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Biomedical subjects

H Jia

Publications and source records attributed to H Jia.

At least 73 records · Page 4Linked to original sources

Involvement of the frontal ventrolateral orbital cortex in descending inhibition of nociception mediated by the periaqueductal gray in rats.

Our previous findings which indicated that electrical stimulation of ventrolateral orbital cortex (VLO) can depress the rat tail flick (TF) reflex and that the VLO-evoked inhibitory effect is blocked by electrolytic lesions of periaqueductal gray (PAG) suggest a role of the VLO in the modulation of nociception. To further investigate the involvement of VLO in this nociceptive modulatory pathway, we tested the effects of microinjections of glutamate (200 mM, 0.7 microliter) into the VLO on the TF reflex. An unilateral microinjection of glutamate into the VLO significantly depressed the TF reflex; and this effect was repeatable. Furthermore, bilateral microinjections of gamma-aminobutyric acid (GABA: 100 mM, 0.5 microliter on each side) into the ventrolateral parts of PAG could eliminate this VLO-evoked inhibition of the TF reflex. These results, along with our previous findings provide further support for a hypothesis that VLO, as a higher center in the frontal cortex, plays an important role in modulation of nociception, and this role is mediated by PAG leading to activation of the brainstem descending inhibitory system which depresses the nociceptive information at the spinal level.

Animals↗

Inhibitory effects of electrically evoked activation of ventrolateral orbital cortex on the tail-flick reflex are mediated by periaqueductal gray in rats.

The present study found in lightly anesthetized rats that the radiant heat-evoked tail flick (TF) reflex was markedly inhibited by a unilateral electrical stimulation (a 20 ms train of 0.2 ms, 100 Hz, 30-100 microA pulses) of the ventrolateral orbital cortex (VLO), with the tail flick latency (TFL) being increased. The mean threshold of VLO stimulation for producing inhibition of the TF reflex was 39.2 +/- 8.7 microA (n = 26), and this inhibitory effect increased following increasing stimulation intensity from 40 to 70 microA. The inhibition developed and remained during the stimulation and disappeared rapidly after termination of the stimulation. When the VLO was stimulated at an intensity of 100 microA in addition to the inhibition an after-facilitation of the TF reflex (a decrease in TFL) was observed at 5-10 s after termination of the stimulation. Bilateral electrolytic lesions of the lateral or ventrolateral parts of the periaqueductal gray matter (PAG) dramatically reduced or eliminated the VLO-evoked inhibition, and the after-facilitation as well. The difference was significant between the TFL changes produced by VLO stimulation before and after PAG lesion (P < 0.01). The results suggest that the antinociception elicited by VLO stimulation is mediated by PAG, leading to activation of the brainstem descending inhibitory system which depresses the nociceptive transmission at the spinal level. The role played by VLO in pain modulation was discussed in association with the proposed endogenous analgesic system consisting of spinal cord-Sm-VLO-PAG-spinal cord.

Animals↗

[Effect of hypoxia on spleen mono nuclear cell DNA content and proliferation of neonatal rats].

Effects of hypoxia on the immune function of neonatal rats at the age of 14 days as well as on the levels of ACh, catecholamine in spleen were studied. After the animals were exposed to hypoxia at 5 km simulated altitude in hypobaric chamber for 5 days, there was 43.4% decrease in DNA content in spleen mono nuclear cell and a 13.2% decrease in mono nuclear cell proliferation. Similar suppression of these two parameters of immune function in exposure to 7 km for 24 h was also noted, which decreased by 39% and 19.8% respectively. The suppressive effect of 7 km for 24 h hypoxia on DNA content was partly blocked when rats were pretreated with DSP-4 intracerebroventricularly one day before hypoxia. The levels of catecholamine in spleen increased, while the levels of ACh decreased after 7 km exposure for 24 h. These observations indicate that hypoxia may suppress cellular function of neonatal rats and its action may be mediated by activation of sympathetic nervous system and inhibition of parasymphathetic one.

Acetylcholine↗

[Evaluating clinical significance of tumor necrosis factor-alpha and hydroxyproline in blood of patients with active pulmonary tuberculosis].

