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H Li

Publications and source records attributed to H Li.

At least 1,279 records · Page 71Linked to original sources
PubMed1997

Single neurons in the spinal trigeminal and dorsal column nuclei project to both the cochlear nucleus and the inferior colliculus by way of axon collaterals: a fluorescent retrograde double-labeling study in the rat.

A number of single neurons in the spinal trigeminal nucleus (STN) and the dorsal column nucleus (DCN) were found to project simultaneously to the cochlear nucleus (CoN) and the external cortex of the inferior colliculus (ICe) by way of axon collaterals. Each rat was injected with Fluoro-Gold (FG) into CoN on one side and with tetramethylrhodamine-dextran amine (TMR-DA) into ICe on the side ipsilateral or contralateral to the FG injection. In these rats, a number of neuronal cell bodies in DCN and the interpolar and caudal subnuclei of STN were double-labeled retrogradely with both FG and TMR-DA, mainly on the side ipsilateral to the FG injection into CoN. These neurons in STN and DCN might mediate somatosensory inputs simultaneously to the two lower brainstem nuclei, CoN and ICe, which constitute the relays of the auditory pathway.

Animals↗
PubMed1997

Surgical anatomy of the rat middle ear.

This study was designed to aid experimental otologic studies of the rat middle ear. The topographic anatomy of the albino rat middle ear is described. A set of microphotographs with matching illustrations presents the structural details at several surgical exposures. Anatomic differences between the rat, guinea pig, and cat are noted.

Anatomy, Comparative↗
PubMed1997

Protection against oral and gastrointestinal diseases: importance of dietary nitrate intake, oral nitrate reduction and enterosalivary nitrate circulation.

Over the last 20 years, dietary nitrate has been implicated in the formation of methemoglobin and carcinogenic nitrosamines in humans. This has led to restrictions of nitrate and nitrite levels in food and drinking water. However, there is no epidemiological evidence for an increased risk of gastric and intestinal cancer in population groups with high dietary vegetable or nitrate intake. A reevaluation of our currently very negative perception of dietary nitrates comes from recent research into the metabolism and enterosalivary circulation of nitrate in mammals. These studies showed that nitrate is converted to nitrite in the oral cavity that then "fuels" an important mammalian resistance mechanism against infectious diseases. Moreover, there is now evidence that the conversion of nitrate into oxides of nitrogen prevents the formation carcinogenic nitrosamines.

Animals↗
PubMed1997

Quantitative autoradiography of 5-[3H]6-cyano-7-nitro-quinoxaline-2,3-dione and (+)-3-[3H]dizocilpine maleate binding in rat vestibular nuclear complex after unilateral deafferentation, with comparison to cochlear nucleus.

The distributions of non-N-methyl-D-aspartate and N-methyl-D-aspartate receptors in the rat vestibular nuclear complex were estimated by quantitative autoradiography of 5-[3H]6-cyano-7-nitro-quinoxaline-2,3-dione and (+)-3-[3H]dizocilpine maleate binding, respectively. The binding of 5-[3H]6-cyano-7-nitro-quinoxaline-2,3-dione in the vestibular nuclear complex was also compared with that in the cerebellar cortex and cochlear nucleus. Measurements were made in control rats and in rats with unilateral destruction of the inner ear and removal of the vestibular ganglion. Compared to the unlesioned side, 5-[3H]6-cyano-7-nitro-quinoxaline-2,3-dione binding in the lesioned-side vestibular nuclear complex was decreased significantly in all regions at two to four postoperative days. However, the bilateral asymmetry disappeared in most regions by 30 days. 5-[3H]6-Cyano-7-nitro-quinoxaline-2,3-dione binding increased in the molecular layer of the cerebellar cortex at 30 days after lesion, although there were no clear changes at two to seven days. 5-[3H]6-Cyano-7-nitro-quinoxaline-2,3-dione binding in the cochlear nucleus decreased on the lesioned side, compared to the unlesioned side, in regions receiving significant auditory nerve innervation, but increased in the molecular layer of the dorsal cochlear nucleus. (+)-3-[3H]Dizocilpine maleate binding in regions of the vestibular nuclear complex was reduced on the lesioned side, compared to the unlesioned side, after deafferentation, with the largest reductions usually at 30 postoperative days. It is suggested that: (i) non-N-methyl-D-aspartate receptors are involved in synaptic transmission for both vestibular and auditory nerve fibers, while the involvement of N-methyl-D-aspartate receptors is less certain; (ii) unilateral deafferentation of the vestibular nuclear complex can result in bilateral asymmetries for non-N-methyl-D-aspartate and N-methyl-D-aspartate receptors, which are most prominent at earlier and later survival times, respectively; and (iii) vestibular compensation may involve regulation of both non-N-methyl-D-aspartate and N-methyl-D-aspartate receptors in the vestibular nuclear complex and activation of non-N-methyl-D-aspartate receptor-related processes in cerebellar cortex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

In vivo bone marrow lipid characterization with line scan Carr-Purcell-Meiboom-Gill proton spectroscopic imaging.

