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Y W Li

Publications and source records attributed to Y W Li.

At least 19 recordsLinked to original sources
PubMed1992

Expression of c-fos protein in the medulla oblongata of conscious rabbits in response to baroreceptor activation.

Neuronal expression of c-fos protein (Fos) in the medulla in response to baroreceptor activation was studied in conscious rabbits. Raising arterial pressure resulted in a marked increase, compared to control animals, in Fos immunoreactivity in the nucleus tractus solitarius, area postrema and ventrolateral medulla (VLM). Fos-immunoreactive neurons in the VLM extended from the level just rostral to the obex to 3 mm more caudal. Only a small proportion of these neurons showed tyrosine hydroxylase immunoreactivity. The results indicate that baroreceptor activation induces Fos expression in circumscribed medullary regions which have previously been shown to receive excitatory baroreceptor inputs.

Animals↗
PubMed1992

Characteristics of caudal ventrolateral medullary neurons antidromically activated from rostral ventrolateral medulla in the rabbit.

We made extracellular recordings from 107 spontaneously active neurons in the caudal ventrolateral medulla, after identifying the cells by antidromically activating them from the rostral ventrolateral medulla, in urethane-anesthetized rabbits. We tested the response of these neurons to inputs from baroreceptors and chemoreceptors. The median conduction velocity for antidromically activated neurons was 0.84 m/s. Raising blood pressure with intravenous noradrenaline excited 22% of 96 neurons tested, inhibited 61%, and had no effect on the remaining 17%. The spontaneous discharge rate of neurons excited by an increase in blood pressure was 1.6 +/- 0.3 spikes/s, lower than the discharge rate of neurons inhibited by this procedure (4.9 +/- 0.5 spikes/s). Excitation of chemoreceptors by hypoxia increased the discharge rate of 14/16 neurons tested in the group excited by baroreceptor inputs. In the group inhibited by baroreceptor inputs 21/35 neurons tested were excited and 12/35 neurons were inhibited by chemoreceptor inputs. Neurons excited by an increase in blood pressure were located in the previously defined caudal vasodepressor region and in a region just rostral to the obex, intermediate between the vasodepressor region and the rostral sympathoexcitatory region. These neurons may form part of the central inhibitory link in the baroreceptor-vasomotor pathway. Other antidromically activated neurons in the vasodepressor region may be inhibitory vasomotor cells with a function relatively independent of baroreceptor inputs, or they may be A1 catecholamine neurons, with axons passing through the rostral medulla en route to the forebrain.

Animals↗
PubMed1992

Angiotensin II excites vasomotor neurons but not respiratory neurons in the rostral and caudal ventrolateral medulla.

We examined the vasomotor and respiratory effects of angiotensin II microinjection into the rabbit ventrolateral medulla (VLM). Angiotensin II in the rostral and caudal VLM increased and decreased arterial pressure, respectively, but had no effect on phrenic nerve activity. In contrast, L-glutamate injections in the same areas altered both arterial pressure and phrenic nerve activity. The results suggest that angiotensin II may activate specifically vasomotor neurons but not respiratory neurons in the VLM.

Angiotensin II↗
PubMed1992

Projections from rabbit caudal medulla to C1 and A5 sympathetic premotor neurons, demonstrated with phaseolus leucoagglutinin and herpes simplex virus.

We combined Phaseolus vulgaris leucoagglutinin anterograde tracing and Herpes simplex virus transneuronal retrograde tracing to determine whether neurons in the vasodepressor region of the rabbit caudal ventrolateral medulla project to brainstem neurons containing the virus after its transneuronal transport from the adrenal medulla. Five days after adrenal injection of virus, 764 +/- 159 virus-positive neurons were found bilaterally in the brainstem: 61% in the C1 sympathoexcitatory region of the rostral ventrolateral medulla, 30% in the A5 region, 5% in the parapyramidal region, and 3% in the paraventricular nucleus of the hypothalamus. Many of the virus-positive neurons in the C1 and A5 areas also contained tyrosine hydroxylase and, in the parapyramidal area, many contained 5-hydroxytryptamine. After iontophoretic deposit of leucoagglutinin into the vasodepressor region of the caudal ventrolateral medulla, brain regions containing varicose processes labeled with leucoagglutinin included the regions containing virus-positive neurons. We examined the C1 and A5 regions following injections of both tracers in the same rabbits, leucoagglutinin into the caudal ventrolateral medulla and virus into the adrenal gland. Varicosities containing leucoagglutinin were seen in contiguity with perikarya and dendritic branches of neurons containing HSV1, in both the C1 and A5 regions. Studies also revealed labeled varicosities in contiguity with TH-containing C1 and A5 neurons. The projection from the caudal medulla to presumed sympathetic premotor neurons in the C1 area, including some C1 cells, represents a potential pathway whereby activity of neurons in the caudal medulla could reduce blood pressure by inhibiting sympathoexcitatory neurons in the rostral medulla.