OBJECTIVE: To evaluate the clinical significance of tumor necrosis factor-alpha (TNF-alpha) and hydroxyproline (HYP) in blood of patients with active pulmonary tuberculosis (APT). METHOD: Contents of TNF-alpha and HYP in blood of 28 patients with APT and 17 normal subjects were determined with enzyme-linked immunosorbent assay and ultraviolet spectrophotometer respectively. RESULT: It was found that the concentrations of TNF-alpha and HYP in patients with APT before antituberculosis treatment were obviously higher than those of the normal subjects (192.85 +/- 37.14 ng/L vs 89.36 +/- 23.18 ng/L and 4.96 +/- 1.13 mg/L vs 1.64 +/- 0.33 mg/L respectively, all P < 0.001) and those who received 3- month anti-tuberculosis treatment (192.65 +/- 37.14 ng/L vs 112.50 +/- 44.93 ng/L and 4.96 +/- 1.13 mg/L vs 2.17 +/- 0.39 mg/L respectively, all P < 0.001). TNF-alpha level was significantly correlated with HYP (r = 0.5132, P < 0.001). CONCLUSION: The results indicate that TNF-alpha might play an important role in inducing pulmonary tissue damage of APT, and the lowering of HYP content in blood might indicate that pulmonary tuberculosis is recovering from active stage.

Adolescent↗

[A primary study on antagonizing effects of anti-snake venom Chinese herbs on endothelin-1 and sarafotoxin 6b].

Some anti-snake venom Chinese herbs were used to test the antagonizing effect on ET-1 and S6b. Oral administration has shown that both the water and alcohol extracts from Cissus assamica and Aristolochia fordiana, and the water extracts from Desmodium microphyllum, Cynanthum paniculatum and Polygonum cillinerve are very helpful in reducing the acute death caused by ET-1 and S6b(i.v.), while the extracts from Cissus assamica, Aristolochia fordiana and Cynanthum paniculatum can dilate the vasoconstriction by ET-1 in a dose dependent manner. Pharmacodynamic parameters have shown that the potencies of alcohol extracts from Cissus assamica and Aristolochia fordiana are greater than that of Cynanthum paniculatum. These data suggest that traditional anti-snake venom herbs have antagonizing effects on ET-1.

Animals↗

[Immunophenotyping study on the blood cells of the patients with paroxysmal nocturnal hemoglobinuria].

OBJECTIVE: To detect the expression of glycosyl-phosphatidyl-inositol (GPI) anchored protein on the blood cell membrane and its implication in the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH). METHODS: The GPI anchored protein was detected by indirect immunofluorescence method with a panel of monoclonal antibodies (CD55, CD59, CD16, CD58, HIR2, CD15, CD2) in 22 PNH patients. RESULTS: The abnormal granulocytes and erythrocytes with deficient GPI anchored proteins were identified in all PNH patients whether the routine hemolysis tests for PNH, including Ham test and mCLST, were positive or negative. However, lymphocytes with PNH-defect were found in only 14 patients. CONCLUSION: GPI anchored protein assay provided sensitive and specific method for the diagnosis of PNH.

Adult↗

Blood pressure and the M235T polymorphism of the angiotensinogen gene.

The angiotensinogen gene locus (1q42-43) has been linked to hypertension in affected relative-pair studies (including a previous UK study), but the role of the Met-->Thr polymorphism at position 235 remains controversial. Using this marker, we investigated the relationship between angiotensinogen genotype and blood pressure in two data sets from the East Anglia region of the United Kingdom. Two hundred twenty-three untreated hypertensive and 187 normotensive control subjects were recruited through local general practices. Blood pressure (including pretreatment measurements in the hypertensive group), age, sex, body mass index, alcohol consumption, cholesterol level, and angiotensinogen genotype were recorded for all subjects. The influence of angiotensinogen genotype on blood pressure was assessed with a general linear model ANOVA with adjustment for age, sex, body mass index, and alcohol consumption. There was no evidence for an association between angiotensinogen genotype and blood pressure level in either the hypertensive or normotensive data set. Angiotensinogen genotype did not influence blood pressure in subjects aged < 50 years, women, or those with a body mass index < 26 kg/m2. We conclude that the angiotensinogen Met-->Thr polymorphism is not a marker for blood pressure level in these East Anglian subjects. Further studies are required to confirm the involvement of the 1q locus in the development of hypertension in UK subjects and to delineate the functional variant(s) in this chromosomal region that influences blood pressure.

