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Biomedical subjects

J Zheng

Publications and source records attributed to J Zheng.

At least 217 records · Page 12Linked to original sources
PubMed1999

Four new triterpenoidal saponins acylated with one monoterpenic acid from Gleditsia sinensis.

Four new oleanane-type triterpenoidal glycosides, named gleditsiosides A-D (1-4), were isolated from the anomalous fruits of Gleditsia sinensis. Using modern NMR techniques, including DQF-COSY, HETCOR, HOHAHA, HMBC, and ROESY experiments and MS analysis as well as chemical methods, their structures were determined as 3-O-beta-D-xylopyranosyl-(1-->2)-alpha-L-arabinopyranosyl-(1-->6)- bet a-D-glucopyranosyl oleanolic acid 28-O-beta-D-xylopyranosyl-(1-->3)-beta-D-xylopyranosyl-(1-->4)-alpha- L-rhamnopyranosyl-(1-->2)-[(6S,2E)-6-hydroxy-2,6-dimethyl-2, 7-octadienoyl-(1-->6)]-beta-D-glucopyranosyl ester (1); 3-O-beta-D-xylopyranosyl-(1-->2)-alpha-L-arabinopyranosyl-(1-->6)- bet a-D-glucopyranosyl oleanolic acid 28-O-beta-D-xylopyranosyl-(1-->3)-beta-D-xylopyranosyl-(1-->4)-alpha- L-rhamnopyranosyl-(1-->2)-[(2E)-2-hydroxylmethyl-6-hydroxy-6-methy l-2 ,7-octadienoyl-(1-->6)]-beta-D-glucopyranosyl ester (2); 3-O-beta-D-xylopyranosyl-(1-->2)-alpha-L-arabinopyranosyl-(1-->6)- bet a-D-glucopyranosyl echinocystic acid 28-O-beta-D-xylopyranosyl-(1-->3)-beta-D-xylopyranosyl-(1-->4)-[beta- D-galactopyranosyl-(1-->2)]-alpha-L-rhamnopyranosyl-(1-->2)-[(2E)-2-h ydroxylmethyl-6-hydroxy-6-methyl-2, 7-octadienoyl-(1-->6)]-beta-D-glucopyranosyl ester (3); and 3-O-beta-D-xylopyranosyl-(1-->2)-alpha-L-arabinopyranosyl-(1-->6)- bet a-D-glucopyranosyl echinocystic acid 28-O-beta-D-xylopyranosyl-(1-->3)-beta-D-xylopyranosyl-(1-->4)-[beta- D-galactopyranosyl-(1-->2)]-alpha-L-rhamnopyranosyl-(1-->2)-[(6S, 2E)-6-hydroxy-2,6-dimethyl-2, 7-octadienoyl-(1-->6)]-beta-D-glucopyranosyl ester (4).

Carbohydrate Sequence↗
PubMed1999

Gleditsiosides N-Q, new triterpenoid saponins from Gleditsia sinensis.

The structures of gleditsiosides N, O, P, and Q (1-4), isolated from anomalous fruits of Gleditsia sinensis, were characterized as novel complex bisdesmosidic triterpenoid glycosides acylated with monoterpenoid units, by means of extensive 1D and 2D NMR studies. The four compounds shared a common structural feature with a trisaccharide [(beta-D-xylopyranosyl-(1-->2)-alpha-L-arabinopyranosyl-(1-->6)-be ta- D-glucopyranoside)] affixed to C-3 and a tetrasaccharide [(beta-D-xylopyranosyl-(1-->3)-beta-D-xylopyranosyl-(1-->4)-alpha-L-r hamnopyranosyl-(1-->2)-beta-D-glucopyranosyl ester)] attached to C-28. Gleditsioside P (3) is the first saponin of this type found to date bearing three monoterpenoid units.

Carbohydrate Sequence↗
PubMed1999

Inhibition of GABA-gated chloride channels by 12,14-dichlorodehydroabietic acid in mammalian brain.

