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Biomedical subjects

H Hu

Publications and source records attributed to H Hu.

At least 181 records · Page 10Linked to original sources
PubMed1998

[Observation on the infectivity of different densities of Plasmodium vivax to Anopheles sinensis].

AIM: To study the infectivity of different densities of P. vivax to An. sinensis. METHODS: Venous blood samples from 38 volunteers artificially infected with P. vivax of South-Yunnan collected at the time of initial parasitaemia, primary attack and relapse, were used to infect Anopheles sinensis by feeding on parasitaemia blood in vitro. The finding of oocysts in the mid-gut of the mosquito by microscope was taken as criteria of positive infection. RESULTS: P. vivax in the initial parasitaemia did not infect the mosquito. In the cases of primary attack, when the density of parasite was more than 100/microliter blood, the infectivity and intensity rose with the prolongation of the course of the disease and the increase in the density of the parasite. The infectivity of the P. vivax in the relapse cases was higher than in the primary attack cases, the mosquitoes could be infected at a parasite density of 1/microliter blood. The mosquitoes acquired a higher infection rate, a higher positive rate of mosquito mid-gut and a higher oocyst index in the primary attack cases whose parasite density were higher than 1,000/microliter blood and in the relapse cases whose parasite density were higher than 100/microliter blood. CONCLUSION: The P. vivax in the period of clinical attack was one of the most dangerous period of the spread of malaria. The cases of relapse were the more dangerous infective sources in malaria transmission.

Adult↗
PubMed1998

[Selection of ningnanmycin overproduction strains by resistance of self-secondary metabolites].

The S. noursei var. xichangensis FR-5 protoplasts was treated by UV, NTG in sequence, and the mutated strains were selected by use of self-secondary metabolites, the microorganisms were isolated by fermentation after agarblock rational method. The seven strains of microorganisms which were one fold production higher than that of original strain were obtained from 122 mutants. The method should be a simple, high speed selection model of breed Ningnanmycin overproduction strains of microorganisms.

Anti-Bacterial Agents↗
PubMed1998

Isoform-specific inhibition of L-type calcium channels by dihydropyridines is independent of isoform-specific gating properties.

Dihydropyridines (DHPs) block L-type Ca2+ channels more potently at depolarized membrane potentials, consistent with high affinity binding to the inactivated state. Nisoldipine (a DHP antagonist) blocks the smooth muscle channel more potently than the cardiac one, a phenomenon observed not only in native channels but also in expressed channels. We examined whether this tissue specificity was attributable to differences of inactivation in the two channel types. We expressed cardiac or smooth muscle alpha1C subunits in combination with beta2a and alpha2/delta subunits in human embryonic kidney cells, and used 2 mM Ca2+ as the permeant ion. This system thus reproduces the in vivo topology and charge carrier of the channels while facilitating comparison of the two alpha1C splice variants. Both voltage-dependent and isoform-specific sensitivity of 10 nM nisoldipine inhibition of the channel were demonstrated, with the use of -100 mV as the holding potential for fully reprimed channels and -65 mV to populate the inactivated state. Under drug-free conditions, we characterized fast inactivation (1-sec prepulses) and slow inactivation (3 min prepulses) in the two isoforms. Inactivation parameters were not statistically different in the two channel isoforms; if anything, cardiac channels tended to inactivate more than the smooth muscle channels at relevant voltages. Likewise, the voltage-dependent activation was identical in the two isoforms. We thus conclude that the more potent nisoldipine inhibition of smooth muscle versus cardiac L-type Ca2+ channels is not attributable to differences in channel inactivation or activation. Intrinsic, gating-independent DHP receptor binding affinity differences must be invoked to explain the isoform-specific sensitivity of the DHP block.

Animals↗
PubMed1998

Future directions in CT technology.

Progress in helical CT acquisition and processing over the last 5 years has lead to new applications and new requirements. Recent progress to meet these requirements is discussed in this article. The potential of future acquisition developments and their potential to further import application are explored.