Line scan Carr-Purcell-Meiboom-Gill spectroscopic imaging sequences have been used to extract lipid chemical composition indices in healthy adult bone marrow in the knee at 1.5 T. Since several spectroscopic echo readouts follow each excitation, the information acquired reflects a balance between spectral T2 decay processes and spectral resolution. To examine this balance in detail, data sets with two different echo spacings and spectral resolutions have been acquired to compare the information available from each in studies of bone marrow. Oils for which high field (7 T) proton spectra were recorded were used to evaluate the accuracy of lipid chemical composition indices extracted from the line scan Carr-Purcell-Meiboom-Gill spectroscopic imaging methods at 1.5 T. The extension of the method to fast spectroscopic imaging of bone marrow with multiple echoes is demonstrated.

Adult↗
PubMed1997

Conformational studies of dithymidine boranomonophosphate diastereoisomers.

The boranophosphate ester nucleotides are a new class of nucleic acid analogues that are isoelectronic and isostructural to normal phosphodiester nucleic acids and that maintain the anionic charge of the nucleic acid backbone. The two P-diastereoisomers of dithymidine boranomonophosphates were separated using reverse phase HPLC; the faster and slower eluting isomers are designated as d(TpBT)-1 and d(TpBT)-2, respectively. Conformations of the isomers were studied using-circular dichroism (CD) and NMR, and compared to the analogous phosphate diester, d(TpT). This comparison allowed the effects of the borane group and chirality of the boranophosphate linkage on sugar and base conformations to be assessed. The CD spectra of the diastereoisomers are consistent with both having a B-type conformation. Analysis of the 1H-1H and 1H-31P coupling constants showed that these conformations are similar to those of the unmodified parent dimer; specifically, the 2'-deoxyribose rings prefer the S (C2'-endo) conformation, and the C4'-C5' and C5'-O5' rotamers are primarily in the gamma + and beta + conformations, respectively. Conformational differences between the diastereoisomers and between the modified and unmodified dimers are manifested by differences in the preferences of the 3'-residues to adopt S sugar pucker and beta + conformations. There is reduced preference for the S sugar pucker of the 3'-residue in d(TpBT)-1 relative to d(TpBT)-2, which is similar to d(TpT). There is less preference for the beta + conformation of the 3'-residue in d(TpBT)-2 relative to d(TpBT)-1 and d(TpT). Based on the CD results, the temperature dependences of the thymidine H6 chemical shifts, and the derived sugar ring and backbone conformational parameters, we conclude that the borane group exerts a minimal influence on the sugar conformations and base stacking interactions. Preliminary assignment of the absolute configuration of the pair of SP and RP diastereoisomers to d(TpBT)-1 and d(TpBT)-2, respectively, is made on the basis of enzyme selectivity and NOE difference experiments.

Boron↗
PubMed1997

The heating phenomenon produced by an ultrasonic fountain.

When a piece of plastic sheet is placed in the path of an ultrasonic fountain generated using a medical nebulizer in water, temperatures of up to 250 degrees C can be produced on the face of the sheet opposite the fountain impact. This paper describes the experimental methodology and results, and suggests that this phenomenon is the combined result of both the heating and mechanical effect of ultrasonic cavitation within the fountain.

Journal Article↗
PubMed1997

Schwann cells responding to primary demyelination in vivo express p75NTR and c-erbB receptors: a light and electron immunohistochemical study.

We have used quantitative and qualitative light microscope immunohistochemistry to examine the expression of p75NTR and c-erbB receptors in Schwann cells in a demyelinating lesion induced by the intraneural injection of lysophosphatidyl choline (LPC). We report that levels of p75NTR, c-erbB2 and c-erbB4, as assessed using image analysis of immuno-peroxidase labelled sections, and c-erbB3, as assessed by eye, increased within each lesion site soon after the initiation of myelinolysis, peaked between 5 and 8 days after induction of demyelination and fell to undetectable levels at the onset of remyelination. Pre-embedding immunoelectron microscopy confirmed that Schwann cells ensheathing demyelinated axons were p75NTR positive. Immunolabel decorated overlapping processes of neighbouring Schwann cells, suggesting that in this context p75NTR could play a role in juxtacrine signalling between reacting cells. We conclude that upregulation of p75NTR and c-erbB receptors is a constitutive Schwann cell response to an acute disruption of the axon-Schwann cell relationship.

