Biomedical subjects

J Y Li

Publications and source records attributed to J Y Li.

At least 91 records · Page 5Linked to original sources

PubMed1999

Inhibition of glucose uptake and suppression of glucose transporter 1 mRNA expression in L929 cells by tumour necrosis factor-alpha.

Recombinant human tumour necrosis factor-alpha (rhTNF-alpha) arrested the growth and suppressed glucose uptake of mouse fibrosarcoma L929 cells in vitro. When the cells were treated with rhTNF-alpha for 24 hours, the mRNA level of glucose transporter 1 (GLUT 1), which is the only GLUT found to be present in L929 cells in our study, was suppressed in a dose-dependent manner. Since the growth of tumour cells depends mainly on glucose catabolism, our findings may indicate that rhTNF-alpha inhibits L929 cells growth by lowering the glucose transport through suppression of GLUT 1 mRNA expression in the cells.

Animals↗

PubMed1999

Modulation of naloxone-precipitated morphine withdrawal syndromes in rats by neuropeptide FF analogs.

Neuropeptide FF (NPFF) has been reported to be an endogenous anti-opioid peptide that has significant effects on morphine tolerance and dependence. In the present study, we examined the chronic effects of NPFF and its synthetic analogs: the putative agonist, PFRFamide, and the putative antagonists, dansyl-PQRamide and PFR(Tic)amide on naloxone-precipitated morphine withdrawal syndromes in rats. After a 5-day co-administration with morphine [5 mg/kg, intraperitoneally (i.p.), twice per day (b.i.d.)] and the tested peptide [intracerebroventricularly (i.c.v.) or i.p., b.i.d.], naloxone (4 mg/kg, i.p.) was given systemically to evaluate the severity of the morphine withdrawal syndromes. Our results revealed that NPFF significantly potentiated the overall morphine withdrawal syndromes and, on the contrary, dansyl-PQRamide attenuated these syndromes. These results clearly indicate that modulation of the NPFF system in the mammalian central nervous system has significant effects on opiate dependence. In addition, morphine withdrawal syndromes could be practically applied as a valid parameter to functionally characterize the putative NPFF agonists and antagonists.

Animals↗

PubMed1999

Axonal transport of ribonucleoprotein particles (vaults).

RNA was previously shown to be transported into both dendritic and axonal compartments of nerve cells, presumably involving a ribonucleoprotein particle. In order to reveal potential mechanisms of transport we investigated the axonal transport of the major vault protein of the electric ray Torpedo marmorata. This protein is the major protein component of a ribonucleoprotein particle (vault) carrying a non-translatable RNA and has a wide distribution in the animal kingdom. It is highly enriched in the cholinergic electromotor neurons and similar in size to synaptic vesicles. The axonal transport of vaults was investigated by immunofluorescence, using the anti-vault protein antibody as marker, and cytofluorimetric scanning, and was compared to that of the synaptic vesicle membrane protein SV2 and of the beta-subunit of the F1-ATPase as a marker for mitochondria. Following a crush significant axonal accumulation of SV2 proximal to the crush could first be observed after 1 h, that of mitochondria after 3 h and that of vaults after 6 h, although weekly fluorescent traces of accumulations of vault protein were observed in the confocal microscope as early as 3 h. Within the time-period investigated (up to 72 h) the accumulation of all markers increased continuously. Retrograde accumulations also occurred, and the immunofluorescence for the retrograde component, indicating recycling, was weaker than that for the anterograde component, suggesting that more than half of the vaults are degraded within the nerve terminal. High resolution immunofluorescence revealed a granular structure-in accordance with the biochemical characteristics of vaults. Of interest was the observation that the increase of vault immunoreactivity proximal to the crush accelerated with time after crushing, while that of SV2-containing particles appeared to decelerate, indicating that the crush procedure with time may have induced perikaryal alterations in the production and subsequent export to the axon of synaptic vesicles and vault protein. Our data show that ribonucleoprotein-immunoreactive particles can be actively transported within axons in situ from the soma to the nerve terminal and back. The results suggest that the transport of vaults is driven by fast axonal transport motors like the SV2-containing vesicles and mitochondria. Vaults exhibit an anterograde and a retrograde transport component, similar to that observed for the vesicular organelles carrying SV2 and for mitochondria. Although the function of vaults is still unknown studies of the axonal transport of this organelle may reveal insights into the mechanisms of cellular transport of ribonucleoprotein particles in general.

