Biomedical subjects

Wei Chen

Publications and source records attributed to Wei Chen.

At least 235 records · Page 13Linked to original sources

PubMed2005

Inhibition of p38 mitogen-activated protein kinase may decrease intestinal epithelial cell apoptosis and improve intestinal epithelial barrier function after ischemia- reperfusion injury.

AIM: To investigate the role of p38 mitogen-activated protein kinase in rat small intestine after ischemia-reperfusion (I/R) insult and the relationship between activation of p38 MAPK and apoptotic cell death of intestine. METHODS: Ninety Wistar rats were divided randomly into three groups, namely sham-operated group (C), I/R vehicle group (R) and SB203580 pre-treated group (S). In groups R and S, the superior mesenteric artery (SMA) was separated and occluded for 45 min, then released for reperfusion for 0.25, 0.5, 1, 2, 6, 12 and 24 h. In group C, SMA was separated without occlusion. Plasma D-lactate levels were examined and histological changes were observed under a light microscope. The activity of p38 MAPK was determined by Western immunoblotting and apoptotic cells were detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUDP-biotin nick end labeling (TUNEL). RESULTS: Intestinal ischemia followed by reperfusion activated p38 MAPK, and the maximal level of activation (7.3-fold vs sham-operated group) was reached 30 min after I/R. Treatment with SB 203580, a p38 MAPK inhibitor, reduced intestinal apoptosis (26.72+/-3.39% vs 62.50+/-3.08% in I/R vehicle, P<0.01) and decreased plasma D-lactate level (0.78+/-0.15 mmol/L in I/R vehicle vs 0.42+/-0.17 mmol/L in SB-treated group) and improved post-ischemic intestinal histological damage. CONCLUSION: p38 MAPK plays a crucial role in the signal transduction pathway mediating post-ischemic intestinal apoptosis, and inhibition of p38 MAPK may attenuate ischemia-reperfusion injury.

Animals↗

PubMed2005

Proton transfer of NH3-HCl catalyzed by only one molecule.

The proton transfer in NH(3)-HCl by only one molecule of catalyst was studied by using the MP2 method with the large 6-311++G(2d,2p) basis set. The 18 structures are obtained for the smallest units, NH(3)-HCl-A trimers, for which the proton transfer maybe occurred. The final results show that the proton transfers have occurred in the 15 cyclic shape structures for A = H(2)SO(4), H(2)SO(3), HCOOH (a), HF, H(2)O(2), HNO(3), HNO(2) (a), CH(3)OH, HCl, HNC, H(2)O, HNO(2) (b), NH(3), HCOOH (b), and HCHO, and not occurred in another 3 trimer structures for A = HCN, H(2)S, and PH(3). These results show that the proton transfer occurs from HCl to NH(3) when catalyst molecule A (acidic, neutral, or basic) not only as a proton donor strongly donates the proton to the Cl atom but as an acceptor strongly accepts the proton from the NH(3) molecule in the cyclic H-bond structure. In this work, a proton circumfluence model is proposed to explain the mechanism of the proton transfer. We find that, for the trimer, when the sum of two hydrogen bond lengths (R = R(1) + R(2)) is shorter than 5.0 A, molecule A has the ability to catalyze the proton transfer. In addition, we also find that the interaction energy E(int) between NH(3)-HCl and A is nearly related to the extent (R(H1)(-)(Cl)) of proton transfer, that is, the interaction energy E(int) increases with the proton transfer.

Ammonia↗

PubMed2005

Increased oxidative DNA damage, as assessed by urinary 8-hydroxy-2'-deoxyguanosine concentrations, and serum redox status in persons exposed to mercury.

BACKGROUND: Mercury is a ubiquitous and highly toxic environmental pollutant. In this study, we evaluated the relationship between mercury exposure and oxidative stress, serum and urinary mercury concentrations, oxidative DNA damage, and serum redox status in chronically mercury-exposed persons compared with healthy controls. METHODS: We measured urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), which we used as a biomarker of oxidative DNA damage in the mercury-exposed persons, by HPLC with electrochemical detection (ECD). We evaluated antioxidant status by measuring the activities of superoxide dismutase and glutathione peroxidase and the concentrations of total reduced glutathione and protein-bound thiols in serum. RESULTS: The significant increase in 8-OHdG concentrations in urine indicated that mercury-induced oxidative damage to DNA occurred in vivo. Differences in body mercury burden and antioxidant enzyme activities were statistically significant between the mercury-exposed persons and controls. Serum and urinary mercury concentrations in the mercury-exposed persons were more than 40-fold higher than in controls. CONCLUSIONS: Mercury exposure can induce oxidative DNA damage, whereas the antioxidative repair systems can be expected to minimize DNA lesions caused by mercury. Measurement of urinary 8-OHdG could be useful for evaluating in vivo oxidative DNA damage in mercury-exposed populations.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2005

Different G protein-coupled receptor kinases govern G protein and beta-arrestin-mediated signaling of V2 vasopressin receptor.

