Biomedical subjects

G Cai

Publications and source records attributed to G Cai.

At least 37 records · Page 2Linked to original sources

PubMed2000

Activation of extracellular signal-regulated protein kinases is associated with a sensitized locomotor response to D(2) dopamine receptor stimulation in unilateral 6-hydroxydopamine-lesioned rats.

Evidence indicates that mitogen-activated protein kinase (MAPK) pathways play a crucial role in the neurobiology of the nervous system. In the present study, dopamine receptor-mediated regulation of extracellular signal-regulated kinases (ERKs) was examined in rats in which the nigrostriatal dopaminergic pathway was unilaterally lesioned by 6-hydroxydopamine (6-OHDA). Subcutaneous injections of the D(2) receptor agonist quinpirole significantly increased tyrosine-phosphorylated ERK1/2 in lesioned striatum, whereas the D(1) receptor agonist SKF38393 failed to activate ERKs. Quinpirole-induced phosphorylation of ERK1/2 was seen as early as 3 min and peaked at 15 min after the challenge. In parallel, striatal ERK kinase activity, measured by the in vitro kinase assay, was increased 2.5-fold on the lesioned side after the administration of quinpirole. Immunohistochemical examination of brain sections after quinpirole administration revealed significant increases in ERK1/2 immunostaining in perinuclear and intranuclear areas of striatal neurons. This increase was much more pronounced on the lesioned than the intact side. Furthermore, quinpirole-induced contralateral rotation was decreased by 48.7 and 50.7%, respectively, when the striatal ERK pathway was selectively inhibited by a single intrastriatal injection of the MAPK/ERK kinase inhibitor PD098059 or after a continuous 7 d intrastriatal infusion of ERK1/2 antisense oligodeoxynucleotide. The results demonstrate, for the first time, that the ERK signaling pathway is activated in denervated striatum in response to stimulation of D(2) dopamine receptors and that the resulting imbalance in striatal ERK activity contributes, at least in part, to neuronal plasticity that underlies D(2) dopamine receptor-mediated contralateral rotation in unilateral 6-OHDA denervated rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed2000

A comparison of self-report and clinical diagnostic interviews for depression: diagnostic interview schedule and schedules for clinical assessment in neuropsychiatry in the Baltimore epidemiologic catchment area follow-up.

BACKGROUND: The field of psychiatric epidemiology continues to employ self-report instruments, but the low degree of agreement between diagnoses achieved using these instruments vs. that achieved by psychiatrists in the clinical modality threatens the credibility of the results. METHODS: In the Baltimore Epidemiologic Catchment Area follow-up, 349 individuals who had a Diagnostic Interview Schedule (DIS) interview were blindly examined by psychiatrists using the Schedules for Clinical Assessment in Neuropsychiatry (SCAN). Comparisons were made at the level of diagnosis, syndrome, and DSM-IV symptom group. Indexes of agreement were computed and characteristics of discrepant cases were identified. RESULTS: Agreement on diagnosis of major depressive disorder was only fair (kappa = 0.20), with the DIS missing many cases judged to meet criteria for diagnosis using the SCAN (29% sensitivity). A major source of discrepancy was respondents with false-negative diagnoses who repeatedly failed to report DIS symptoms attributed to life crises or medical conditions. Older age, male sex, and lower impairment were associated with underdetection by the DIS, using logistic regression analysis. In spite of the diagnostic discrepancy, there was substantial correlation in numbers of symptom groups in the 2 modalities (r = 0.49). Agreement was highest (about 55% sensitivity and 90% specificity) when both the SCAN and DIS thresholds were set at the level of depression syndrome instead of diagnosis. CONCLUSIONS: Weak agreement at the level of diagnosis continues to threaten the credibility of estimates of prevalence of specific disorders. A bias toward underreporting, as well as stronger agreement at the level of the depression syndrome and on ordinal measures of depressive symptoms, suggests that associations with risk factors are conservative.

Adolescent↗

PubMed2000

Evaluation of endothelial cell migration with a novel in vitro assay system.

