment with a selective adenosine A(1) receptor antagonist 8-cyclopentyl-1,diproylxanthine (DPCPX ) (32 nmol/kg) partially abolished the cardioprotection of LIP on myocardium. Taken together, it is concluded that LIP reduces infarct size following myocardial ischemia-reperfusion, and that the locally released adenosine and thereby the activated relevant neural pathway play an important role in the cardioprotection provided by LIP.

Intrarenal artery injection of L-arginine inhibits spontaneous activity of renal afferent nerve fibers / 生理学报

The purpose of this study was to determine the effect of intrarenal artery injection of L-arginine on multi- and single-unit spontaneous discharges of renal afferent nerve fibers in anesthetized rabbits. The results obtained are as follows: (1) intrarenal artery injection of L-arginine (0.05, 0.24, and 0.48 mmol/kg) decreased the renal afferent nerve activity (ARNA) in a dose-dependent manner with arterial pressure unchanged; (2) pretreatment with a nitric oxide synthase inhibitor L-NAME (N6-nitro-L-arginine methylester, 0.11 mmol/kg), completely abolished the effect of L-arginine; and (3) intrarenal artery injection of a nitric oxide donor SIN-1 (3-morpholinosydnonimine, 3.75 micromol/kg) also resulted in an inhibition of ARNA. The results suggest that intrarenal artery injection of NO precursor (L-arginine) and donor (SIN-1) can inhibit ARNA in anesthetized rabbits.