Adrenal Medulla↗
PubMed1992

Renal and adrenal sympathetic preganglionic neurons in rabbit spinal cord: tracing with herpes simplex virus.

We mapped sympathetic renal preganglionic neurons in the rabbit spinal cord using Herpes simplex virus retrograde transneuronal tracing after application of the virus to the renal nerve. Virus-positive neurons were found in the spinal cord from T7 to L2, principally in the ipsilateral intermediolateral cell column. Renal and adrenal preganglionic neurons are largely separate populations. Extensive nonspecific spread of virus from infected cells to neighboring neurons does not appear to occur.

Adrenal Glands↗
PubMed1992

Mouse model of neurodegeneration: atrophy of basal forebrain cholinergic neurons in trisomy 16 transplants.

Vulnerability of specific brain regions and neuronal populations is a characteristic feature of Alzheimer disease and Down syndrome. Cholinergic neurons of the basal forebrain degenerate in both disorders. The basis for neuronal degeneration is unknown. Mouse trisomy 16 (Ts 16) is an animal model of Down syndrome. We sought an experimental system in which the survival and development of Ts 16 basal forebrain cholinergic neurons could be examined beyond the fetal period. As Ts 16 mice do not survive birth, we transplanted fetal Ts 16 and control basal forebrain into the hippocampus of young adult mice. Transplanted neurons survived and grew neurites in all grafts. Over time, we observed selective atrophy of cholinergic neurons in Ts 16 grafts. Denervation of the hippocampus produced a significant increase in the size of Ts 16 cholinergic neurons. This suggests that hippocampal-derived neurotrophic factors acted to prevent degeneration. beta/A4-amyloid-containing plaques were not seen. Ts 16 provides a model of spontaneous, genetically determined neurodegeneration that may be used to understand better the molecular pathogenesis of neuronal dysfunction in Alzheimer disease and Down syndrome.

Alzheimer Disease↗
PubMed1992

Dysregulation of gene expression in mouse trisomy 16, an animal model of Down syndrome.

In humans, trisomy 21 results in a specific phenotype known as Down syndrome (DS). The mechanism by which an extra copy of normal genes leads to the DS phenotype is unknown. Most studies in DS and other aneuploid organisms have shown that gene dose is proportional to gene expression. To date, most genes examined have encoded either metabolic enzymes or constitutively expressed products. In the trisomy 16 mouse, an animal model of DS, we found marked dysregulation of two developmentally regulated genes, App and Prn-p. Dysregulation varied from tissue to tissue and during development in the same tissue. We conclude that abnormal phenotypes seen in aneuploid conditions may result in part from disordered expression of developmentally regulated genes.

Aneuploidy↗
PubMed1992

Analysis of retinoblastoma (RB) gene deletion in human prostatic carcinomas.

The retinoblastoma tumor suppressor gene (RB gene) has been reported to be deleted and/or modified in a number of human cancers, indicating that dysfunction of this tumor suppressor gene is perhaps critical in the development of many human tumors. In addition to deletion of one copy and/or mutational inactivation of the RB gene, this gene has also been reported to be altered by a small deletion in the promoter sequence in one case of small cell mixed adenocarcinoma of the prostate. A deletion of 105 nucleotides of the RB gene in exon 21, leading to an aberrant short-sized mRNA transcript, has also been reported in one cell line (DU 145) derived from brain metastasis of prostatic adenocarcinoma. We have analyzed tissues from 10 prostate specimens (3 hyperplastic and 7 neoplastic) and one prostate cancer cell line (DU 145) for the presence of short-sized mRNA transcript (exon 21 alterations) by polymerase chain reaction (PCR) using total RNA extracted from frozen tumors and the cell line. None of the prostate tissue showed any evidence of aberrant short-sized mRNA, although it was confirmed in the DU 145 cell line. Simultaneously, we have used DNA-PCR to investigate RB promoter deletion in 23 adenocarcinomas and one small cell carcinoma of the prostate. We also failed to demonstrate any indication of RB promoter deletion at the DNA level in adenocarcinomas. The single case of small cell carcinoma failed to show evidence of any aberration in RB promoter. We therefore conclude that neither RB promoter alterations nor the exon 21 deletion are associated with typical prostate adenocarcinoma.