In this study we introduce a novel in vitro 'oil-drop' assay system for the measurement of endothelial cell (EC) migration, based on the original concept of the Teflon fence assay (Pratt et al., 1984; Am. J. Pathol. 117: 349-354). An aliquot of 15-20,000 human umbilical vein EC (HUVEC) is pipetted through a layer of mineral oil. The cells readily attach, spread and migrate on the surface of a matrix-coated tissue culture dish as a confluent circular monolayer. Migration is measured as the net increase in the total area covered at 24 hours. We have used this system to quantify EC migration on matrices composed of a mixture of type I collagen and either von Willebrand factor (vWF) or fibronectin (FN) in the presence or absence of tumor necrosis factor alpha (TNFalpha). Plating efficiency on both vWF/collagen and FN/collagen, measured by counting cells after attachment and spreading, is about 80%. With this method, migration on vWF/collagen was about 6.4 mm(2) and 5.3 mm(2) for TNFalpha-treated and untreated HUVEC, respectively. HUVEC migration on FN/collagen was slightly greater - 6.4 mm(2) and 6.5 mm(2) with and without TNFalpha treatment, respectively. During the 24 hour time period, HUVEC numbers increased 30-40% on vWF/collagen, and 60-80% on FN/collagen, with increased proliferation observed with TNF-alpha treatment. EC proliferation could be completely inhibited by 2 mM hydroxyurea. This assay system has proven useful in our studies to quantify cell migration and proliferation.

Cell Movement↗

PubMed2000

Cholesteryl ester enrichment of plasma low-density lipoproteins in hamsters fed cereal-based diets containing cholesterol.

Male Syrian hamsters were fed 0.02, 0.03, or 0.05% cholesterol to test the hypothesis that moderate cholesterol intake increases the cholesteryl ester content of the plasma low-density lipoproteins (LDL). Dietary cholesterol levels of 0.02%-0.05% were chosen to reflect typical human intakes of cholesterol. Hamsters were fed ad libitum a cereal-based diet (modified NIH-07 open formula) for 15 weeks. Increasing dietary cholesterol from 0.02% to 0.05% resulted in significantly increased plasma LDL and high-density lipoprotein cholesterol concentration, increased liver cholesterol concentration, and increased total aorta cholesterol content. The cholesteryl ester content of plasma LDL was determined as the molar ratio of cholesteryl ester to apolipoprotein B and to surface lipid (i.e., phospholipid + free cholesterol). Increasing dietary cholesterol from 0.02% to 0.05% resulted in significantly increased cholesteryl ester content of LDL particles. Furthermore, cholesteryl ester content of LDL was directly associated with increased total aorta cholesterol, whereas a linear relationship between plasma LDL cholesterol concentration and aorta cholesterol was not observed. Thus, the data suggest that LDL cholesteryl ester content may be an important atherogenic feature of plasma LDL.

Animals↗

PubMed2000

Identification and characterization of a novel microtubule-based motor associated with membranous organelles in tobacco pollen tubes.

Pollen tube growth depends on the differential distribution of organelles and vesicles along the tube. The role of microtubules in organelle movement is uncertain, mainly because information at the molecular level is limited. In an effort to understand the molecular basis of microtubule-based movement, we isolated from tobacco pollen tubes polypeptides that cosediment with microtubules in an ATP-dependent manner. Major polypeptides released from microtubules by ATP (ATP-MAPs) had molecular masses of 90, 80, and 41 kD. Several findings indicate that the 90-kD ATP-MAP is a kinesin-related motor: binding of the polypeptide to microtubules was enhanced by the nonhydrolyzable ATP analog AMP-PNP; the 90-kD polypeptide reacted specifically with a peptide antibody directed against a highly conserved region in the motor domain of the kinesin superfamily; purified 90-kD ATP-MAP induced microtubules to glide in motility assays in vitro; and the 90-kD ATP-MAP cofractionated with microtubule-activated ATPase activity. Immunolocalization studies indicated that the 90-kD ATP-MAP binds to organelles associated with microtubules in the cortical region of the pollen tube. These findings suggest that the 90-kD ATP-MAP is a kinesin-related microtubule motor that moves organelles in the cortex of growing pollen tubes.

Adenosine Triphosphatases↗

PubMed2000

Interleukin-18 (IL-18) enhances innate IL-12-mediated resistance to Toxoplasma gondii.