Angiotensinogen↗

[Effects of bilateral lesions of ventrolateral orbital cortex on the rat tail flick reflex inhibition evoked by electroacupuncture].

This study found that bilateral electrolytic lesions of the ventrolateral orbital cortex (VLO) markedly reduced the inhibitory effects of high intensity electroacupuncture (EA) at "Zusanli" point on tail flick reflex in lightly anesthetized rats, but did not influence the inhibitory effects of low intensity EA stimulation. The results show that the VLO is involved in acupuncture analgesia produced by activation of small afferent fibers with high intensity electroacupunture. Results of this study provide further support for a hypothesis that spinal cord-Sm-VLO-PAG-spinal cord may constitute a negative feedback loop of nociceptive modulation. The analgesic effects produced by high intensity electroacupuncture may be mediated by this loop leading to depression of the nociceptive inputs at the spinal cord level.

Acupuncture Analgesia↗

[Responses of neurons in thalamic nucleus submedius to electrical stimulation of peroneal nerve and "zusanli" point in rats].

The experiments were performed on the anesthetized rats. Single unit was recorded extracellularlly from the thalamic nucleus submedius (Sm) with glass micropipettes. The responses of Sm neurons were examined to electrical stimulation of the peroneal nerve and "Zusanli" point. The results show that most (81%) of the neurons in Sm responded to electrical stimulation of the peroneal nerve with afferent C fiber excitation, and this response increased following increase of the stimulation intensity and pulse numbers. It was found that electrical stimulation of the "Zusanli" point could activate the Sm neuronal activities with higher intensity threshold compared to that of the peroneal nerve stimulation, and the response properties of Sm neurons to acupoint stimuli were similar to those to stimulation of peroneal nerve. These results provide support for the hypothesis that a negative feedback loop consisting of spinal cord-Sm-VLO-PAG-spinal cord responsible for nociceptive modulation is involved in acupuncture analgesia, especially in analgesia produced by electroacupuncture-evoked activation of the afferent C fibers.

Acupuncture Analgesia↗

[The coronary artery structure and early atherosclerotic lesions of 80 young adults cases in the Ningbo fishing region].

In order to study the coronary artery structure in relation to early atherosclerotic lesions of young adults residing in a fishing region, coronary arteries from 80 autopsies of people aged 15 to 39 years who died from accidents were collected and studied by pathohistological, immunohistochemical and morphometric methods. The results showed an 18.67% prevalence of Sudanophilic lesions in the right, coronary artery, the thickness of the intima of the left anterior descending branch increased with increasing age in males, but no significant difference was observed in females, the density of the coronary artery cell nuclei decreased with increasing age. The prevalence of fatty streaks and stenosis of left anterior descending branch was 25.0% and 5.0% respectively, and that of the left circumflex branch was 7.5% and 3.9% respectively. The amount of chondroinn sulfate proteoglycan in the left anterior descending branch was 23.3 +/- 8.8% in intima and 12.0 +/- 4.0% in the media. The above findings suggest that the custom of eating large amounts of sea food may have a beneficial effect on lipid deposit, smooth muscle cell proliferation, thickness of intima and percentage of proteoglycan. Thus it is one of the important factors for the low incidence of coronary heart disease in this fishing region.

Adolescent↗

Inhibitory effects of electrical stimulation of thalamic nucleus submedius area on the rat tail flick reflex.

This study in lightly anesthetized rats found that unilateral electrical stimulation delivered to the ventral part of the thalamic nucleus submedius (Sm), the thalamic reuniens nucleus (Re) and the hypothalamic dorsal area (DA) markedly depressed the TF reflex, and this inhibitory effect increased following increasing stimulation intensity. Stimulation in the dorsal part of Sm did not produce any or only slight depression of the TF reflex. Furthermore, an ipsilateral electrolytic lesion of the ventrolateral orbital cortex (VLO) eliminated the unilateral Sm-evoked inhibition, but not the inhibition elicited by Re and DA and contralateral Sm stimulation. Finally, after bilateral electrolytic lesions of the ventrolateral periaqueductal gray (PAG) the DA and Re and contralateral Sm-evoked inhibitions were also eliminated. The results suggest that the Sm plays an important role in modulation of nociceptive inputs, and this role of Sm is mediated by the VLO and leads to activation of the PAG descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.

