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Biomedical subjects

C Huang

Publications and source records attributed to C Huang.

At least 163 records · Page 9Linked to original sources
PubMed2000

Lactose (mal)digestion evaluated by the 13C-lactose digestion test.

BACKGROUND: The prevalence of genetically determined lactase nonpersistence is based on the results of the lactose H2 breath test. This test, however, is an indirect test, which might lead to misinterpretation. DESIGN: We determined lactase activity in healthy Chinese and Dutch students using a novel 13C-lactose digestion test. The cut-off value of this test was established in a Chinese population with a homogenous genetic background of lactase nonpersistence and was compared with the results obtained in a Caucasian population. Twenty-five grams of a 13C-lactose solution was consumed by 12 known H2-positive and 5 H2-negative Chinese students and 48 Dutch students and, subsequently, 13C-glucose concentration in plasma and H2 excretion in breath were measured. RESULTS: A similar 13C-glucose response curve was found in all Chinese students. The mean response curve in the Dutch students was more pronounced (P < 0.01). The 1 h (peak) plasma 13C-glucose concentration was the best discriminator between lactose digesting and maldigesting subjects. The cut-off level of 2 mmol L-1 13C-glucose in plasma was defined in the H2-positive Chinese students group. Based on the 13C-glucose response the prevalence of lactose maldigestion in the Dutch subjects was 25%; based on the lactose H2 breath test 17%. CONCLUSIONS: Using the 13C-lactose digestion test the results demonstrate a higher prevalence of lactose maldigestion in a Caucasian population than indicated by the results of the H2 breath test. A moderate increase in the plasma 13C-glucose concentration after consumption of 13C-lactose in the young adult Chinese subjects indicates a residual lactase activity in that age group, even when a positive H2 breath test result is obtained. These results indicate that the 13C-glucose concentration in plasma more accurately reflects the small intestinal lactose digestion capacity than the lactose H2 breath test.

Adult↗
PubMed2000

Role of brain angiotensin II in the somatosensory induced antinatriuresis in the anaesthetized rat.

1. The present study set out to explore the importance of angiotensin (Ang)II in the brain in allowing the somatosensory system to cause a reflex renal nerve-mediated reduction in renal sodium and water excretion. 2. In chloralose-urethane-anaesthetized rats receiving saline i.c.v. (2 microL + 1 microL/h), the administration of capsaicin (0.5 mg, s.c.) increased blood pressure by 14% (P < 0.001) and, while renal perfusion pressure was regulated at an unchanged level, neither renal blood flow (RBF) nor glomerular filtration rate was changed. However, urine flow and absolute and fractional sodium excretion was reduced between 29 and 38% (P<0.05-0.01). All variables had returned to control levels 30 min later. 3. The administration of captopril (40 microg + 20 microg/h i.c.v.) decreased blood pressure and sodium excretion by 6 and 17%, respectively (both P < 0.05). Under these conditions, capsaicin s.c. increased blood pressure by 9% (P<0.05); however, with renal perfusion pressure regulated at a constant level, neither renal haemodynamics nor water nor sodium excretion were changed. 4. A final group of animals received AngII (100 ng + 50 ng/h) concomitantly with captopril i.c.v., which increased blood pressure, RBF and urine flow, absolute and fractional sodium excretions by 8 (P < 0.05), 22 (P < 0.001 ) and 52-149% (P < 0.05-0.01), respectively. Capsaicin given s.c. under these conditions increased blood pressure by 6% (P < 0.05) and, while renal perfusion pressure was maintained at an unchanged value and renal haemodynamics remained constant, urine flow and absolute and fractional sodium excretion were reduced by 35-38% (all P < 0.05). 5. These data show that for the somatosensory system to induce a reflex increase in renal sympathetic nerve activity sufficient to cause an antinatriuresis and antidiuresis, the presence of AngII is necessary in the brain. How AngII exerts this facilitatory action within the central nervous system remains to be investigated.

Anesthesia↗
PubMed2000

Stimulation of macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, and RANTES by Candida albicans and Cryptococcus neoformans in peripheral blood mononuclear cells from persons with and without human immunodeficiency virus infection.