Adenocarcinoma↗
PubMed1992

The transient nature of the effect of ischemic preconditioning on myocardial infarct size and ventricular arrhythmia.

We sought to determine whether short periods of preconditioning ischemia limited infarct size in a model of low coronary collateral flow and whether the effects of preconditioning were transient or long-lasting. Rats underwent 90 minutes of coronary occlusion followed by reperfusion. In one group, the rats were preconditioned by three 3-minute occlusions, each separated by 5 minutes of reperfusion. The size of the myocardial infarcts were smaller in the preconditioned group (24.9 +/- 7.8% of the risk zone developed necrosis) versus the nonpreconditioned group (60.7 +/- 5.3%, p less than 0.01). In addition, the incidence of ventricular arrhythmias was reduced by preconditioning. However, when there was a delay of 1 hour or more between the brief episodes of preconditioning and the longer 90-minute occlusion, the beneficial effects of preconditioning were lost. Thus preconditioning reduced the volume of myocardium infarcted and the incidence of ventricular arrhythmias during a subsequent period of prolonged ischemia; however, these beneficial effects were transient.

Animals↗
PubMed1992

Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus.

Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.

Animals↗
PubMed1992

Comparative method for detection of RNA-PCR-amplified signals.

During the development of a micro-method for the quantitative analysis of gene expression, we observed that the sensitivity for detection of PCR-amplified product was higher when silver staining was used, compared with either ethidium bromide staining (as reported previously) or Southern hybridization with 32P-labeled oligonucleotide probe. This observation may have an important impact on the analysis of RNA-PCR-amplified signal for the quantitation of mRNA expression, simply by densitometric scanning of silver-stained polyacrylamide gel. We believe that this is the first report to show such a comparison, demonstrating the greater sensitivity of silver staining compared with either ethidium bromide staining or Southern hybridization utilizing an oligonucleotide probe prepared by 3'-end labeling with 32P-dATP.

Base Sequence↗
PubMed1992

Biological monitoring of deltamethrin in sprayers by HPLC method.

Using HPLC, the authors had investigated the three metabolites of deltamethrin (DM) in the urine of spraymen and one suicide, namely: dibromovinyl-dimethylcyclopropane carboxylic acid (Br2A), 3-phenoxybenzyl-hydroxy-ethyl acetate (PHE) and 3-phenoxyl-benzoic acid (BA). Br2A was chosen as the biological monitoring parameter for DM exposed people, and the urine samples of one suicide and 11 farmers sprayed DM or DM plus methamidophos were examined for Br2A quantitatively which was detected in 8 of 11 sprayers and in the suicide case.

Agricultural Workers' Diseases↗
PubMed1991

Transneuronal labeling of neurons in rabbit brain after injection of herpes simplex virus type 1 into the aortic depressor nerve.

Herpes simplex virus type 1 (HSV1) was injected into either the aortic depressor nerve or the vagus nerve in the rabbit. Four or 5 days after injection of virus, the rabbit brain was processed immunohistochemically to demonstrate viral antigen. After injection into the aortic nerve HSV1 positive cells were found principally ipsilaterally within the nucleus tractus solitarius, area postrema, caudal and rostral ventrolateral medulla oblongata, the spinal trigeminal complex, raphe nuclei, A5 area, locus coeruleus, parabrachial nucleus, periaqueductal gray, ventrolateral hypothalamic area, paraventricular nucleus, amygdala, bed nucleus of the stria terminalis and insular cortex. Double labeling studies indicated that approximately 85% of the virus-containing neurons in the ventrolateral medulla, and virtually all the HSV-positive neurons in the A5 area and locus coeruleus also contained tyrosine hydroxylase. In the raphe nuclei and parapyramidal region approximately 33% of virus-containing cells reacted positively with PH8 antibody, a marker for serotonin synthesis. After injection of HSV1 into the vagus nerve labeled cells were found in similar brain areas, with a more bilateral distribution. The HSV-positive neurons may be involved in the processing of baroreceptor-derived information.

Animals↗
PubMed1991

Construction, expression, and biologic activity of murine/human chimeric antibodies with specificity for the human alpha/beta T cell receptor.