Data Display↗
PubMed1998

[Reduction of helical artifact using SmartHelical algorithm].

Stair-step artifact is a serious problem in reconstructed images of multiplanar reformation (MPR), surface rendering and maximum-intensity projection (MIP). We developed a new algorithm, SmartHelical Algorithm (SHA), to reduce helical artifacts. SmartHelical Algorithm reduced helical artifacts significantly with slight worsening of longitudinal resolution. Noise was reduced and SNR was increased. SHA reduced stair-step artifact in reconstructed images of MPR, surface rendering and MIP, and improved image quality.

Adult↗
PubMed1998

Factors influencing malaria endemicity in Yunnan Province, PR China (analysis of spatial pattern by GIS). Geographical Information System.

This study is an initial attempt to apply disease mapping through Geographical Information System (GIS) with multiple regression analysis to determine the nature and extent of factors influencing malaria transmission in Yunnan Province, PR China, particularly in border areas. Secondary county-based data covering the period 1990 to 1996 were collected and analyzed. The malaria situation in Yunnan Province as a whole is influenced mainly by the combined effects of the physical environment, the presence of efficient vector species, and mobile population along international borders with Myanmar, Lao PDR and Vietnam.

China↗
PubMed1997

Age and secular trends in bone lead levels in middle-aged and elderly men: three-year longitudinal follow-up in the Normative Aging Study.

The goal of this study was to examine age and secular trends in bone and blood lead levels of community-exposed men. Bone and blood lead levels were measured twice, with a 3-year interval between measurements, among participants in a longitudinal study of aging. Seventy subjects (mean age = 66 years, age range = 52-83 years) with repeated measurements of bone and blood lead levels were studied. At the first evaluation, geometric mean lead levels in patella, tibia, and blood were 29.1 (standard deviation (SD) 1.8) microg/g, 17.5 (SD 2.0) microg/g, and 6.7 (SD 1.8) microg/dl, respectively. At the second evaluation, these levels were 22.2 (SD 1.8) microg/g, 17.9 (SD 1.7) microg/g, and 5.1 (SD 1.4) microg/dl, respectively. Cross-sectional analysis of each set of measurements indicated that, on average, a 1-year-older individual would have 2.7% and 2.4-3.2% higher levels of lead in patella and tibia, respectively. In contrast to the increasing age trend in cross-sectional analysis, the secular trend over time was decreasing for patella lead levels and stable for tibia lead levels. The authors conclude that in community-exposed middle-aged and elderly men, the biomarkers of exposure to lead are decreasing in patella and blood and unchanging in tibia as of the early 1990s. The increasing age trend in bone lead levels in cross-sectional studies should be carefully interpreted in light of the birth cohort effect.

Aged↗
PubMed1997

Direct analysis of sugar alcohol borate complexes in plant extracts by matrix-assisted laser desorption/ionization fourier transform mass spectrometry.

Matrix-assisted laser desorption/ionization Fourier transform mass spectrometry (MALDI/FTMS), operating in the negative ion mode, is used to directly observe sugar alcohol borate complexes in a number of plant fractions. The method involves virtually no sample workup and, in the case of celery phloem sap, requires only 40 nL of sap to observe the borate complex. The isolation and characterization of such soluble borate complexes is important in understanding the distribution of boron in plants. The results show that the complexes are composed of two mannitol or sorbitol ligands (L) complexed to a single borate center (B). In some cases, the boron is complexed to non-alditol monosaccharides. Sustained off-resonance collision irradiation dissociation of the BL2- complex, where L is a mannitol, gives fragments that confirm the proposed structure. Complexes of larger oligosaccharides have also been successfully observed using MALDI/FTMS. Semiempirical molecular orbital calculations (AM1) of the mannitol BL2- complex show that the most favorable configuration is with carbons 3 and 4 of both mannitol residues complexed to the borate. This allows maximum interaction of the remaining hydroxyls with the borate center.

Borates↗
PubMed1997

Expression of the murine CD21 gene is regulated by promoter and intronic sequences.