Signaling through beta-arrestins is a recently appreciated mechanism used by seven-transmembrane receptors. Because G protein-coupled receptor kinase (GRK) phosphorylation of such receptors is generally a prerequisite for beta-arrestin binding, we studied the roles of different GRKs in promoting beta-arrestin-mediated extracellular signal-regulated kinase (ERK) activation by a typical seven-transmembrane receptor, the Gs-coupled V2 vasopressin receptor. Gs- and beta-arrestin-mediated pathways to ERK activation could be distinguished with H89, an inhibitor of protein kinase A, and beta-arrestin 2 small interfering RNA, respectively. The roles of GRK2, -3, -5, and -6 were assessed by suppressing their expression with specific small interfering RNA sequences. By using this approach, we demonstrated that GRK2 and -3 are responsible for most of the agonist-dependent receptor phosphorylation, desensitization, and recruitment of beta-arrestins. In contrast, GRK5 and -6 mediated much less receptor phosphorylation and beta-arrestin recruitment, but yet appeared exclusively to support beta-arrestin 2-mediated ERK activation. GRK2 suppression actually increased beta-arrestin-stimulated ERK activation. These results suggest that beta-arrestin recruited in response to receptor phosphorylation by different GRKs has distinct functional potentials.

Arrestins↗

PubMed2005

Influence of metabolic syndrome on arterial stiffness and its age-related change in young adults: the Bogalusa Heart Study.

Increased arterial stiffness is associated with risk variables of metabolic syndrome in middle-aged and older adults. However, information regarding the influence of the metabolic syndrome on arterial stiffness and its rate of change with age in young adults is limited. These aspects were examined in a sample of 806 asymptomatic, healthy young adults aged 24-44 years from a black-white community. Brachial to ankle pulse wave velocity (baPWV) measured by an oscillometric method was used as an index of arterial stiffness. baPWV increased with the increasing number of metabolic syndrome components, defined by National Cholesterol Education Program Adult Treatment Panel III (1256, 1314, and 1422 cm/s for those with 0, 1-2, and 3-5 components, respectively, P for trend <0.001). Furthermore, the rate of change (slope) of baPWV with age increased as the number of metabolic syndrome components increased (4.1, 10.7, and 18.7 cm/s per year for those with 0, 1-2, and 3-5 components, respectively; P for comparison of slopes <0.001). These findings by showing the deleterious effects of metabolic syndrome on arterial stiffness and its age-related increase in young adults underscore the importance of this syndrome in cardiovascular risk assessment even in a younger population. Further longitudinal studies are needed to confirm the current cross-sectional findings.

Adult↗

PubMed2005

Theoretical investigation of the large nonlinear optical properties of (HCN)n clusters with Li atom.

Two new classes of (HCN)(n)...Li and Li...(HCN)(n) (n = 1, 2, 3) clusters with the electride characteristic are formed in theory by the metal Li atom attaching to the (HCN)(n) (n = 1, 2, 3) clusters. Because of the interaction between the Li atom and the (HCN)(n) part, the 2s valence electron of the Li atom becomes a loosely bound excess electron. Our high-level ab initio calculations show that these new clusters with the excess electron have large first hyperpolarizabilities, for example, beta(0) = -15,258 au for (HCN)...Li and beta(0) = -3401 au for Li...(HCN) at the QCISD/6-311++G(3df,3pd) level (only beta(0) = -2.8 au for HCN monomer(26)). Obviously, the excess electron from the Li atom plays a crucial role in the large first hyperpolarizabilities of these clusters. The beta(0) value of (HCN)(n)...Li (beta(0) > 10(4) au, from sigma --> pi* transition) is larger than that of Li...(HCN)(n) (beta(0) > 10(3) au, from sigma --> sigma* transition) for n = 1, 2, or 3. In addition, two interesting rules have been observed. They are that |beta(0)| decreases with lengthening of the HCN chain for (HCN)(n)...Li clusters and that |beta(0)| increases as n increases for Li...(HCN)(n) clusters. In this paper, we discuss two classes of clusters that are highly similar to the electride structure model, of which the structural characteristics are that alkali metal atoms ionize to form cations and trapped electrons under the action of other polar molecules. Thus, the investigation on the large first hyperpolarizabilities of (HCN)(n)...Li and Li...(HCN)(n) (n = 1, 2, 3) may prompt one to study the unusual nonlinear optical responses of some electrides.

Journal Article↗

PubMed2005

[The effect and mechanism of arsenic trioxide on hepatocellular carcinoma].