Innate resistance to Toxoplasma gondii is dependent on the ability of interleukin-12 (IL-12) to stimulate natural killer (NK) cell production of gamma interferon (IFN-gamma). Since IL-18 is a potent enhancer of IL-12-induced production of IFN-gamma by NK cells, SCID mice (which lack an adaptive immune response) were used to assess the role of IL-18 in innate resistance to T. gondii. Administration of anti-IL-18 to SCID mice infected with T. gondii resulted in an early reduction in serum levels of IFN-gamma but did not significantly decrease resistance to this infection. In contrast, administration of exogenous IL-18 to infected SCID mice resulted in increased production of IFN-gamma, reduced parasite burden, and a delay in time to death. The protective effects of IL-18 treatment correlated with increased NK cell numbers and cytotoxic activity at the local site of administration and with elevated levels of inducible nitrous oxide synthose in the spleens of treated mice. In addition, in vivo depletion studies demonstrated that the ability of exogenous IL-18 to enhance resistance to T. gondii was dependent on IL-12, IFN-gamma, and NK cells. Together, these studies demonstrate that although endogenous IL-18 appears to have a limited role in innate resistance to T. gondii, treatment with IL-18 can augment NK cell-mediated immunity to this pathogen.

Animals↗

PubMed2000

The CD40/CD40 ligand interaction is required for resistance to toxoplasmic encephalitis.

Since the CD40/CD40 ligand (CD40L) interaction is involved in the regulation of macrophage production of interleukin 12 (IL-12) and T-cell production of gamma interferon (IFN-gamma), effector cell functions associated with resistance to Toxoplasma gondii, the role of CD40L in immunity to this parasite was assessed. Infection of C57BL/6 mice with T. gondii results in an upregulation of CD40 expression on accessory cell populations at local sites of infection as well as in lymphoid tissues. Splenocytes from C57BL/6 mice infected with T. gondii for 5 days produced high levels of IL-12 and IFN-gamma when stimulated with toxoplasma lysate antigen, and blocking CD40L did not significantly alter the production of IFN-gamma or IL-12 by these cells. Similar results were observed with splenocytes and mononuclear cells isolated from the brains of chronically infected mice. Interestingly, although CD40L(-/-) mice infected with T. gondii produced less IL-12 than wild-type mice, they produced comparable levels of IFN-gamma but succumbed to toxoplasmic encephalitis 4 to 5 weeks after infection. The inability of CD40L(-/-) mice to control parasite replication in the brain correlated with the ability of soluble CD40L, in combination with IFN-gamma, to activate macrophages in vitro to control replication of T. gondii. Together, these results identify an important role for the CD40/CD40L interaction in resistance to T. gondii. However, this interaction may be more important in the control of parasite replication in the brain rather than the generation of protective T-cell responses during toxoplasmosis.

Animals↗

PubMed2000

Comparison of PCR, antigenemia assay, and rapid blood culture for detection and prevention of cytomegalovirus disease after lung transplantation.

The goal of this study was to evaluate serial cytomegalovirus (CMV) blood culture, antigenemia testing, and qualitative and quantitative plasma CMV PCR for their ability to predict CMV disease and thus to direct preemptive therapy after lung transplantation. Forty-one patients provided 414 samples for blood culture, 290 samples for antigenemia testing, and 432 samples for PCR. Seven patients developed 11 episodes of CMV disease. CMV PCR had sensitivity, specificity, and positive predictive and negative predictive values of 79, 99, 84, and 99%, respectively, compared with 48, 99, 85, and 98%, respectively, for antigenemia testing, and 8, 100, 100, and 97%, respectively, for culture. Only quantitative CMV PCR correlated with disease stage: asymptomatic patients had a mean of 1,500 CMV DNA copies/ml, whereas patients who developed CMV disease had 5,087 copies/ml 12 to 4 weeks before symptoms and 32,000 copies/ml at diagnosis. Furthermore, CMV PCR-measured DNA increased 5- to 10-fold immediately preceding symptoms. PCR and antigenemia test values decreased with anti-CMV therapy. CMV DNA (as detected by PCR), but not antigenemia, persisted in patients who later developed recurrent CMV disease. The data indicate that lung transplant recipients will benefit from monitoring of CMV disease by plasma CMV PCR.