Murine CD21 gene products are expressed primarily on the surface of B lymphocytes and follicular dendritic cells. To identify the genetic elements that control the tissue-specific expression of the CD21 gene, we analyzed, via transient transfections, the 5' proximal promoter region of the CD21 gene (1272 bp 5' of the initiating ATG). This region possessed strong promoter activity, but it was not tissue specific, in that T cell expression was equivalent to that of B cells. These data suggested that the anticipated tissue-specific control element(s) lies 3' of the initiating ATG. Analysis of a novel minigene construct that possessed both the 5' promoter region and a large region (9 kb) of the CD21 gene 3' of the initiating ATG demonstrated the expected tissue-specific expression. Further analysis using the luciferase reporter system indicated that such control elements reside in the first intron (5.5 kb in size), which separates the exons encoding the signal sequence and the first extracellular short consensus repeat domain of the mature protein. Further dissection of intron 1 demonstrated that the sequences controlling the tissue-specific expression of the murine CD21 gene are contained in the 5' 1.6-kb region of this intron. This 1.6-kb fragment was fractionated into an 800-bp sequence at the 5' end that showed very significant inhibitory activity in both B and T cells and a 3' 800-bp sequence that demonstrated moderate repression in T cells, but enhancer activity in B cells. These data suggest this region of the CD21 gene possesses a number of functionally distinct sites that positively and negatively regulate CD21 gene transcription.

Animals↗
PubMed1997

Depletion of T lymphocytes with immunotoxin retards the progress of experimental allergic encephalomyelitis in rhesus monkeys.

FN18-CRM9 is an anti-rhesus anti-CD3 immunotoxin that can transiently deplete T cells to 1% of initial values in both the blood and lymph node compartments and can induce long-term tolerance to mismatched renal allografts. We have investigated the ability of this immunotoxin to interdict the course of an experimental rhesus T-cell-driven autoimmune disease, experimental allergic encephalomyelitis (EAE) induced by myelin basic protein. Monkeys showing CSF pleocytosis were then treated with FN18-CRM9 alone or in combination with cranial irradiation (325 or 650 cGy). EAE in nontreated control monkeys progressed rapidly. Paralysis occurred 4-6 days after CSF pleocytosis. Paralysis was either delayed or never occurred in treated monkeys, and histopathology revealed few inflammatory plaques that were notable for their low or absent T cell content. While T cells repopulate in the periphery posttreatment, they do not return to the CNS in large numbers, suggesting that the newly repopulated T cells have lost their previously acquired CNS homing capability. Anti-CD3 immunotoxin may be useful in treating clinical T-cell-driven autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.

Animals↗
PubMed1997

FN18-CRM9 immunotoxin promotes tolerance in primate renal allografts.

BACKGROUND: Transplant tolerance, rather than immunity, may be favored in the setting of a lower mature lymphoid mass in the recipient induced by anti-T cell agents. A novel immunosuppressive agent, FN18-CRM9, known to specifically kill T cells with great potency, was evaluated in a transplant model. METHODS: In order to ablate recipient T cells, the immunotoxin FN18-CRM9 was administered to rhesus monkey recipients of MHC-mismatched renal allografts. Donor lymphocytes were injected intrathymically into some animals. RESULTS: All monkeys with T-cell depletion by immunotoxin had prolonged allograft survival, and tolerance confirmed by skin grafting has been confirmed in five of six long-surviving recipients. CONCLUSIONS: In this clinically relevant model, profound but transient T-cell depletion by a single agent substantially promotes tolerance.

Animals↗
PubMed1997

The reaction pathway of the isomerization of D-xylose catalyzed by the enzyme D-xylose isomerase: a theoretical study.