Animals↗

Effects of thalamic nucleus submedius lesions on the tail flick reflex inhibition evoked by hindlimb electrical stimulation in the rat.

Bilateral electrolytic lesions of the thalamic nucleus submedius (Sm) facilitated the TF reflex and attenuated the antinociception evoked by hindlimb electrical stimulation with high intensities in lightly anaesthetized rats. However, the antinociception produced by low intensity hindlimb stimulation was unchanged, except that the after-effect was reduced. The results show that the Sm is probably involved in pain modulation and plays an important role in mediation of the antinociception elicited by high intensity peripheral stimulation.

Animals↗

An analysis of lidocaine block of sodium current in isolated human atrial and ventricular myocytes.

Lidocaine is a Na+ channel blocker that is highly effective for the treatment of ventricular tachyarrhythmias, but is largely ineffective against atrial arrhythmias. If is not known if this differential efficacy is the result of differences in lidocaine inhibition of atrial v ventricular Na+ channels. The purpose of the present study was to characterize lidocaine block of Na+ channels in human atrium and ventricle. We used the whole cell voltage clamp technique with low external and internal Na+ concentrations (5 mM) to study the Na+ current (INa) in single human atrial and ventricular cells isolated enzymatically from specimens obtained during surgery. We found that tonic block of peak INa by lidocaine (200 microM, holding potential = -140 mV, 0.1 Hz, at 17 degrees C) was not voltage dependent in either cell type. Reduction of maximal peak Na+ conductance in 41 atrial cells (19.8 +/- 2.7%) and nine ventricular cells (22.6 +/- 1.7%) was virtually identical. The rate of onset of block development was determined during depolarization to either -80 mV or -20 mV. The time course of onset of block was described by a single exponential at -80 mV and by a double exponential at -20 mV. When the rate of block onset during a single conditioning depolarization was compared to that which developed during conditioning by a train of brief pulses (3 ms, 30 Hz), onset was faster during the pulse train. The results were nearly identical for atrial and ventricular INa. The time constants of recovery from block following either single pulse or multiple-pulse conditioning did not differ. These data suggest that lidocaine binds to both the activated and inactivated states of the human cardiac Na+ channel. Using an analytical method based upon the Guarded Receptor Hypothesis, we calculated apparent rate constants describing lidocaine's interaction with the three primary states of the human Na+ channel (resting, activated and inactivated). Rate constants were similar to those reported for other mammalian species. Our results demonstrate that lidocaine block of INa is virtually identical for human atrial and ventricular cells; thus additional mechanisms must be invoked to explain the differential efficacy of lidocaine against ventricular as compared to atrial dysrhythmias.

Adolescent↗

Expression of the alpha- and beta-subunits of the stimulatory and inhibitory G-proteins in beta 1-adrenoceptor-blocked and non-beta-adrenoceptor-blocked human atrium.

1. Chronic beta 1-adrenoceptor blocker therapy induces hyperresponsiveness of the beta 2-adrenoceptor in human atrium. To investigate whether the beta 2-adrenoceptor sensitization induced by beta 1-adrenoceptor blockade is associated with altered gene expression of G-proteins, which couple the receptors to adenylate cyclase, we determined the mRNA expression of the alpha- and beta-subunits of the stimulatory G-protein, Gs, and inhibitory G-protein, Gi, in human right atrial appendage by polymerase chain reaction and by enhanced chemiluminescence Northern blot analysis. 2. The polymerase chain reaction revealed bands of predicted size of Gs alpha, both short form and long form, all three Gi alpha subtypes and three G beta subtypes. In Northern blots, the digoxigenin-labelled antisense cRNA probe specific for Gi alpha 2 hybridized to a predominant band at 2.3 kb, whereas the Gi alpha 3 cRNA probe detected a message of 1.8 kb in total RNA extracted from human atrium. The cRNA probe encoding Gs alpha revealed one major band at 1.9 kb and one minor band at 1.7 kb. The G beta cRNA probes detected messages of 3.4 kb for G beta 1, 1.8 kb for G beta 2 and 1.9 kb for G beta 3 in human atrium. 3. The mRNA levels of Gs alpha in beta 1-adrenoceptor-blocked atria (n = 12) were not significantly different from those in non-beta-adrenoceptor-blocked atria (n = 12), nor were there any significant differences in the Gi alpha 2 mRNA levels between atria from patients treated with beta 1-adrenoceptor blockers and untreated patients. The ratios of 1.9-kb Gs alpha mRNA to 1.7-kb Gs alpha mRNA and of 1.9-kb Gs alpha mRNA to 2.3-kb Gi alpha 2 mRNA in beta 1-adrenoceptor-blocked patients were almost identical to those in non-beta-adrenoceptor-blocked patients. Neither G beta 1 mRNA nor G beta 2 mRNA expression in beta 1-adrenoceptor-blocked atria differed significantly from that in non-beta-adrenoceptor-blocked atria. 4. We conclude that the previously observed sensitization following beta 1-adrenoceptor-blockade of beta 2-adrenoceptors in human atria is unlikely to be mediated by altered gene expression of the alpha- and beta-subunits of G-proteins.