Animals↗

PubMed1999

Seimatoantlerium tepuiense gen. nov., a unique epiphytic fungus producing taxol from the Venezuelan Guyana.

Seimatoantlerium gen. nov., type species, S. tepuiense sp. nov. is proposed for an acervular fungus producing 4-septate, holoblastic conidia with 6-8 unbranched, apical appendages that dehisce as an appendage apparatus and also commonly possessing one or two exogenous basal appendages as well as a pedicel. It is compared with Seimatosporium, Seimatosporiopsis, and other genera. It is epiphytic on Maguireothamnus speciosus, a rubiaceous plant endemic to the tepuis of southeastern Venezuela. It produces the anti-oomycetous anticancer compound, taxol, as shown by immunological and spectroscopic methods. Taxol production is discussed relative to the ability of this fungus to exist in an extremely moist ecosystem, as well as to its relationship to other plant associated fungi.

Antineoplastic Agents, Phytogenic↗

PubMed1999

P53 deletion is not a frequent event in multiple myeloma.

Recently a high incidence of interstitial deletion of the P53 locus has been reported in multiple myeloma (MM) patients. Considering the importance of such an event, we analysed 79 patients with advanced-stage disease using fluorescence in situ hybridization (FISH). Strikingly, we found only 7/79 patients with a P53 deletion. In order to rule out any differences in probe selection, we reanalysed all the patients with the same probe as that used in a previous study, and confirmed the low incidence of P53 deletion (7/79, 9%). The only explanation is a difference in hybridization efficiency. Since hybridization is far less efficient on malignant plasma cells than on other bone marrow cells we suggest that this poor hybridization efficiency may lead to a false P53 deletion.

Gene Deletion↗

PubMed1999

Proteolytic processing, axonal transport and differential distribution of chromogranins A and B, and secretogranin II (secretoneurin) in rat sciatic nerve and spinal cord.

The chromogranin family comprises chromogranin A and B, and secretogranin II. The present study has focused on the axonal transport of chromogranins/secretogranin II and their detailed distribution in peripheral nerves and the spinal cord. With radioimmunoassay (RIA) and column chromatography, we first studied the processing of chromogranin B and secretogranin II during axonal transport. No larger precursors of these peptides were detected in the sciatic nerves, indicating that they are already processed to a high degree early during axonal transport. We also analysed nerve segments above and below a crush, using RIA, in order to compare these accumulation data with those obtained by the cytofluorimetric-scanning (CFS) technique. For the latter technique, the amounts of accumulation distal to the crush (presumably representing recycling and retrogradely transported peptides) were 30-40% of the amounts in the proximal accumulation for chromogranin A and secretoneurin, in contrast to chromogranin B, which showed 15% recycling. With the RIA, the corresponding values for secretoneurin and PE-11 (antibody against chromogranin B) were 42% and 14%, respectively. Therefore, the data obtained by CFS were in excellent agreement with those obtained by RIA. In crushed sciatic nerves, chromogranin A was present in large axons as well as in small- and medium-sized axons. Chromogranin B was mainly restricted to large axons, while secretoneurin was localized to bundles of small axons. This differential distribution was also found in the spinal roots and in the peripheral terminals. Chromogranin A was present in both ventral and dorsal roots, and chromogranin B was detected in ventral roots and in large sensory axons in the dorsal roots. Secretoneurin was dominant in the dorsal root. Double-labelling studies with antibodies against choline acetyltransferase/vesicular acetylcholine transporter, or against tyrosine hydroxylase, confirmed that chromogranin A was distributed in cholinergic, sensory, as well as adrenergic neurons. Chromogranin B was mainly present in cholinergic motor neurons and large sensory neurons, and secretoneurin was restricted to adrenergic and sensory neurons. The present study demonstrates that chromogranins A and B, and secretoneurin are transported with fast axonal transport in the peripheral nerves, with different amounts of recycling, and that they are differentially distributed in different types of neurons in the peripheral nervous system and the spinal cord, suggesting that each of them may play a special role in subsets of neurons.