1. 12,14-dichlorodehydroabietic acid (12,14-Cl2DHA) reduced GABA-stimulated uptake of 36Cl- into mouse brain synaptoneurosomes suggesting inhibition of mammalian GABA(A) receptor function. 2. 12,14-Cl2DHA did not affect the binding of [3H]-muscimol to brain membranes but displaced specifically bound [3H]-EBOB. The inhibitory effect on [3H]-EBOB binding was not reversible. 12,14-Cl2DHA reduced the availability of [3H]-EBOB binding sites (Bmax) without changing the KD of the radioligand for remaining sites. 12,14-Cl2DHA did not affect the rate of association of [3H]-EBOB with its chloride channel receptor, but increased the initial rate of [3H]-EBOB dissociation. 3. 12,14-Cl2DHA enhanced the incidence of EPSCs when rapidly applied to cultured rat cortical neurones. Longer exposures produced block of IPSCs with marked increases in the frequency of EPSCs and min EPSCs. 12,14-Cl2DHA also irreversibly suppressed chloride currents evoked by pulses of exogenous GABA in these cells. 4. Ultimately, 12,14-Cl2DHA inhibited all synaptic traffic and action currents in current clamped cells indicating that, in contrast to picrotoxinin (which causes paroxysmal bursting), it is not fully selective for the GABA(A) receptor-chloride channel complex. 5. The depolarizing block seen with 12,14-Cl2DHA in amphotericin-perforated preparations implicates loss of Ca2+ buffering in the polarity change and this may account for inhibition of spontaneous action potentials. 6. Our investigation demonstrates that 12,14-Cl2DHA blocks GABA-dependent chloride entry in mammalian brain and operates as a non-competitive insurmountable GABA(A) antagonist. The mechanism likely involves either irreversible binding of 12,14-Cl2DHA to the trioxabicyclooctane recognition site or a site that is allosterically coupled to it. We cannot exclude, however, the possibility that 12,14-Cl2DHA causes localized proteolysis or more extensive conformational change within a critical subunit of the chloride channel.

Abietanes↗
PubMed1999

HIV-associated dementia: new insights into disease pathogenesis and therapeutic interventions.

Remarkable progress was made in recent years in the therapeutics of HIV-1-associated dementia (HAD) and in unraveling the complex pathophysiology that follows viral invasion of the central nervous system (CNS). Viral replication in and outside of the CNS was significantly reduced in HIV-1 infected subjects by new potent antiretroviral therapies. This has resulted in partial repair of cellular immune function with improvement in, and the prevention of, neurologic deficits associated with progressive HIV-1 disease. In regard to HAD pathophysiology, it is now known that CNS damage induced by HIV-1 infection occurs indirectly. Neuronal loss is mediated through immune activation and viral infection of mononuclear phagocytes (MPs) (brain macrophages and microglia). Cellular and viral factors secreted by brain MPs produce, over time, neuronal damage and drop out. Viral growth in the brain appears necessary, but not sufficient, to produce cognitive and motor impairments in affected individuals. Indeed, the best predictor for neurologic impairment following HIV-1 infection is the absolute number of immune-competent macrophages; not the level of viral production in affected brain tissue. As yet, an understanding of macrophage-related neurodegeneration has not translated into significant improvements in the treatment of this devastating complication of HIV disease. Nonetheless, adjunctive antiinflammatory and neuroprotective therapies are being developed. New ideas regarding HAD neuropathogenesis, and implications for the diagnosis and treatment of HAD are summarized in this article.

AIDS Dementia Complex↗
PubMed1999

The neuropathogenesis of HIV-1 infection.

HIV encephalitis is the common pathologic correlate of HIV-dementia (HAD). HIV-infected brain mononuclear phagocytes (MP) (macrophages and microglia) are reservoirs for persistent viral infection. When activated, MP contribute to neuronal damage. Such activated and virus-infected macrophages secrete cellular and viral factors, triggering neural destructive immune responses. Our Center's laboratories have begun to decipher the molecular and biochemical pathways for MP-mediated neuronal damage in HAD. This review will discuss the salient clinical and pathological features of HAD and highlight the recent advances made, by our scientists and elsewhere, in unraveling disease mechanisms, including the role of chemokines and their receptors in the neuropathogenesis of HIV-1 encephalitis.