Adrenergic beta-1 Receptor Antagonists↗

[The disturbance of Ca2+ transport and the changes of some relative factors in arterial smooth muscle cells from spontaneously hypertensive rats with different age].

The purpose of this study was to observe the abnormalities of calcium transport of cultured arterial smooth muscle cells (ASMC) in both prehypertensive and hypertensive SHR and their control WKY rats. The changes in cAMP, ANG II and CaM contents in ASMC were also studied. The results indicated that the Ca2+ influx in ASMC of prehypertensive SHR was increased compared with that of the control, although the value of that in hypertensive SHR was higher significantly more than that of the prehypertensive rat, but there was no significant difference between them. On the other hand, the Ca2+ efflux in ASMC of prehypertensive SHR was decreased compared with that of WKY rats. A more seriously decreased efflux value was found in hypertensive SHR. The cAMP and CaM content were higher than those in WKY rats. In addition, ANG II content in ASMC had a direct bearing on blood pressure, showing a marked difference between prehypertensive and hypertensive SHR. The disturbance of transmembrane Ca2+ transport in ASMC of hypertensive rats appears to be related to genetic defect and the changes of cAMP contents might play a role in membrane Ca2+ transport in ASMC during the development of hypertension. Furthermore the level of arterial ANG II may be related to the elevation of blood pressure in hypertension.

Age Factors↗

Renin-angiotensin system gene polymorphisms influence blood pressure and the response to angiotensin converting enzyme inhibition.

OBJECTIVES: To investigate the relationship between polymorphisms in the angiotensin converting enzyme (ACE), angiotensinogen (AGT) and type 1 angiotensin-II (AT1R) genes and (1) quantitative variations in blood pressure and (2) the blood pressure response to ACE inhibition in a hypertensive cohort. DESIGN AND METHODS: We administered monotherapy with ACE inhibitors to 125 previously untreated essential hypertensives. Genotypes for ACE insertion and deletion, AGT M235T and AT1R A1166-->C polymorphisms were determined in DNA extracted from peripheral blood leucocytes. The influence of genotype on pretreatment blood pressure and the ACE inhibitor-induced decrease in blood pressure was tested by analysis of variance and multiple regression analysis, adjusting for age, sex, body mass index, alcohol intake and, where appropriate, pretreatment blood pressure. RESULTS: ACE and AT1R genotypes were independent predictors of pretreatment systolic and diastolic blood pressure, with an apparent interaction between these two gene loci. Although it did not influence pretreatment blood pressure in this population, AGT genotype was an independent predictor of the blood pressure response to ACE inhibition. CONCLUSIONS: The ACE and AT1R gene loci (chromosomes 17q and 3q, respectively) may carry alleles influencing blood pressure variation in this hypertensive population, with a possible epistatic interaction between the two loci. The AGT T235 allele does not appear to be a marker for blood pressure variation in this group, but variants on chromosome 1q lying in or near the AGT gene may contribute to individual differences in the blood pressure response to ACE inhibition. Among essential hypertensives, differences in the ACE inhibitor response appear, in part, to be genetically determined.

Adolescent↗