Animals↗

PubMed1999

Axonal transport of synucleins is mediated by all rate components.

Synucleins are abundant nerve terminal proteins of hitherto unknown function. In diseases with Lewy bodies, human alpha-synuclein concentrates in these lesions in the cell body and mutations in alpha-synuclein lead to heritable Parkinson's disease with Lewy bodies. This indicates that changes in the normal metabolism and axonal transport of alpha-synuclein is perturbed in these diseases. To investigate the normal axonal transport of synucleins we studied the rat visual system by nerve crush operations and metabolic labelling of the retinal ganglion cells followed by immunoprecipitation of nerve segments. We found by immunofluorescence microscopy of the crush-operated nerves that synucleins are transported by fast antero- and retrograde transport and colocalize with synaptophysin and SNAP-25 around the lesion. The metabolic labelling studies demonstrated that synucleins were moved through the nerve with all the rate components, the fast component and the slow components a and b, with component b predominating. Two-dimensional gel electrophoresis revealed that both alpha- and beta-synuclein migrate through the nerve by slow component b in a ratio of 2:1.

Animals↗

PubMed1999

Genetically engineered brain drug delivery vectors: cloning, expression and in vivo application of an anti-transferrin receptor single chain antibody-streptavidin fusion gene and protein.

A single chain Fv antibody-streptavidin fusion protein was expressed and purified from bacterial inclusion bodies following cloning of the genes encoding the variable region of the heavy chain and light chain of the murine OX26 monoclonal antibody to the rat transferrin receptor. The latter undergoes receptor mediated transcytosis through the brain capillary endothelial wall in vivo, which makes up the blood-brain barrier (BBB); therefore, the OX26 monoclonal antibody and its single chain Fv analog may act as brain drug delivery vectors in vivo. Attachment of biotinylated drugs to the antibody vector is facilitated by production of the streptavidin fusion protein. The bi-functionality of the OX26 single chain Fv antibody-streptavidin fusion protein was retained, as the product both bound biotin and the rat transferrin receptor in vitro and in vivo, based on pharmacokinetic and brain uptake analyses in anesthetized rats. The attachment of biotin-polyethyleneglycol-fluorescein to the OX26 single chain Fv antibody-streptavidin fusion protein resulted in illumination of isolated rat brain capillaries in confocal fluorescent microscopy. In conclusion, these studies demonstrate that genetically engineered single chain Fv antibody-streptavidin fusion proteins may be used for non-invasive neurotherapeutic delivery to the brain using endogenous BBB transport systems such as the transferrin receptor.

Animals↗

PubMed1999

Transcriptional and translational regulation of angiotensin II type 2 receptor by angiotensin II and growth factors.