AIDS Dementia Complex↗
PubMed1999

Lymphotropic virions affect chemokine receptor-mediated neural signaling and apoptosis: implications for human immunodeficiency virus type 1-associated dementia.

Chemokine receptors pivotal for human immunodeficiency virus type 1 (HIV-1) infection in lymphocytes and macrophages (CCR3, CCR5, and CXCR4) are expressed on neural cells (microglia, astrocytes, and/or neurons). It is these cells which are damaged during progressive HIV-1 infection of the central nervous system. We theorize that viral coreceptors could effect neural cell damage during HIV-1-associated dementia (HAD) without simultaneously affecting viral replication. To these ends, we studied the ability of diverse viral strains to affect intracellular signaling and apoptosis of neurons, astrocytes, and monocyte-derived macrophages. Inhibition of cyclic AMP, activation of inositol 1,4,5-trisphosphate, and apoptosis were induced by diverse HIV-1 strains, principally in neurons. Virions from T-cell-tropic (T-tropic) strains (MN, IIIB, and Lai) produced the most significant alterations in signaling of neurons and astrocytes. The HIV-1 envelope glycoprotein, gp120, induced markedly less neural damage than purified virions. Macrophage-tropic (M-tropic) strains (ADA, JR-FL, Bal, MS-CSF, and DJV) produced the least neural damage, while 89.6, a dual-tropic HIV-1 strain, elicited intermediate neural cell damage. All T-tropic strain-mediated neuronal impairments were blocked by the CXCR4 antibody, 12G5. In contrast, the M-tropic strains were only partially blocked by 12G5. CXCR4-mediated neuronal apoptosis was confirmed in pure populations of rat cerebellar granule neurons and was blocked by HA1004, an inhibitor of calcium/calmodulin-dependent protein kinase II, protein kinase A, and protein kinase C. Taken together, these results suggest that progeny HIV-1 virions can influence neuronal signal transduction and apoptosis. This process occurs, in part, through CXCR4 and is independent of CD4 binding. T-tropic viruses that traffic in and out of the brain during progressive HIV-1 disease may play an important role in HAD neuropathogenesis.

AIDS Dementia Complex↗
PubMed1999

Basic FGF decreases clearance receptor of natriuretic peptides in fetoplacental artery endothelium.

Atrial natriuretic peptide (ANP) is present in the fetoplacental circulation of humans and sheep. The ANP-A receptor is the specific membrane receptor for ANP, which produces cGMP. The clearance receptor of natriuretic peptide (CR) is postulated to modulate local concentrations of ANP, thereby modulating cGMP production through the ANP-A receptor. Recently we reported that fetoplacental basic fibroblast growth factor (bFGF) and cGMP levels are increased dramatically during the third trimester of ovine gestation. Therefore we hypothesized that bFGF will downregulate CR expression in cultured ovine fetoplacental artery endothelial (OFPAE) cells via the mitogen-activated protein kinase (MAPK) signal cascade mechanism, thereby causing augmentation of ANP-mediated cGMP production. Western analysis and/or RT-PCR of CR expression were performed after treatment of OFPAE cells with bFGF (10 pg/ml-1 microgram/ml) with or without 50 microM PD-98059, a selective inhibitor of MAPK kinase. To investigate the possible effects of CR downregulation on the functional modulation of ANP-A receptor activation, cGMP production (20 min) by OFPAE cells was measured in response to ANP (10 pM-1 microM) with or without pretreatment (24 h) of 10 ng/ml bFGF. CR expression in OFPAE cells was dose dependently downregulated by 1-10 ng/ml bFGF treatment (maximum -69%), which was completely reversed by pretreatment with PD-98059. Treatment of OFPAE cells with 10 ng/ml bFGF (24 h) did not alter maximum ANP-A activity (cGMP production/20 min), but decreased the apparent ED(50) of ANP to stimulate cGMP production from 2.5 to 0.83 nM, suggesting the possibility that bFGF-mediated downregulation of CR may elevate ANP-mediated cGMP production responses. Thus bFGF downregulates CR mRNA and protein expressions via the MAPK cascade in OFPAE cells.