The beta-chemokine macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES are critical for recruitment of inflammatory cells into infected tissue. Moreover, by binding to the human immunodeficiency virus (HIV) coreceptor CCR5, release of these chemokines could influence the course of HIV infection. beta-chemokine gene expression and release was determined by ELISA and RNase protection assay, respectively, in peripheral blood mononuclear cells (PBMC) from HIV-negative and -positive persons stimulated with Candida albicans and Cryptococcus neoformans, 2 fungi common in HIV-infected persons. Gene expression and/or release of all 3 chemokines was seen in response to both fungi although C. albicans was more potent than C. neoformans. Fungal stimulated chemokine production by HIV-positive PBMC was similar to that in HIV-negative PBMC, suggesting that the scant inflammatory response often seen in AIDS patients with cryptococcosis and candidiasis is not secondary to suboptimal beta-chemokine release.

AIDS-Related Opportunistic Infections↗
PubMed2000

The bioavailability of beta-carotene in stir- or deep-fried vegetables in men determined by measuring the serum response to a single ingestion.

To evaluate the bioavailability of beta-carotene from plant foods, the serum beta-carotene response to a single ingestion of various beta-carotene sources was determined in 10 healthy men. Tested beta-carotene sources included stir-fried shredded carrot, stir-fried water convolvulus leaves, deep-fried sweet potato ball, purified beta-carotene in a capsule (beadlets) and beadlets with beta-carotene free oriental radish (beadlets + radish). The maximal change in serum beta-carotene concentration occurred at 24 or 32 h post ingestion. This response to beadlets was significantly higher than that to the other four tested beta-carotene sources (P < 0.05). The maximal serum response to beadlets + radish was also significantly higher than that to the three food beta-carotene sources (P < 0.05). The maximal serum response to sweet potato was significantly higher than that to water convolvulus leaves (P < 0. 05). The bioavailability relative to beta-carotene beadlets was calculated by dividing the maximal change in serum concentration to each test meal of each subject by his own serum maximal change in response to beadlets. Accordingly, the bioavailability was 65% for beadlets + radish, 33% for carrots, 26% for water convolvulus leaves and 37% for sweet potatoes. Concurrent ingestion of oriental radish reduced the bioavailability of beadlets to two-thirds of its original value, which partially accounted for the difference between the bioavailability of beadlets and natural foods. The relative bioavailability of beta-carotene from stir-fried and deep-fried vegetables was about one-third to one-fourth that of the purified beta-carotene beadlets. These bioavailabilities are higher than previously reported values.

Adult↗
PubMed2000

Function and mechanism of zinc metalloenzymes.

Zinc is required for the activity of > 300 enzymes, covering all six classes of enzymes. Zinc binding sites in proteins are often distorted tetrahedral or trigonal bipyramidal geometry, made up of the sulfur of cysteine, the nitrogen of histidine or the oxygen of aspartate and glutamate, or a combination. Zinc in proteins can either participate directly in chemical catalysis or be important for maintaining protein structure and stability. In all catalytic sites, the zinc ion functions as a Lewis acid. Researchers in our laboratory are dissecting the determinants of molecular recognition and catalysis in the zinc-binding site of carbonic anhydrase. These studies demonstrate that the chemical nature of the direct ligands and the structure of the surrounding hydrogen bond network are crucial for both the activity of carbonic anhydrase and the metal ion affinity of the zinc-binding site. An understanding of naturally occurring zinc-binding sites will aid in creating de novo zinc-binding proteins and in designing new metal sites in existing proteins for novel purposes such as to serve as metal ion biosensors.

Animals↗
PubMed2000

Zinc deficiency up-regulates expression of high-affinity phosphate transporter genes in both phosphate-sufficient and -deficient barley roots.

Phosphate (P) is taken up by plants through high-affinity P transporter proteins embedded in the plasma membrane of certain cell types in plant roots. Expression of the genes that encode these transporters responds to the P status of the plants, and their transcription is normally tightly controlled. However, this tight control of P uptake is lost under Zn deficiency, leading to very high accumulation of P in plants. We examined the effect of plant Zn status on the expression of the genes encoding the HVPT1 and HVPT2 high-affinity P transporters in barley (Hordeum vulgare L. cv Weeah) roots. The results show that the expression of these genes is intimately linked to the Zn status of the plants. Zn deficiency induced the expression of genes encoding these P transporters in plants grown in either P-sufficient or -deficient conditions. Moreover, the role of Zn in the regulation of these genes is specific in that it cannot be replaced by manganese (a divalent cation similar to Zn). It appears that Zn plays a specific role in the signal transduction pathway responsible for the regulation of genes encoding high-affinity P transporters in plant roots. The significance of Zn involvement in the regulation of genes involved in P uptake is discussed.

Carrier Proteins↗
PubMed2000

Involvement of the zinc-binding capacity of Sendai virus V protein in viral pathogenesis.