The regulatory effects of angiotensin-II (AngII) and several growth factors, including insulin-like growth factor 1 (IGF-1), basic fibroblast growth factor (bFGF), and transforming growth factor beta1 (TGFbeta1) on the AngII subtype 2 (AT2) receptor were studied using R3T3 cells, a mouse fibroblast cell line that expresses only AT2 receptors. AngII increased (in a time- and dose-dependent manner) AT2 binding sites but had no effects on AT2 messenger RNA (mRNA) levels. At maximal concentration (10(-7) M) AngII caused a 4-fold increase of AT2 receptor number. In contrast, IGF-1 increased (3- to 4-fold), whereas bFGF and TGFbeta1 decreased (by about 90% and 80%, respectively) AT2 receptor and mRNA levels. Moreover, AngII potentiated the effect of IGF-1 on receptor number, but not on AT2 mRNA levels, and significantly reduced the inhibitory action of bFGF and TGFbeta1 on AT2 binding sites but not on AT2 mRNA levels. None of these factors modified AT2 mRNA half-life. The potential effects of these factors on transcription of the AT2 gene were measured by means of nuclear run-on assays. IGF-1 increased the rate of transcription by about 2.5-fold, whereas bFGF and TGFbeta1 reduced it by 90 and 80%, respectively. In contrast, AngII did not modify either the basal or IGF-1-stimulated transcription rate. Finally, AngII alone or together with IGF-1, but not IGF-1 alone, increased the attachment of AT2 mRNA to polysomal fractions. The present findings demonstrate that the main mechanism by which AngII regulates the AT2 receptor is by increasing the rate of AT2 mRNA translation, whereas the stimulatory (IGF-1) or inhibitory (bFGF and TGFbeta1) effects of these growth factors on AT2 expression are exerted at the transcriptional level.

Angiotensin II↗

PubMed1999

Characterisation of the muscarinic receptor subtype M3 in the bovine zona fasciculata-reticularis cells by receptor binding, mRNA and functional studies.

In the present work we have investigated which muscarinic (M) receptor subtype is responsible for the steroidogenic effect of muscarinic agonists in bovine zona fasciculata-reticularis (ZFR) cells in culture. Radioligand binding studies using the muscarinic antagonist [(3)H]quinuclidinyl benzilate ([(3)H]QNB) demonstrated binding sites of high affinity (K(d)=0.45 nM) and low capacity ( approximately 8000 sites/cell). Pharmacological characterisation of muscarinic receptors was assessed by evaluating the effects of the M(3)>M(1)>>M(2) antagonist 4-DAMP (4-diphenylacetyl-N-methylpiperidine) and the M(1)=M(4)> M(3)>>M(2) antagonist pirenzepine on the binding of [(3)H]QNB and carbachol-induced cortisol production. For both parameters, the potency of 4-DAMP was about two orders of magnitude higher than that of pirenzepine. Reverse transcriptase (RT)-PCR analysis of bovine ZFR mRNAs using specific primers for M(2), M(3) and M(4) receptors revealed the expression of only M(3) mRNA. Moreover, carbachol significantly stimulated inositol phosphate accumulation, but had no inhibitory effect on basal or ACTH-induced cAMP production. Indeed, carbachol potentiated ACTH-induced cAMP production and this effect was, in part, mediated through protein kinase C. Lastly, neomycin, an inhibitor of phosphoinositide turnover, significantly attenuated carbachol-evoked cortisol production. Thus, pharmacological, biochemical and mRNA studies indicate that the M(3) receptor subtype is responsible for the biological effects of muscarinic agonists in bovine ZFR cells.

Animals↗

PubMed1999

Amplification of the 11q23 region in acute myeloid leukemia.

Cytogenetic abnormalities involving the 11q23 region are found in both acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML). Molecular consequences of 11q23 translocations are the formation of chimeric genes, all of them involving the MLL (mixed-lineage leukemia) gene. To evaluate the usefulness of fluorescence in situ hybridization (FISH) in detecting MLL rearrangements in AML, we analyzed 181 patients with an MLL-specific probe. Among them, we detected three patients with multiple FISH signals, reflecting genomic amplification of this chromosomal region. Extra copies of MLL have been reported previously in four patients, but did not correspond to a true gene amplification. For the first time, we describe genomic amplification of the 11q23 region (up to more than 50 copies) in AML patients. This genomic amplification could affect MLL, but other genes in the vicinity could also be the primary target. Genes Chromosomes Cancer 26:166-170, 1999.

Aged↗

PubMed1999

Cytomegalovirus pneumonitis as an initial presentation in an HIV-infected patient.