Animals↗
PubMed1999

Electrophysiological recordings in pallidotomy localized to 3D stereoscopic imaging.

A quantitative on-line analysis of electrical activity in the pallidum of Parkinsonian patients has been developed to determine the focal point of lesioning. A 3D volume image system has been developed to display basal ganglia anatomy and coregister the electrophysiological data within the globus pallidus. Thirty patients undergoing 41 pallidotomies are presented. Neuronal activity from the pallidum is recorded using a semi-microelectrode. Based on this activity, lesioning is performed. Postlesion recordings are made to determine the necessity of additional lesioning. A stereoscopic 3D volume MR image system has been developed that along with on-line signal processing allows visualization of high neural activity in the pallidum and postlesion residual activity.

Action Potentials↗
PubMed1999

Activation of the mitogen-activated protein kinase cascade is necessary but not sufficient for basic fibroblast growth factor- and epidermal growth factor-stimulated expression of endothelial nitric oxide synthase in ovine fetoplacental artery endothelial cells.

Basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) may play important roles in the placental vasculature, not only by controlling cell growth and differentiation, but also by mediating production of local vasodilators such as nitric oxide. As the mitogen-activated protein kinase (MAPK) signal cascade has been widely associated with cell growth in response to growth factors, herein we investigate whether bFGF, EGF, and VEGF also stimulate expression of endothelial nitric oxide synthase (eNOS) via activation of the MAPK cascade in ovine fetoplacental artery endothelial cells. The presence of the receptors for all three growth factors was confirmed by both immunocytochemistry and a functional cell proliferation assay. All three growth factors at 10 ng/ml rapidly (<10 min) activated MAPK. This activation was inhibited by PD 98059, a specific MAPK kinase inhibitor. bFGF and EGF, but not VEGF, dose- and time-dependently increased eNOS protein levels. Maximal stimulatory effects of bFGF and EGF on eNOS protein expression were observed at 10 ng/ml for 24 h of treatment and were associated with elevated eNOS messenger RNA. PD 98059 also significantly inhibited bFGF- and EGF-induced increases in eNOS protein expression. Because treatment with all three growth factors resulted in activation of the MAPK cascade, while bFGF and EGF, but not VEGF, increased eNOS expression, we conclude that activation of the MAPK cascade is necessary, but not sufficient, for bFGF- and EGF-induced increases in eNOS protein expression in ovine fetoplacental artery endothelial cells. Thus, additional signaling pathways are implicated in the different controls of eNOS expression and mitogenesis by growth factors.

Animals↗
PubMed1999

New saponins from the seeds of Aesculus chinensis.

Eight new acylated polyhydroxyoleanene triterpenoidal saponins, aesculiosides A-H (1-8), along with four known ones, have been isolated from the seeds of Aesculus chinensis. On the basis of extensive NMR studies, the structures of the new compounds were determined to be 21-O-tigloylprotoaescigenin 3-O-[beta-D-glucopyranosyl-(1-->2)][beta-D-glucopyranosyl-(1-->4)]- beta-D-glucuronopyranosyl acid (1), 21-O-angeloylprotoaescigenin 3-O-[beta-D-glucopyranosyl- (1-->2)][beta-D-glucopyranosyl-(1-->4)]-beta-D-glucuronopyranosyl acid (2), 21,22-O-ditigloylprotoaescigenin 3-O-[beta-D-glucopyranosyl-(1-->2)][beta-d-glucopyranosyl- (1-->4)]-beta-D-glucuronopyranosyl acid (3), 21-O-tigloyl-22-O-angeloylprotoaescigenin 3-O-[beta-D-glucopyranosyl- (1-->2)][beta-D-glucopyranosyl-(1-->4)]-beta-D-glucuronopyranosyl acid (4), 21,22-O-ditigloylprotoaescigenin 3-O-[beta-D-glucopyranosyl- (1-->2)][beta-D-glucopyranosyl-(1-->4)]-methyl beta-d-glucuronopyranosate (5), 21-O-tigloyl-22-O-angeloylprotoaescigenin 3-O-[beta-D-glucopyranosyl-(1-->2)-[beta-D-glucopyranosyl-(1-->4)]-methy l beta-D-glucuronopyranosate (6), 21-O-tigloyl-28-O-acetylprotoaescigenin 3-O-[beta-D-glucopyranosyl-(1-->2)][beta-D-glucopyranosyl-(1-->4)]-methy l beta-D-glucuronopyranosate (7) and 21-O-angeloyl-28-O-acetylprotoaescigenin 3-O-[beta-D-glucopyranosyl-(1-->2)][beta-D-glucopyranosyl-(1-->4)]-methy l beta-D-glucuronopyranosate (8).