Adult↗

PubMed2000

Mechanism of decreased adenosine protection in reperfusion injury of aging rats.

The purpose of this study was to determine whether the protective effects of adenosine on myocardial ischemia-reperfusion injury are altered with age, and if so, to clarify the mechanisms that underlie this change related to nitric oxide (NO) derived from the vascular endothelium. Isolated perfused rat hearts were exposed to 30 min of ischemia and 60 min of reperfusion. In the adult hearts, administration of adenosine (5 micromol/l) stimulated NO release (1. 06 +/- 0.19 nmol. min(-1). g(-1), P < 0.01 vs. vehicle), increased coronary flow, improved cardiac functional recovery (left ventricular developed pressure 79 +/- 3.8 vs. 57 +/- 3.1 mmHg in vehicle, P < 0.001; maximal rate of left ventricular pressure development 2,385 +/- 103 vs. 1,780 +/- 96 in vehicle, P < 0.001), and reduced myocardial creatine kinase loss (95 +/- 3.9 vs. 159 +/- 4.6 U/100 mg protein, P < 0.01). In aged hearts, adenosine-stimulated NO release was markedly reduced (+0.42 +/- 0.12 nmol. min(-1). g(-1) vs. vehicle), and the cardioprotective effects of adenosine were also attenuated. Inhibition of NO production in the adult hearts significantly decreased the cardioprotective effects of adenosine, whereas supplementation of NO in the aged hearts significantly enhanced the cardioprotective effects of adenosine. The results show that the protective effects of adenosine on myocardial ischemia-reperfusion injury are markedly diminished in aged animals, and that the loss in NO release in response to adenosine may be at least partially responsible for this age-related alteration.

Adenosine↗

PubMed2000

[The effect of V-shaped nitinol alloy implantation on acetabular dysplasia: an experimental study].

OBJECTIVE: To observe the effect of V-shaped nitinol alloy implantation into the acetabular roof of puppies with acetabular dysplasia on acetabular dysplasia. METHODS: The puppies with acetabular dysplasia were divided randomly into two groups. Osteotomy was begun about 0.5 cm above the acetabulum, using a curved osteotome this cut must proceed between the medial wall of the ilium and medial wall of the acetabulum. The osteotomy does not have to be carried to the triradiate cartilage. When the osteotomy is completed, the superior aspect of the acetabulum can be hinged downward by curved osteotome. The V-shaped nitinol alloy was wedged securely in the osteotomy site. Roentgenogram was made 4 and 12 weeks after operation in all animals. RESULTS: The inclination of the acetabular roof was redirected and the acetabular index was decreased. Microscopic study showed a marked proliferation of cartilaginous cells of the acetabular cartilage. CONCLUSION: The V-shaped nitinol alloy implantation into the acetabular roof can correct the sloping acetabular roof, increase the coverage on the femoral head, and improve the growth of the acetabulum.

Acetabulum↗

PubMed2000

[The research progress of using electromagnetic technology in treatment of bone diseases].

In these years, the study of the bioeffects of electromagnetic fields (EMFs) has been listed as the national important task in the field of biological physics. Using EMFs to treat bone diseases is associated with electric technology, biology and medicine. Previous medical studies have shown that EMFs can stimulate healing in bone fractures. But the effects are still controversial and the mechanism is not yet clear. Therefore, it is necessary to carry out experiments in vitro at cellular and molecular levels. Research workers have been exploring the effects of EMFs on bone formation and metabolism. The suggestion of using EMFs in the treatment of osteoporosis and other osseous diseases has been put forward.

Animals↗

PubMed2000

[Zero-stress state of renal artery in spontaneously hypertensive rats].