Human immunodeficiency (HIV) infection often presents with an unusual symptom complex. Although cytomegalovirus (CMV) is a frequent opportunistic infection in the late stage of acquired immunodeficiency syndrome (AIDS), CMV pneumonitis as an initial manifestation of HIV infection is not documented in the medical literature. We report a previously healthy patient with bilateral interstitial pulmonary infiltrates who was found to have CMV pneumonitis; only later was HIV virus infection diagnosed. Cytomegalovirus is a frequently isolated pathogen from respiratory secretions in AIDS patients. The role of CMV as a sole pulmonary pathogen is controversial. After exclusion of other pathogens, CMV was demonstrated by histological changes and viral culture in our case. This case indicates that pulmonary infiltrates presenting as the first manifestation of HIV infection can be caused by CMV infection.

AIDS-Related Opportunistic Infections↗

PubMed1998

High incidence of translocations t(11;14)(q13;q32) and t(4;14)(p16;q32) in patients with plasma cell malignancies.

Abnormalities involving the 14q32 region are recurrent chromosomal changes in plasma cell malignancies. Recent preliminary molecular analyses found IGH rearrangements in almost 100% of human myeloma cell lines and in 75% of patients. However, no systematic study analyzing the nature of the partner chromosomal regions have been reported thus far. To define the exact incidence of illegitimate IGH rearrangements and the respective incidence of partner genes cloned to date, we analyzed 141 patients with either multiple myeloma (MM, n = 127) or primary plasma cell leukemia (PCL, n = 14) using fluorescence in situ hybridization. The overall incidence of illegitimate recombinations was 57% (80 of 141 patients). Analysis of this incidence according to Durie and Salmon stage, patients' status, i.e., MM versus primary PCL and diagnosis versus relapse, immunoglobulin type and subtype, and beta2-microglobulin value, did not show any correlation. To analyze the nature of the partner chromosomal region, we selected probes specific for the following genes: FGFR3 (4p16), MYC (8q24), CCND1 (11q13), MAF (16q23), and BCL2 (18q21). These probes, combined with differentially labeled 14q32 probes, were used for dual-color fluorescence in situ hybridization on interphase plasma cells. Among the 80 patients with illegitimate IGH rearrangement, we identified 23 IGH-CCND1 fusion cases [i.e., t(11;14)], 17 IGH-FGFR3 fusion cases [i.e., t(4;14)], 3 IGH-MYC fusion cases [i.e., t(8;14)], and only one IGH-MAF fusion case. No IGH-BCL2 fusion case was detected. In 37 of 80 patients, none of these partner genes was involved. Analysis of cases with specific translocations according to their bioclinical features at diagnosis did not show any correlation. This study demonstrated that CCND1 and FGFR3 genes are involved together in about 50% of MM and primary PCL patients with illegitimate IGH rearrangements.

Aneuploidy↗

PubMed1998

Emerging tobacco hazards in China: 1. Retrospective proportional mortality study of one million deaths.

OBJECTIVE: To assess the hazards at an early phase of the growing epidemic of deaths from tobacco in China. DESIGN: Smoking habits before 1980 (obtained from family or other informants) of 0.7 million adults who had died of neoplastic, respiratory, or vascular causes were compared with those of a reference group of 0.2 million who had died of other causes. SETTING: 24 urban and 74 rural areas of China. SUBJECTS: One million people who had died during 1986-8 and whose families could be interviewed. MAIN OUTCOME MEASURES: Tobacco attributable mortality in middle or old age from neoplastic, respiratory, or vascular disease. RESULTS: Among male smokers aged 35-69 there was a 51% (SE 2) excess of neoplastic deaths, a 31% (2) excess of respiratory deaths, and a 15% (2) excess of vascular deaths. All three excesses were significant (P<0.0001). Among male smokers aged >/70 there was a 39% (3) excess of neoplastic deaths, a 54% (2) excess of respiratory deaths, and a 6% (2) excess of vascular deaths. Fewer women smoked, but those who did had tobacco attributable risks of lung cancer and respiratory disease about the same as men. For both sexes, the lung cancer rates at ages 35-69 were about three times as great in smokers as in non-smokers, but because the rates among non-smokers in different parts of China varied widely the absolute excesses of lung cancer in smokers also varied. Of all deaths attributed to tobacco, 45% were due to chronic obstructive pulmonary disease and 15% to lung cancer; oesophageal cancer, stomach cancer, liver cancer, tuberculosis, stroke, and ischaemic heart disease each caused 5-8%. Tobacco caused about 0.6 million Chinese deaths in 1990 (0.5 million men). This will rise to 0.8 million in 2000 (0.4 million at ages 35-69) or to more if the tobacco attributed fractions increase. CONCLUSIONS: At current age specific death rates in smokers and non-smokers one in four smokers would be killed by tobacco, but as the epidemic grows this proportion will roughly double. If current smoking uptake rates persist in China (where about two thirds of men but few women become smokers) tobacco will kill about 100 million of the 0.3 billion males now aged 0-29, with half these deaths in middle age and half in old age.