The V protein of Sendai virus (SeV) is nonessential to virus replication in cell culture but indispensable to viral pathogenicity in mice. The highly conserved cysteine-rich zinc finger-like domain in its carboxyl terminus is believed to be responsible for this viral pathogenicity. In the present study, we showed that the cysteine-rich domain of the SeV V protein could actually bind zinc by using glutathione-S-transferase fusion proteins. When the seven conserved cysteine residues at positions 337, 341, 353, 355, 358, 362, and 365 were replaced individually, the zinc-binding capacities of the mutant proteins were greatly impaired, ranging from 22 to 68% of that of the wild type. We then recovered two mutant SeVs from cDNA, which have V-C(341)S and V-C(365)R mutations and represent maximal and minimal zinc-binding capacities among the corresponding mutant fusion proteins, respectively. The mutant viruses showed viral protein synthesis and growth patterns similar to those of wild-type SeV in cultured cells. However, the mutant viruses were strongly attenuated in mice in a way similar to that of SeV V(DeltaC), which has a truncated V protein lacking the cysteine-rich domain, by exhibiting earlier viral clearance from the mouse lung and less virulence to mice. We therefore conclude that the zinc-binding capacity of the V protein is involved in viral pathogenesis.

Amino Acid Sequence↗
PubMed2000

Transglutaminase-mediated fibronectin multimerization in lung endothelial matrix in response to TNF-alpha.

Exposure of lung endothelial monolayers to tumor necrosis factor (TNF)-alpha causes a rearrangement of the fibrillar fibronectin (FN) extracellular matrix and an increase in protein permeability. Using calf pulmonary artery endothelial cell layers, we determined whether these changes were mediated by FN multimerization due to enhanced transglutaminase activity after TNF-alpha (200 U/ml) for 18 h. Western blot analysis indicated that TNF-alpha decreased the amount of monomeric FN detected under reducing conditions. Analysis of (125)I-FN incorporation into the extracellular matrix confirmed a twofold increase in high molecular mass (HMW) FN multimers stable under reducing conditions (P < 0.05). Enhanced formation of such HMW FN multimers was associated with increased cell surface transglutaminase activity (P < 0.05). Calf pulmonary artery endothelial cells pretreated with TNF-alpha also formed nonreducible HMW multimers of FN when layered on surfaces precoated with FN. Inhibitors of transglutaminase blocked the TNF-alpha-induced formation of nonreducible HMW multimers of FN but did not prevent either disruption of the FN matrix or the increase in monolayer permeability. Thus increased cell surface transglutaminase after TNF-alpha exposure initiates the enhanced formation of nonreducible HMW FN multimers but did not cause either the disruption of the FN matrix or the increase in endothelial monolayer permeability.

Animals↗
PubMed2000

Free radical-mediated transgene inactivation of macrophages by endotoxin.

Endotoxin, the lipopolysaccharide component of gram-negative bacteria, is a common contaminant of plasmid DNA preparations. The present study investigated the effect of endotoxin on gene transfection efficiency and the role of reactive oxygen species (ROS) in this process. Gene transfection studies were performed in various cell types with cytomegalovirus-luciferase as a reporter plasmid and cationic liposome as a transfecting agent. The presence of endotoxin in plasmid DNA preparations severely limited transgene expression in macrophages but had little or no effect in other cell types tested. This decreased transfection was dependent on ROS-mediated cellular toxicity induced by endotoxin. Neutralizing the endotoxin by the addition of polymyxin B effectively increased transfection efficiency and reduced toxicity. Electron spin resonance studies confirmed the formation of ROS in endotoxin-treated cells and their inhibition by free radical scavengers. The ROS scavenger N-t-butyl-alpha-phenylnitrone, the H(2)O(2) scavenger catalase, and the.OH scavenger sodium formate effectively inhibited endotoxin-induced effects, whereas the O(2)(-) scavenger superoxide dismutase had lesser effects. These results indicate that multiple oxidative species are involved in the transfection inactivation process and that.OH formed by H(2)O(2)-dependent, metal-catalyzed Fenton reaction play a major role in this process.

Animals↗
PubMed2000

A functional angiotensin II receptor-GFP fusion protein: evidence for agonist-dependent nuclear translocation.