Animals↗
PubMed1997

Retinal changes associated with tamoxifen treatment for breast cancer.

PURPOSE: This study was undertaken to estimate the incidence of retinal changes and determine the prevalence of ocular toxicity associated with tamoxifen treatment in a breast cancer population. METHODS: The study was based on a population cross-sectional survey, including 290 patients taking tamoxifen from 6 months to 12 years; 274 patients were analysed. The main outcome measures were the incidence of retinal changes and visual impairment. RESULTS: The incidence of retinal changes was 0.9% (3 of 274 patients). All 3 patients were asymptomatic. The length of tamoxifen treatment ranged from 39 months to 120 months in the affected patients, with cumulative tamoxifen doses ranging from 23.7 g to 73 g. CONCLUSIONS: Retinopathy in patients receiving low doses of tamoxifen is rare and, in our study, did not result in changes in visual acuity. We found no retinopathy in patients receiving tamoxifen within the first 3 years of treatment or in patients receiving a total tamoxifen dosage of less than 23.7 g. Although retinopathy can occur in a tamoxifen-treated population, its low incidence and an associated good prognosis for vision does not merit special screening for this problem.

Aged↗
PubMed1997

The structure of the cytochrome p450BM-3 haem domain complexed with the fatty acid substrate, palmitoleic acid.

The substrate-bound structures of two cytochrome P450s, P450cam and P450eryF, are known. While these structures reveal important features that control substrate specificity, the problem of how conformational changes allow for substrate entry and product release remains unsolved. The structure of the haem domain of the bacterial fatty acid hydroxylase, P450BM-3, previously was solved in the substrate-free form. Unlike the substrate-bound P450cam and P450eryF structures, the substrate access channel is open in substrate-free P450BM-3. Here we present the X-ray structure of P450BM-3 at 2.7 A bound with a fatty acid substrate, palmitoleic acid. A comparison of the substrate-bound and -free forms reveals major conformational differences and provides the first detailed picture of substrate-induced conformational changes in a P450.

Amino Acid Sequence↗
PubMed1997

Structure of translation factor eIF4E bound to m7GDP and interaction with 4E-binding protein.

eIF4E, the mRNA cap binding protein, is a master switch that controls eukaryotic translation. To be active, it must bind eIF4G and form the eIF4F complex, which also contains eIF4A. Translation is downregulated by association of eIF4E with 4E-BP, which occupies the eIF4G binding site. Signalling events acting on 4E-BP cause it to dissociate from eIF4E, and eIF4E is then free to bind eIF4G to form the active eIF4F complex. We have solved the structure of the yeast eIF4E/m7Gpp complex in a CHAPS micelle. We determined the position of the second nucleotide in a complex with m7GpppA, and identified the 4E-BP binding site. eIF4E has a curved eight-stranded antiparallel beta-sheet, decorated with three helices on the convex face and three smaller helices inserted in connecting loops. The m7G of the cap is intercalated into a stack of tryptophans in the concave face. The 4E-BP binding site is located in a region encompassing one edge of the beta-sheet, the adjacent helix a2 and several regions of non-regular secondary structure. It is adjacent to, but does not overlap the cap-binding site.

Amino Acid Sequence↗
PubMed1997

Irreversible inhibition of mitochondrial complex I by 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxyli c acid (DHBT-1): a putative nigral endotoxin of relevance to Parkinson's disease.

Based on a number of lines of evidence, we have proposed recently that a very early step in the pathogenesis of idiopathic Parkinson's disease might be elevated translocation of L-cysteine into neuromelanin-pigmented dopaminergic cell bodies in the substantia nigra. In vitro studies suggest that such an influx of L-cysteine would divert the neuromelanin pathway by scavenging dopamine-o-quinone, the proximate autoxidation product of dopamine, to give 5-S-cysteinyldopamine, which is oxidized further to 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxylic acid (DHBT-1) and other cysteinyldopamines and dihydrobenzothiazines. In this study, it is demonstrated that DHBT-1 inhibits ADP-stimulated oxidation of malate and pyruvate (state 3 or complex I respiration) when incubated with intact rat brain mitochondria with an IC50 of approximatelly 0.80 mM. Incubation of DHBT-1 with freeze-thawed rat brain mitochondria in both the presence and absence of KCN and/or NADH causes an irreversible, time-dependent decrease of NADH-coenzyme Q1 reductase activity. Significantly lower concentrations of DHBT-1 are necessary to cause this effect when mitochondrial membranes are incubated in the absence of KCN and NADH. The irreversible inhibition of mitochondrial complex I caused by DHBT-1 under the latter conditions could be blocked only partially by glutathione, ascorbic acid, superoxide dismutase, or catalase. Together, these results suggest that DHBT-1 can cross the outer mitochondrial membrane and irreversibly inhibit complex I by a mechanism that is not primarily related to oxygen radical-mediated damage. Formation of DHBT-1 requires only dopamine, L-cysteine, and an oxidizing environment, conditions that may well exist in the cytoplasm of neuromelanin-pigmented dopaminergic neurons in the parkinsonian substantia nigra. The results of this study raise the possibility that DHBT-1 might be an endotoxin formed specifically in pigmented dopaminergic neurons that can contribute to irreversible damage to mitochondrial complex I and substantia nigra cell death in Parkinson's disease.