Different pathways of the metal-induced isomerization of D-xylose to D-xylulose are investigated and compared in detail using energy minimization and molecular dynamics simulation. Two theoretical models are constructed for the reaction: in vacuum and in the enzyme D-xylose isomerase. The vacuum model is constructed based on the X-ray structure of the active site of D-xylose isomerase. It contains the atoms directly involved in the reaction and is studied using a semi-empirical molecular orbital method (PM3). The model in the enzyme includes the effects of the enzyme environment on the reaction using a combined quantum mechanical and molecular mechanical potential. For both models, the structures of the reactants, products, and intermediate complexes along the isomerization pathway are optimized. The effects of the position of the "catalytic Mg2+ ion" on the energies of the reactions are studied. The results indicate: 1) in vacuum, the isomerization reaction is favored when the catalytic metal cation is at site A, which is remote from the substrate; 2) in the enzyme, the catalytic metal cation, starting from site A, moves and stays at site B, which is close to the substrate; analysis of the charge redistribution of the active site during the catalytic process shows that the metal ion acts as a Lewis acid to polarize the substrate and catalyze the hydride shift; these results are consistent with previous experimental observations; and 3) Lys183 plays an important role in the isomerization reaction. The epsilon-NH3+ group of its side chain can provide a proton to the carboxide ion of the substrate to form a hydroxyl group after the hydride shift step. This role of Lys183 has not been suggested before. Based on our calculations, we believe that this is a reasonable mechanism and consistent with site-directed mutation experiments.

Aldose-Ketose Isomerases↗
PubMed1997

Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro.

Autoimmune diseases induced by mercuric chloride are genetically determined, at least one gene being major histocompatibility complex (MHC)-linked. Previously, we showed that in vitro mercury stimulation induced a high proliferative response in lymphocytes from susceptible mice (high-responders) and that the proliferative response could be restored in lymphocytes from low-responders by pretreating the cells with mercury. We also found that the continuous presence of mercury induced IL-2 and IFN-gamma production, while pretreatment with mercury induced IL-4 production. In this study, we showed that anti-MHC class II monoclonal antibodies blocked both the mercury-induced proliferative responses in lymphocytes from high-responders and the restored proliferative responses in low-responders. In addition, anti-MHC class II antibodies also inhibited the mercury-induced IL-2, IFN-gamma and IL-4 cytokine production in vitro. The results demonstrate that MHC class II antigens directly participate in mercury-induced cytokine production and cell activation, and are required at the onset of the initiation.

Animals↗
PubMed1997

Synthesis and protein kinase C inhibitory activities of balanol analogues with modification of 4-hydroxybenzamido moiety.

A series of racemic balanol analogues with modification of the benzamido moiety of balanol have been synthesized and evaluated for their inhibitory activities against human protein kinase C isozymes (PKC-alpha, -beta I, -beta II, -gamma, -delta, -epsilon, and -eta). The structural modification includes replacement of the 4-hydroxyphenyl group with variously substituted phenyl rings, substitution of the amide linkage with a sulfonamide or an ester, and replacement of the 4-hydroxyphenyl substructure with a hydroxyl substituted indole or a hydroxybenzyl group. in general, these analogues were found to be less potent than balanol, but a number of analogues were identified with improved isozyme selectivity. The structure-activity relationship studies of these analogues also indicated that (1) the optimal general PKC inhibition requires a free 4-hydroxyl group in the benzamido portion of the molecule, (2) the amide linkage of the benzamido moiety is important for PKC inhibition, and (3) the conformation associated with the benzamido moiety seems to have a profound effect on PKC inhibition. The requirement of a free 4-hydroxyl group in conjunction with an appropriate conformation of the benzamido moiety for optimal PKC inhibition suggests that the 4-hydroxyphenyl group may be involved in a specific inhibitor-enzyme interaction important for PKC inhibition.

Animals↗
PubMed1997

Mercury-induced renal immune complex deposits in young (NZB x NZW)F1 mice: characterization of antibodies/autoantibodies.