We constructed an expression vector for a fusion protein [ANG II type 1a receptor-green fluorescent protein (AT(1a)R-GFP)] consisting of enhanced GFP attached to the COOH terminus of the rat AT(1a)R. Chinese hamster ovary (CHO) cells transfected with AT(1a)R-GFP demonstrated specific, high-affinity (125)I-labeled ANG II binding (IC(50) 21 nM). ANG II exposure stimulated sodium-proton exchange and cytoplasmic calcium release to a similar extent in cells transfected with AT(1a)R or AT(1a)R-GFP; these responses were desensitized by prior exposure to ANG II and were sensitive to the AT(1)R blocker losartan. ANG II-driven internalization of AT(1a)R-GFP in transfected CHO cells was demonstrated both by radioligand binding and by laser scanning confocal microscopy. Colocalization of GFP fluorescence with that of the nuclear stain TOTO-3 in confocal images was increased more than twofold after 1 h of ANG II exposure. We conclude that AT(1a)R-GFP exhibits similar pharmacological behavior to that of the native AT(1a)R. Our observations also support previous evidence for the presence of AT(1a)R in the nucleus and suggest that the density of AT(1a)R in the nucleus may be regulated by exposure to its ligand.

Angiotensin II↗
PubMed2000

Extracellular Ca(2+)-sensing receptor is a promiscuous divalent cation sensor that responds to lead.

The extracellular Ca(2+)-sensing receptor (CaR) responds to polycations, including Ca(2+) and neomycin. This receptor is a physiological regulator of systemic Ca(2+) metabolism and may also mediate the toxic effects of hypercalcemia. A number of divalent cations, including Pb(2+), Co(2+), Cd(2+), and Fe(2+), are toxic to the kidney, brain, and other tissues where the CaR is expressed. To determine which divalent cations can activate the CaR, we expressed the human CaR in HEK-293 cells and measured activation of phospholipase A(2) (PLA(2)) and the mitogen-activated protein kinase p42ERK in response to potential agonists for the receptor. HEK-293 cells expressing the nonfunctional mutant CaR R796W served as controls. Extracellular Ca(2+), Ba(2+), Cd(2+), Co(2+), Fe(2+), Gd(3+), Ni(2+), Pb(2+), and neomycin activated the CaR, but Hg(2+) and Fe(3+) did not. We analyzed the kinetics of activation of p42ERK and PLA(2) by the CaR in response to Ca(2+), Co(2+), and Pb(2+). The EC(50) values ranged from approximately 0.1 mM for Pb(2+) to approximately 4.0 mM for Ca(2+). The Hill coefficients were >3, indicating multiple cooperative ligand binding sites or subunits. Submaximal concentrations of Ca(2+) and Pb(2+) were additive for activation of the CaR. The EC(50) for Ca(2+) or Pb(2+) was reduced four- to fivefold by the presence of the other ion. These divalent cations also activated PLA(2) via the CaR in Madin-Darby canine kidney cells that stably express the CaR. We conclude that many divalent cations activate the CaR and that their effects are additive. The facts that the CaR is a promiscuous polycation sensor and that the effects of these ions are additive to activate it suggest that the CaR may contribute to the toxicity of some heavy metals such as Pb(2+), Cd(2+), Co(2+), and Fe(2+) for the kidney and other tissues where it is expressed.

Animals↗
PubMed2000

Inhibition of atypical PKC blocks ultraviolet-induced AP-1 activation by specifically inhibiting ERKs activation.

Since ultraviolet (UV) radiation is a major etiologic factor in the development of human skin cancers, investigating the signal transduction pathways initiated by UV radiation may help with the understanding of the molecular mechanisms of UV-induced carcinogenesis. Our previous studies demonstrated that UV-induced activator protein-1 (AP-1) activation is blocked by dominant negative atypical PKCs (aPKCs). Here we investigated the role of aPKC in UV-induced activation of mitogen activated protein (MAP) kinase family members which are considered to be the mediators of AP-1 activation. We found that UV radiation led to translocation of protein kinase C (PKC) zeta and activation of MAP kinase family members as well as an increase of AP-1-dependent transcription activation at the same dose range. Pretreatment of cells or mouse skin with antisense oligonucleotides of PKCzeta impaired UV-induced activation of AP-1 in JB6 cells as well as in AP-1-luciferase transgenic mice. It also inhibited UV-induced activation of ERKs but not of JNK and p38 kinases in JB6 cells. In contrast, no significant inhibition of AP-1 activation and MAP kinase activation were observed in cells treated with sense oligonucleotides of PKCzeta. Furthermore, overexpression of a dominant negative mutant of PKClambda/iota specifically inhibited activation of extracellular signal-regulated protein kinases (ERKs) but not of c-jun N-terminal kinases (JNKs) nor p38 kinases induced by UV radiation. These results demonstrated that inhibition of aPKC impairs UV-induced AP-1 activation via suppression of ERKs activation but not of JNKs or p38 kinase activation.