Adult↗

PubMed1998

Primary non-Hodgkin's lymphoma of the nasal cavity: prognostic significance of paranasal extension and the role of radiotherapy and chemotherapy.

BACKGROUND: This study was conducted to determine whether the paranasal extension of a primary non-Hodgkin's lymphoma (NHL) of the nasal cavity has any deleterious effect on patient outcome. METHODS: One hundred and seventy-five patients with previously untreated nasal NHL were reviewed. There were 2 with low grade, 107 with intermediate grade, 17 with high grade, and 49 with unclassifiable lymphomas. In 48 cases the immunophenotype was available and 46 were T-cell lymphoma. According to the Ann Arbor system, there were 133 patients with Stage IE, 28 with Stage IIE, 4 with Stage IIIE, and 10 with Stage IVE lymphomas. Stage IE was subdivided into limited Stage IE (i.e., confined to the nasal cavity [67 patients]) or extensive Stage IE (i.e., presenting with extension beyond the nasal cavity [66 patients]). For patients with limited Stage IE disease the treatment of choice was radiotherapy with or without chemotherapy. In patients with extensive Stage IE disease, treatment was comprised of a combination of chemotherapy and radiotherapy or radiotherapy alone. For patients with a more advanced stage of disease (IIE-IVE), chemotherapy was an integral part of the treatment and was completed by irradiation, especially for patients with Stage IIE disease. RESULTS: The actuarial overall survival (OS) and disease free survival (DFS) rates at 5 years for the whole group were 65% and 57%, respectively. The 5-year OS and DFS rates were influenced by stage, with a gradual decrease from 75% and 68% for Stage IE disease to 35% and 28% for Stage IIE disease, and 31% and 19% for Stage IIIE/IVE disease. Patients with limited Stage IE disease survived significantly longer (90% 5-year OS) compared with those with extensive Stage IE disease (57% 5-year OS; P < 0.001). For 67 patients with limited Stage IE disease, the 5-year OS was 89% with radiotherapy alone and 92% with radiotherapy and chemotherapy, whereas for 66 patients with extensive Stage IE disease, the 5-year OS was 54% with radiotherapy and 58% with combined modality therapy or chemotherapy (P > 0.05). CONCLUSIONS: The prognosis of patients with primary NHL of the nasal cavity is stage dependent. In this large cohort of Stage IE patients, it was demonstrated that the paranasal local extension was a significant prognostic factor associated with poorer treatment outcome. The authors believe that Ann Arbor Stage IE should be subclassified further into limited and extensive Stage IE. The addition of chemotherapy did not appear to modify significantly the survival of patients with either limited or extensive Stage IE disease. The extranodal progression observed in patients with extensive Stage IE and Stage IIE-IVE disease clearly illustrates the need for improvement of systemic treatment.

Adolescent↗

PubMed1998

Effects of growth factors on cell proliferation and angiotensin II type 2 receptor number and mRNA in PC12W and R3T3 cells.