It is well demonstrated that mercury induces a systemic autoimmune disease in susceptible mouse strains. One of the major characteristics of mercury-induced autoimmune disease in mice is the development of renal immune complex deposits. We have previously shown that continual injection of mercury into young autoimmune prone (NZB x NZW)F1 mice induced an increase in antibody/autoantibody production as well as development of early renal immune complex deposits. In the present study, we characterized the isotype, the specificity and the possible pathogenicity of deposited immunoglobulins in the kidneys of mercury-injected (NZB x NZW)F1 hybrids. We found that young (NZB x NZW)F1 mice injected with mercuric chloride (HgCl2) for 6 weeks developed intense antibody formation of all immunoglobulin isotypes (except for IgG2b) as well as high levels of granular deposits of IgM, IgG1, IgG2a and IgG3 antibodies in the renal mesangium. Increased levels of the same antibody isotypes were also found in the kidney eluate of mercury- but not saline-injected mice. The dominant antibody in the kidney eluate of mercury-injected mice was of IgG1 isotype and found to be directed against double-stranded DNA, collagen, cardiolipin, phosphatidylethanolamine, and the hapten trinitrophenol, but not against nucleolar antigens. Further studies demonstrated that mercury-induced renal immune complex deposits in young (NZB x NZW)F1 mice did not lead to a severe kidney injury. Thus, in response to mercury, young (NZB x NZW)F1 mice develop renal immunoglobulin deposits with an isotype and specificity pattern correlating with that seen in the spleen and in the serum.

Age Factors↗
PubMed1997

Thiol compounds inhibit mercury-induced immunological and immunopathological alterations in susceptible mice.

In vitro mercury induces a high proliferative response in splenic lymphocytes and in vivo it induces a systemic autoimmune disease in susceptible mouse strains. This disease is characterized by increased serum levels of IgE and IgG1 antibodies, by the production of anti-nucleolar antibodies and by the formation of renal immune complex deposits. We have previously found that the presence of 2-mercaptoethanol (2-ME) inhibited mercury-induced cell proliferation in vitro. In this study, we tested the effects of four other thiol compounds, namely dithiothreitol (DTT), L-cysteine, meso-2,3-dimercaptosuccinic acid (meso-DMSA) and 2,3-dimercapto-1-propanesulfonic acid, Na salt (DMPS) on mercury-induced immunological changes both in vitro and in vivo. We found that in vitro, the addition of all thiol compounds abrogated mercury-induced cell aggregation and proliferation. In vivo, injection of meso-DMSA and/or DMPS (s.c. or i.p.) immediately following exposure to mercury markedly decreased IgG1 synthesis in spleen cells and serum IgE levels in mercury-susceptible SJL mice. Treatment with DMPS also prevented mercury-induced IgG1 anti-nucleolar antibody synthesis and the development of mesangial IgG1 immune complex deposits in SJL mice.

Animals↗
PubMed1997

Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low-responders and a shift of the interleukin profile.

Mercury can induce autoimmune disease in susceptible mouse strains. We found that in vitro mercuric chloride induced a high proliferative response in spleen lymphocytes from mercury-susceptible SJL mice, but a low response in resistant mice, such as C57BL/6 (H-2b), A/J (H-2a) and CBA (H-2k) mice. However, a high proliferative response was obtained with lymphocytes from all tested low-responder mice by pretreating them in vitro for 1-3 days with mercuric chloride and then wash away the excess mercury. Both CD4+ and CD8+ T cells were activated in the restored response, but CD4+ T cells was the major responding cell population, as in high-responder mice. We also measured the cytokine production at the protein level after mercury stimulation in vitro. We found that in mercury stimulation the different culture conditions resulted in different patterns of cytokine production. The continuous presence of mercury induced interleukin-2 (IL-2) and interferon-gamma, but not IL-4 production in spleen cells from both high- and low-responder mice. In contrast, by pretreating the cells with mercury and then washing, spleen cells from both high and low-responder mice produced IL-4. Our results suggest that spleen cells from both mercury-susceptible and -resistant mice have the potential to respond to mercury in vitro and produce both Th1- and Th2-type cytokines. But the mercury-induced cytokine profile can shift depending on the conditions for activation.

Animals↗