Murine/human chimeric antibodies with specificity for the human TCR-alpha/beta have been produced by genetic engineering. The L and H chain V region exons encoding the murine mAb BMA 031 were isolated and inserted into mammalian expression vectors containing the human kappa and gamma 1 or gamma 4 C region exons. The chimeric genes were transfected into murine Sp2/O hybridoma cells by electroporation and transfectomas secreting chimeric antibody were isolated. Secretion levels ranged from 1 to 7 pg/cell/24 h. The chimeric antibodies bound specifically to T cells and competed effectively with the parental murine mAb for binding to these sites. The ability to promote antibody-dependent cell-mediated cytolysis was significantly enhanced in the chimeric antibodies as compared with murine BMA 031. C-dependent cytolysis, however, was not detectable with any of the antibodies. Chimeric BMA 031 is a clinically relevant, genetically engineered antibody with potential uses in transplantation, graft-vs-host disease, autoimmune diseases and other T cell-related disorders.

Animals↗
PubMed1991

Transneuronal transport of herpes simplex virus from the cervical vagus to brain neurons with axonal inputs to central vagal sensory nuclei in the rat.

The recent introduction of live viruses as intra-axonal tracing agents has raised questions concerning which central neurons are transneuronally labelled after application of the virus to peripheral organs or peripheral nerves. Since the central connections of the vagus nerve have been well described using conventional neuronal tracing agents, we chose to inject Herpes Simplex Virus Type 1 into the cervical vagus of the rat. After survival times of up to 3 days the rat brains were processed immunohistochemically using a polyclonal antiserum against herpes simplex virus. Two days after injection of the virus we observed viral antigen in the area postrema and in the nucleus tractus solitarius and the dorsal motor nucleus of the vagus (dorsal vagal complex), principally ipsilaterally. At this survival time the viral antigen in the dorsal vagal complex was largely confined to glial cells. After 3 days the viral antigen was localized both in glia and in nerve cells within the dorsal vagal complex and in brain regions previously demonstrated, using conventional tracing procedures, to contain neurons with axonal projections to the dorsal vagal complex. This was true for medullary, pontine, midbrain and hypothalamic regions and for telencephalic regions including the amygdala, the bed nucleus of the stria terminalis, and the insular and medial frontal cortices. Many of the nerve cells containing viral antigen were displayed in a Golgi-like manner, with excellent visualization of the dendritic tree. Axonal processes, in contrast, were not visualized. We used co-localization studies to confirm previous findings concerning monoamine neurotransmitter-related antigens present in medullary and pontine neurons projecting to the dorsal vagal complex. After 3 days there were many Herpes Simplex Virus Type 1-containing glial cells along the intra-medullary course of the vagal rootlets. However, no viral antigen was found in brain regions containing neurons whose axons pass through the region of glial cell-labelled rootlets. Glial cells containing viral antigen were particularly numerous in brain regions known to receive an input from neurons in the area postrema and the dorsal vagal complex. Taken together with our observation concerning the early appearance of viral antigen within glial cells in the dorsal vagal complex, this suggests that when the virus reaches the axon terminal portion it is transferred to nearby glial cells and possibly enters central neurons by way of these structures.

Amidines↗
PubMed1991

Neurons in rabbit caudal ventrolateral medulla inhibit bulbospinal barosensitive neurons in rostral medulla.

We made extracellular recordings from 104 spinally projecting neurons in the rostral ventrolateral medulla of urethan-anesthetized rabbits to test whether inhibitory vasomotor neurons in the caudal ventrolateral medulla act by inhibiting rostral sympathoexcitatory neurons. The median conduction velocity was 8.3 m/s, and the median discharge rate was 2.9 spikes/s. Raising arterial pressure with intravenous phenylephrine inhibited 88% of 77 neurons tested. The remaining units were excited. Lowering arterial pressure with nitroprusside excited 90% of 30 neurons tested. Remaining units were unaffected. Ninety-one percent of 58 rostral neurons inhibited by phenylephrine were also inhibited by injection of L-glutamate into the caudal ventrolateral medulla and 81% of 43 tested were excited by caudal injection of gamma-aminobutyric acid. These results confirm our suggestion [Brain Res. 253: 161-171, 1982; Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H686-H692, 1988] and the findings of S. K. Agarwal, A. J. Gelsema, and F. R. Calaresu [Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R265-R270, 1989]. The depressor neurons in the caudal medulla act substantially by inhibition of spinally projecting sympathoexcitatory neurons in the rostral medulla. All rostral units excited by phenylephrine were also excited by injections of L-glutamate into the caudal ventrolateral medulla, suggesting that some sympathoinhibition of baroreceptor and caudal medullary origin may take place in the spinal cord and be mediated by a subpopulation of rostral sympathoinhibitory neurons.

Animals↗