By observing the opening angle of the renal artery, the zero-stress state of the renal artery was studied in spontaneously hypertensive rats (SHR) prior to and posterior to their hypertension, and the role of endogenous angiotensin II (Ang II) and endothelin (ET) on the zero-stress state was studied by giving SHR Losartan(AT1 receptor antagonist of Ang II) and BMS-182874 (an A type receptor antagonist of ET) respectively. The opening angle of the renal artery in SHR with established hypertension was much greater than that in wistar-Kyoto rats(WKY) (114.2 +/- 42.2 vs 70.2 +/- 30.4, P < 0.01). The opening angles of the renal artery in SHR treated with Losartan and BMS-182874 were much smaller than those in control SHR. The opening angles of the renal artery in Losartan-treated and BMS-182874-treated SHR were 65.9 +/- 32.7 and 66.6 +/- 41.54 respectively. The results suggest that non-unequal growth exists in the renal arterial wall in SHR with established hypertension and the residual stress and strain in SHR are greater than those in age-matched WKY. Endogenous Ang II and ET may play a role in the changes of zero-stress state in SHR with hypertension.

Angiotensin II↗

PubMed2000

[Characterization of the Pt/CeO2-ZrO2/Al2O3 catalysts by spectra].

The performance of Pt/Al2O3 catalysts with CeO2-ZrO2 in difference ways was studied by NIR-FT-Raman, BET, H2 chemisorption, XRD. It shows that the dispersion of Pt on Al2O3 is improved with the increasing of dispersion of CeO2-ZrO2 on the surface of Al2O3, owing to the strong interacting between CeO2-ZrO2 and Pt. And adding with salts is priority.

Aluminum Oxide↗

PubMed1999

Identification of amino acid sequence in the hinge region of human vitamin D receptor that transfers a cytosolic protein to the nucleus.

The localization of human vitamin D receptor (VDR) in the absence of its ligand 1,25-dihydroxyvitamin D(3) was investigated using chimera proteins fused to green fluorescent protein (GFP) at either the N or C terminus, and the nuclear localization signal (NLS) was identified. Plasmids carrying the fusion proteins were transiently or stably introduced into COS7 cells, and the subcellular distribution of the fusion proteins was examined. GFP-tagged wild-type VDRs were located predominantly in nuclei but with a significant cytoplasmic presence, while GFP alone was equally distributed throughout the cells. 10(-8) M 1,25-dihydroxyvitamin D(3) promoted the nuclear import of VDR in a few hours. To identify the NLS, we constructed several mutated VDRs fused to GFP. Mutant VDRs that did not bind to DNA were also localized predominantly in nuclei, while the deletion of the hinge region resulted in the loss of preference for nucleus. A short segment of 20 amino acids in the hinge region enabled cytoplasmic GFP-tagged alkaline phosphatase to translocate to nuclei. These results indicate that 1) VDR is located predominantly in nuclei with a significant presence in cytoplasm without the ligand and 2) an NLS consisting of 20 amino acids in the hinge region facilitates the transfer of VDR to the nucleus.

Amino Acid Sequence↗

PubMed1999

Association analysis between dopamine receptor genes and bipolar affective disorder.

We have performed a case-control analysis of dopamine D2-like receptor (DRD2, DRD3 and DRD4) gene polymorphisms in 118 Han Chinese cases with bipolar affective disorder and 196 control subjects, and replication analysis in 157 English cases and 143 control subjects. We found association between a functional DRD2 promoter variant (P = 0.03 by allele) and the DRD2 taq1A polymorphism (P = 0.001 by allele) in Chinese bipolar disorder patients. However, this finding was not replicated in the Caucasian subjects, indicating that the significant association we observed in the Chinese population is a false positive finding. An alternative explanation is that these polymorphisms are risk factors in Chinese but not Caucasian populations, a hypothesis which seems unlikely in view of the similarity of the clinical characteristics of bipolar disorder in the two populations. We also report a novel, rare one-repeat variant of the DRD4 exon 3 VNTR repeat in Chinese populations, which appears to be absent in Caucasians and is not associated with disease.

Adult↗

PubMed1999

IL-10 enhances NK cell proliferation, cytotoxicity and production of IFN-gamma when combined with IL-18.