Animals↗
PubMed1997

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate.

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2-nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane-induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.

Animals↗
PubMed1997

Molecular genetics of long QT syndrome from genes to patients.

Recently, there has been intense excitement in the field of cardiac arrhythmias. Molecular genetic studies have led to significant progress in characterizing molecular mechanisms underlying long QT syndrome, an inherited cardiac disorder that causes syncope, seizures, and sudden death from ventricular arrhythmias. Three long QT syndrome genes have been identified: SCN5A on 3p21-24, HERG on 7q35-36, and KVLQT1 on 11p15.5; all encode cardiac mycote ion channels. Molecular and electrophysiological characterization of these three long QT syndrome genes has led to identification of three critical electrical currents in the human heart (INa, IKr, IKa) and provides insight into our fundamental understanding of cardiac function. Genetic testing and gene-specific therapies are now available for some families with long QT syndrome.

Chromosome Mapping↗
PubMed1997

Adenovirus-mediated wild-type p53 gene transfer and overexpression induces apoptosis of human glioma cells independent of endogenous p53 status.

Mutation or inactivation of the p53 tumor suppression gene is an early alteration in the transformation of glial cells to gliomas. To study the effect of exogenous wild-type p53 on glioma cell growth, human glioma lines U251 MG, U87 MG and A172 were infected with an adenovirus vector expressing either wild-type p53 or bacterial lacZ. Rapid cell death occurred only in the p53-transduced cell lines and was characterized by nuclear condensation, formation of nucleosomal DNA ladders, and positive in situ end-labeling of DNA, suggesting that apoptosis had been induced. The U87 MG cell line that contains wild-type p53 as evidenced by wild-type p53-dependent transcription activity also underwent apoptosis within 2 to 3 days after infection. These results suggest that the presence of endogenous wild-type p53 does not preclude apoptosis by overexpression of exogenous p53.

Adenoviridae↗
PubMed1997

Characterization of cocaine binding sites in the rat testes.

PURPOSE: An estimated 29 million individuals use cocaine in the United States. Studies have shown a high affinity for dose dependent binding of cocaine in the testes. Recent work done in our laboratory has shown that chronic administration of cocaine to male rats has an adverse effect on fertility and spermatogenesis by producing extensive morphological changes in the testes, leading to reduction in sperm production. As a first step toward understanding this process, we characterized and identified the pharmacological properties of [3H]cocaine binding sites in the testes. MATERIALS AND METHODS: Crude membranes from the testes were prepared from 35 days old male Sprague-Dawley rats. [3H]cocaine binding was measured by using the method of Madras et al. (1989) with modifications. The data from saturation binding assays were analyzed by Inplot (GraphPad Software, San Diego, CA) to determine the Kd and Bmax. RESULTS: Specific binding of [3H]cocaine was linearly dependent on membrane protein concentrations ranging from 0.2 to 8 mg./ml. The pooled data from three independent experiments revealed a mean affinity of 36 +/- 2.0 nM and Bmax of 1.84 +/- 0.13 pmol/mg. The present study demonstrates that testicular tissue has receptor protein that binds [3H]cocaine saturably and specifically. Competition displacement experiments revealed a shallow displacement curve for (-)cocaine and Win 35,428 with r2 = 0.96, indicative of multiple binding components. Computer analysis confirmed that a two component binding model was preferred statistically over a one component model in all three experiments (p < 0.001). CONCLUSION: The results from these studies suggest that the testicular tissue contains a protein that binds [3H]cocaine in a saturable and specific manner. It has a different sensitivity from the [3H]cocaine binding protein in the brain and placenta. Further clarification of the relationship between cocaine and its recognition site is necessary to understand the mechanism of testicular damage after cocaine exposure.

Animals↗
PubMed1997

The significance of white-centered retinal hemorrhages in the shaken baby syndrome.

Retinal hemorrhages in healthy children with or without a history of associated trauma are a strong indicator of child abuse. This report describes six cases of battered infants who presented with white-centered retinal hemorrhages. We discuss potential mechanisms for the presence of white-centered retinal hemorrhages in battered children.

Battered Child Syndrome↗