Carbohydrate Conformation↗
PubMed1999

Triterpenoidal saponins acylated with two monoterpenic acids from Gleditsia sinensis.

The isolation and characterization of three new oleanane-type triterpenoidal saponins, called gleditsiosides E-G, along with two known ones, from the anomalous fruits of Gleditsia sinensis LAM. are described. Their structural details were unambiguously determined by using a combination of modern NMR techniques, including distortionless enhancement by polarization transfer (DEPT), double-quantum filtered 1H-1H correlated spectroscopy (DQF-COSY), homonuclear hartmann-hahn (HOHAHA), 1H-13C heteronuclear correlation (HET-COR), heteronuclear multiple-bond connectivity (HMBC) and rotating-frame overhauser enhancement spectroscopy (ROESY) experiments as well as some chemical methods. The five bisdesmosidic triterpenoidal saponins consisting of the same sugar sequence were all acylated with two different or identical monoterpenic acids to the C-2 and C-3 positions of rhamnose moiety.

Carbohydrate Sequence↗
PubMed1999

Three-dimensional gadolinium-enhanced coronary magnetic resonance angiography: initial experience.

We present our initial experience on first-pass gadolinium-enhanced coronary artery magnetic resonance angiography (MRA). Three-dimensional segmented gradient-echo sequences were developed to image coronary arteries within a single breathhold during the injection of a double-dose contrast agent. Comparisons were made between a short TR of 2.7-msec (n = 5) and a long TR of 5.0-msec (n = 3) sequences in terms of the signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR). An in-plane resolution of roughly 1 x 1 mm2 was achieved. Dramatic vascular signal enhancement by a factor of 3-5 was obtained in volunteers following the contrast agent injection, allowing for clear visualization of proximal coronary arteries. The longer TR scans generally performed better in terms of SNR and CNR improvement (approximately 50%) but allowed for less coverage. These preliminary results suggest that gadolinium-enhanced MRA is a useful tool to study proximal coronary arteries with breathhold, but for a larger coverage, a multiple dose approach may be necessary.

Adult↗
PubMed1999

Soluble HIV-1 infected macrophage secretory products mediate blockade of long-term potentiation: a mechanism for cognitive dysfunction in HIV-1-associated dementia.