Previous studies have shown that IL-10 inhibits the accessory cell functions required for production of IFN-gamma by T cells and NK cells. Our results show that although IL-10 did not induce the production of IFN-gamma by NK cells, it did enhance the ability of IL-18 to stimulate NK cell production of IFN-gamma. In addition, IL-10 augmented NK cell proliferation and cytotoxic activity when combined with IL-18. However, IL-10 did not affect the ability of IL-12 to stimulate NK cells to produce IFN-gamma or proliferate, but there was an additive effect with IL-12 to increase NK cell cytotoxic activity. Interestingly, the type I IFN, whose receptors (R) are related to the IL-10R, also enhanced the effects of IL-18 on NK cell production of IFN-gamma and NK cell cytotoxicity. The ability of IL-10 to elevate the production of IFN-gamma appeared to be specific for NK cells since IL-10 had no effect on the production of IFN-gamma by Th1 clones stimulated with IL-18 or IL-12 in the presence of a monoclonal antibody specific for CD3. These latter results correlated with lower mRNA levels for the alpha and beta chains of the IL-10R in Th1 cells than observed in NK cells. Thus, the ability of IL-10 and IL-18 to up-regulate NK cell function, but not Th1 cell activity, appears to be based on expression of the IL-10R.

Adjuvants, Immunologic↗

PubMed1999

A mild variant of Desbuquois dysplasia.

UNLABELLED: On the basis of three newly observed cases (a pair of siblings and a sporadic case) and one previously reported case, we describe the clinical and radiological phenotype of a skeletal dysplasia resembling Desbuquois dysplasia. The skeletal alterations in the present disorder, including generalized osteopenia, mild modification of the vertebral endplates, epiphyseal flattening of the long bones, broad proximal femora with a spur-like projection of the lesser trochanters (a monkey wrench appearance of the proximal femora), and advanced carpal skeletal age, are almost identical to those of Desbuquois dysplasia. However, postnatal growth failure and minor spondylo-articular problems in the present disorder contrast with the conspicuous prenatal growth failure and severe spondylo-articular deformities of Desbuquois dysplasia. Short stature in the present disorder does not reach the degree of Desbuquois dysplasia. Molecular investigation of one patient excluded abnormalities of the diastrophic dysplasia sulphate transporter gene. CONCLUSION: The combination of skeletal alterations identical to those of Desbuquois dysplasia with milder short stature and spondylo-articular problems in the present patients suggests the nosological proposal of "a mild variant of Desbuquois dysplasia".

Abnormalities, Multiple↗

PubMed1999

Biliary cholesterol and bile acid excretion do not increase in hamsters fed cereal-based diets containing cholesterol.

The major compensatory responses to increased cholesterol consumption are decreased cholesterol synthesis and increased cholesterol excretion through the bile either as free cholesterol or bile acids. The objective of this study was to test the hypothesis that biliary cholesterol excretion is increased in hamsters fed low levels of cholesterol reflecting normal human intake. The hypothesis was based on observations that hamsters generally resist changes in bile acid synthesis when fed large amounts of cholesterol; therefore, increased biliary cholesterol excretion represents a potentially significant pathway for elimination of excess cholesterol in this species. Hamsters were fed modified NIH-07 cereal-based diets containing 0.02%, 0.03%, and 0.05% cholesterol (0.04, 0.06, and 0.10 mg cholesterol/kcal, respectively). The primary response to increasing amounts of dietary cholesterol was downregulation of whole-body cholesterol synthesis, reduced from 3.93+/-0.14 micromol x d(-1) x 100 g(-1) body weight in hamsters fed 0.02% cholesterol to 0.52+/-0.14 micromol x d(-1) x 100 g(-1) in the 0.05% cholesterol group. Biliary cholesterol excretion was also slightly reduced in hamsters fed 0.05% cholesterol, whereas bile acid excretion was not altered by dietary cholesterol. Despite a pronounced downregulation of whole-body cholesterol synthesis, liver and plasma cholesterol concentrations increased in hamsters fed 0.05% cholesterol. The data indicate that increased biliary cholesterol excretion is not a major compensatory route of cholesterol excretion in hamsters consuming cholesterol. Furthermore, cholesterol added to the diet at 0.05% appears to be the approximate threshold at which compensatory mechanisms can prevent increases in liver and plasma cholesterol in male Syrian hamsters. Consequently, this species may be an appropriate animal model for "hyperresponding" individuals in the human population.

Animals↗