Animals↗
PubMed2000

[Effects of extremely low frequency weak magnetic fields on the intracellular free calcium concentration in PC-12 tumor cells].

In this study the effects of the extremely low frequency (ELF) magnetic fields on intracellular Ca2+ concentration ([Ca2+]i) of rat chromaffinoma PC-12 cells were examined by using a digital fluorescence image microscopy system. A 50 Hz, 100 microT sinusoidal ELF magnetic field increased [Ca2+]i to a marked level, whereas a static field or a field of higher frequency (2000 Hz) did not cause a [Ca2+]i increase. The magnetic field-induced [Ca2+]i rise was partly due to an influx of extracellular Ca2+ and partly due to the release of intracellular Ca2+ pool. It seemed likely that the Ca2+ transport ability of the cell membranes was increased by the 50 Hz magnetic field.

Animals↗
PubMed2000

Inhibition of ultraviolet B-induced AP-1 activation by theaflavins from black tea.

Theaflavins are believed to be key active components in black tea for chemoprevention of cancer. However, the molecular mechanisms underlying the inhibitory effects of theaflavins are not clear. With the JB6 mouse epidermal cell line, we investigated the effects of theaflavins on ultraviolet (UV) B radiation-induced activator protein-1 (AP-1)-dependent transcriptional activation and compared them with (-)-epigallocatechin-3-gallate (EGCG), a major green tea polyphenol that has cancer chemopreventative activity. Theaflavins and EGCG inhibited UVB-induced AP-1 activation in a concentration-dependent manner. The inhibitory effects of theaflavins were stronger than those of EGCG. We found that theaflavins significantly inhibited activation of extracellular signal-regulated protein kinases and c-jun NH(2)-terminal kinases. Because the transcription factor AP-1 is important in the process of tumor promotion, the inhibitory effect of these polyphenols on AP-1 activation may further explain the anti-tumor promotion action of these tea constituents. Mol. Carcinog. 28:148-155, 2000.

Animals↗
PubMed2000

Activation of PKC is required for arsenite-induced signal transduction.

Trivalent arsenic (arsenite) is a human carcinogen. However, the molecular mechanism of arsenite-induced carcinogenesis is still not well understood. In this study, we found that arsenite induced translocation of PKCepsilon, PKCdelta, and PKCalpha from cytosol to membranes. Rottlerin, a selective inhibitor for PKCdelta, and safingol, a specific inhibitor for PKCalpha, both markedly inhibited arsenite-induced AP-1 activity. These inhibitory effects by rottlerin and safingol appeared to be dose dependent. Arsenite-induced phosphorylation of Erks was inhibited by rottlerin, while safingol inhibited arsenite-induced phosphorylation of JNKs and p38 kinases. Dominant negative mutant transfectant of PKCepsilon markedly blocked arsenite-induced AP-1 activity and the phosphorylation of Erks, JNKs, and p38 kinases. These data demonstrate that PKCdelta, PKCepsilon, and PKCalpha mediate arsenite-induced AP-1 activation in JB6 cells through different MAP kinase (Erks, JNKs, and p38 kinases) pathways.

Acetophenones↗
PubMed2000

Distribution of a common methylenetetrahydrofolate mutation in six Chinese population groups.

The distribution of the C677T polymorphism was analyzed by the PCR-RFLP technique in the Northeast Han, the Oroqen, the Ewenki, the Daur as well as in Koreans and Mongolians. The results were compared with each other. They revealed that the frequencies of the T allele are quite different (17-47%) among the tested groups and are much higher in Chinese population groups than in others.

Asian People↗
PubMed2000

Analysis of polymorphic mitochondrial DNA in the Han population and three other ethnic groups of northeast China.

By means of the PCR-RFLP technique the polymorphism of a 465 fragment of mtDNA D loop was analyzed in 36 individuals of the Northeast Han, 30 individuals of the Daur, 32 individuals of the Oroqen and 30 individuals of the Ewenki. All these individuals were randomly selected and are healthy. 27 restriction patterns were obtained by assaying the RFLP fragments of the mtDNA D loop. The mean nucleid acid substitute frequencies at each site are the following: Northeast Han = 0.0291, Oroqen = 0.0477, Ewenki = 0.0563, Daur = 0.0541. The genetic relationship between these four populations was analyzed by the UPG cluster analysis.

Asian People↗