It is generally accepted that viral and cellular products from immune competent mononuclear phagocytes (MP) (brain macrophages and microglia) underlie the neuropathogenesis of HIV-1-associated dementia (HAD). What remains unanswered, however, is the composition of and mechanisms for such MP-induced neurological dysfunctions. In attempts to address these issues culture fluids from HIV-1ADA-infected monocyte-derived macrophages (MDMs) (depleted or enriched with progeny virus) were placed onto the CA1 area of rat hippocampal brain slices (the site of mammalian learning and memory) and neuronal long-term potentiation (LTP) assayed. LTP was induced by high frequency stimulation (HFS). Lipopolysaccharide (LPS) served as a surrogate macrophage activator. Synaptic strength was assayed by the initial slope of evoked field excitatory postsynaptic potentials (EPSPs). Synaptic potentiation following HFS was observed in slices incubated with uninfected (control) MDM culture fluids. The magnitude of the LTP response was 150.2 +/- 21.10% compared to basal levels (n=6). Synaptic strength was enhanced in virus-infected (135.7+/-28.9%, n=8) and LPS-activated MDM (123.3+/-5.1%, n=7) but at lower levels than controls. The lowest levels of LTP were in brain slices incubated with virus-infected and LPS-activated MDM fluids at (109.5+/-9.9% n=12). Interestingly, bath application of progeny HIV-1 virions showed minimal LTP effects. Virus-infected, LPS-activated MDM fluids, with progenyvirus, reduced synaptic strength but were not statistically different than replicate culture fluids depleted of virus. In contrast, IL-1beta and quinolinic acid, significantly diminished synaptic strength. These results, taken together, suggest that soluble HIV-1-infected MDM secretory products, but not virus per se, significantly affect LTP. This electrophysiological system, which monitors neuronal function following cell exposure to HIV-1 infected materials could provide a novel testing ground for therapeutics designed to protect brain function in HAD.

AIDS Dementia Complex↗
PubMed1999

Coronary MR angiography.

Coronary MR angiography has developed rapidly over the past several years. Not only is research being performed at academic centers but industry is also investing in dedicated contrast agents and cardiac MR imaging platforms. Although current coronary MR angiography has limited clinical utility, its place within the assessment of ischemic cardiac disease is evolving. The technology currently under investigation holds much promise, especially when one considers that MR has the potential to provide information currently supplied by the performance of a number of screening tests. It would be far more cost-effective to perform a single MR examination than to perform a stress echo, rest-stress nuclear medicine examination and a conventional coronary angiogram. In addition, clinicians need information about coronary flow and myocardial perfusion. Although some of this information can be currently obtained with an intravascular Doppler flow wire or by positron emission tomography, MR angiography offers the advantages of being both noninvasive and more easily accessible in comparison to either method. The combined information promised by a comprehensive cardiac MR examination that includes coronary MR angiography as a component is an exciting prospect.

Contrast Media↗
PubMed1999

Effect of aerobic training on orthostatic tolerance, circulatory response, and heart rate dynamics.

BACKGROUND: This study was performed to investigate the effects of aerobic training on orthostatic tolerance and to quantify the post-training changes in cardiovascular response and heart rate variability (HRV). METHODS: Tolerance and circulatory responses to two types of lower body negative pressure (LBNP) were examined and compared in a group of healthy male students before and after 6 mo of aerobic training, and the results were further compared with a group of athletes (runners). Changes in HRV associated with training were analyzed by conventional and time-varying autoregressive spectral analysis, as well as by approximate entropy measurement (ApEn)--a statistic quantifying heart rate "complexity" derived from non-linear dynamics. RESULTS: After aerobic training, there was an initial transient hypotension during the supine -50 mmHg LBNP testing and a significant decrease in tolerance to upright graded LBNP in most of the student-subjects. Moreover, after training, there was a significant decrease in ApEn value of the HRV time series during both supine control and LBNP testing, and the rate of cardiac vagal withdrawal and sympathetic activation during the onset of LBNP was faster than that before training. CONCLUSIONS: The present study has provided further evidence that certain types of aerobic training may affect orthostatic tolerance and may be associated with a loss of complexity of HRV during supine resting and orthostatic stress.

Adaptation, Physiological↗
PubMed1999

Lack of human papillomavirus types 16 and 18 DNA in esophageal squamous carcinoma cell lines.

OBJECTIVE: To assess the role of human papillomavirus (HPV) in the carcinogenesis of the esophageal carcinomas in a high-incidence geographical area in Northern China. METHODS: The presence of HPV types 16 and 18 DNA in the three esophageal carcinoma cell lines was examined by type-specific polymerase chain reaction (PCR). RESULTS: No HPV type 16 and 18 DNA was found in any of the three esophageal carcinoma cell lines. CONCLUSION: The results suggest that the role of HPV in human esophageal carcinogenesis in a high-incidence geographical area remains to be elucidated.

Adult↗