Previous studies have suggested that the expression of angiotensin type 2 receptor was inversely related to cell proliferation. We examined the effects of insulin-like growth factor (IGF-1), basic fibroblast growth factor (bFGF), transforming growth factor beta1 (TGFbeta1) and fetal calf serum (FCS) on cell proliferation and AT2 binding sites and mRNA level in PC12W (rat pheochromocytoma cell line) and R3T3 (mouse fibroblast cell line) which express abundant AT2 receptors. In both cell lines, serum deprivation markedly increased both AT2 receptor number and mRNA. However, in the absence of serum cell proliferation continued in PC12W and R3T3 at late passages (R3T3 LP) but not at early passages (R3T3 EP). In PC12W, none of the three growth factors studied stimulated cell proliferation, but TGFbeta1 and more particularly bFGF markedly reduced AT2 expression. In R3T3 LP, IGF-1 and bFGF, but not TGFbeta1, slightly stimulated cell proliferation, but the three factors, specially bFGF, reduced AT2 expression. In contrast, in R3T3 EP, the three growth factors significantly increased cell proliferation, but whereas TGFbeta1 and bFGF markedly reduced AT2 binding sites and mRNA, IGF-1 caused the opposite effects. These results indicate that regulation of AT2 expression is not correlated with cell proliferation and appears to be more complex than initially suspected. In addition, they show that the same factor can have an opposite effect on AT2 expression in the same cell line depending upon the cell passage.

Angiotensin II↗

PubMed1998

Measurement of regional N-acetylaspartate after transient global ischemia in gerbils with and without ischemic tolerance: an index of neuronal survival.

We investigated the correlation between N-acetylaspartate (NAA) level and neuronal density in the hippocampal CA1 region of the brain after occlusion of both common carotid arteries for 5 minutes and reperfusion for 3 hours to 4 weeks in gerbils with and without ischemic preconditioning (tolerance). Animals were divided into four groups--the sham operated group, the nonpreconditioning (non-p) group, the single-preconditioning (single-p) group with 2-minute ischemia once 2 days before 5-minute ischemia, and the double-preconditioning (double-p) group with 2-minute ischemia twice 2 days before 5-minute ischemia (n = 6 for each group). The CA1 region was dissected out from freeze-dried sections for high-performance liquid chromatographic assay of NAA, and adjacent sections were stained with cresyl violet for measurement of the neuronal density. Both NAA (pmol/microg dry weight) and the neuronal density (cells/mm) decreased in the non-p group after 3 days (NAA = 24.0 +/- 3.0; neuronal density = 65 +/- 38 cells/mm) and 7 days (NAA = 17.9 +/- 2.5; neuronal density = 20 +/- 15 cells/mm) and in the single-p group after 7 days (26.4 +/- 3.0, 106 +/- 30) compared with the control group (NAA = 32.9 +/- 3.0; neuronal density = 203 +/- 9 cells/mm). There was no decrease in the double-p group. The NAA level and the neuronal density showed a good linear correlation. The regional NAA level may be used as an index of neuronal viability.

Animals↗

PubMed1998

Factorial trial of three interventions to reduce the progression of precancerous gastric lesions in Shandong, China: design issues and initial data.

In the fall of 1995, 3411 subjects in 13 rural villages in Linqu County, Shandong Province, China, began participating in a blinded, randomized 23 factorial trial to determine whether interventions can reduce the prevalence of dysplasia and other precancerous gastric lesions. One intervention is treatment for infection by Helicobacter pylori with amoxicillin and omeprazole. A second is dietary supplementation with capsules containing vitamin C, vitamin E, and selenium. A third is dietary supplementation with capsules containing steam-distilled garlic oil and Kyolic aged garlic extract. Investigators will evaluate histopathologic endpoints after gastroscopies with biopsies from seven standard sites in 1999. Initial data from pill counts and sampled blood levels of vitamin E, vitamin C, and S-allylcysteine indicate excellent compliance. Subjects have tolerated all interventions well, although 3.1% of those assigned to amoxicillin and omeprazole developed rashes, compared to 0.3% to those in the control group. Preliminary breath tests demonstrate substantial reductions in gastric urease activity, an indication of infection by Helicobacter pylori, among those assigned to amoxicillin and omeprazole.

Adult↗