OBJECTIVE: To investigate the effect and mechanism of arsenic trioxide on hepatoma cell line BEL-7402 and observe the effect and best administration method of arsenic trioxide on hepatocellular carcinoma patients who were not suitable for operation. METHODS: The cell activity and morphologic changes were studied after being treated with arsenic trioxide in different concentrations. The apoptosis was detected by flow cytometry assay and DNA fragmentation assay. The caspase-3 level of mRNA and protein were detected by reverse transcription polymerase chain reaction (RT-PCR) and fluoro-spectrophotometer. The growth inhibition of implant tumor was observed in nude mice treated with arsenic trioxide in different concentrations. Arsenic trioxide was used in hepatocellular carcinoma patients by intravenous dropping and continuous regional infusion through hepatic artery. RESULTS: The effect of arsenic trioxide on hepatoma cell lines was dependent on the time and concentration obviously. The decrease in cell number was preceded by morphological changes in the treated BEL-7402 cells that were characteristic of apoptosis, including membrane blebbing, shrunken cytoplasm, nuclear condensation and loss of adhesion. Flow cytometry assay showed an arrestment at G(2)/M phase and sub-G(1) cell peak. DNA fragmentation assay showed a marked DNA ladder. The mRNA level of caspase-3 was no change in RT-PCR whereas the protein of caspase-3 was increased after added As(2)O(3) 1 - 36 h. Caspase-3 activity began to increase after 2 h and reached a maximal level after 12 h in a linear fashion. Then, the level of caspase-3 was decreased, but still in a high level. The growth inhibition of implant tumors was obviously in nude mice. The intravenous usage of arsenic trioxide could improve the quality of life with low toxicity in hepatocellular carcinoma patients not suitable for operation. The tumor size decreased in 30 patients and AFP value decreased in 19 patients by continuous regional infusion through hepatic artery. CONCLUSIONS: Arsenic trioxide can obviously inhibit the growth of hepatoma cell line BEL-7402 through inducing hepatoma cell apoptosis. The activation and increase of Caspase-3 is the possible mechanism of apoptosis, and the acting point is in pro-enzyme level. The best result of arsenic trioxide on non-operative patients should be gotten in continuous infusion through hepatic artery.

Adult↗

PubMed2005

Refining the complex rheumatoid arthritis phenotype based on specificity of the HLA-DRB1 shared epitope for antibodies to citrullinated proteins.

OBJECTIVE: The main genetic risk factor for rheumatoid arthritis (RA), the HLA region, has been known for 25 years. Previous research has demonstrated, within the RA population, an association between HLA-DRB1 alleles carrying the shared epitope (SE) and antibodies directed against cyclic citrullinated peptides (anti-CCP antibodies). We undertook this study to make the first comparison of SE allele frequencies in the healthy population with those in RA patients who do or do not harbor anti-CCP antibodies. METHODS: HLA-DRB1 typing was performed in 408 RA patients from the Leiden Early Arthritis Clinic (the Leiden EAC; a Dutch population-based inception cohort in which disease course was followed up over time), in 423 healthy Dutch controls, and in 720 affected members of 341 US multiplex (sibpair) families of Caucasian origin from the North American RA Consortium (NARAC) with well-established disease and fulfilling the American College of Rheumatology classification criteria for RA. The presence of anti-CCP antibodies was determined by enzyme-linked immunosorbent assay. RESULTS: For the Leiden EAC, the odds ratio (OR) describing the association of 2 copies of the SE allele with anti-CCP positivity (using no copies of the SE allele in the healthy control group as the referent) was 11.79 (P < 0.0001), while the OR for 1 SE allele was 4.37 (P < 0.0001). No association with the SE was observed in the Dutch anti-CCP-negative RA patients. For the NARAC families, linkage and association analysis revealed the SE to be associated only with anti-CCP-positive disease and not with anti-CCP-negative disease. Stratified analyses indicated that anti-CCP antibodies primarily mediated association of the SE with joint damage or disease persistence. CONCLUSION: HLA-DRB1 alleles encoding the SE are specific for disease characterized by antibodies to citrullinated peptides, indicating that these alleles do not associate with RA as such, but rather with a particular phenotype.

Arthritis, Rheumatoid↗

PubMed2005

Transmit and receive transmission line arrays for 7 Tesla parallel imaging.

Transceive array coils, capable of RF transmission and independent signal reception, were developed for parallel, 1H imaging applications in the human head at 7 T (300 MHz). The coils combine the advantages of high-frequency properties of transmission lines with classic MR coil design. Because of the short wavelength at the 1H frequency at 300 MHz, these coils were straightforward to build and decouple. The sensitivity profiles of individual coils were highly asymmetric, as expected at this high frequency; however, the summed images from all coils were relatively uniform over the whole brain. Data were obtained with four- and eight-channel transceive arrays built using a loop configuration and compared to arrays built from straight stripline transmission lines. With both the four- and the eight-channel arrays, parallel imaging with sensitivity encoding with high reduction numbers was feasible at 7 T in the human head. A one-dimensional reduction factor of 4 was robustly achieved with an average g value of 1.25 with the eight-channel transmit/receive coils.

Brain↗

PubMed2005

Higher-order harmonic transmission-line RF coil design for MR applications.

A novel concept based on the use of higher-order harmonic resonances in a transmission-line resonator is introduced for the design of high-frequency RF coils at high and ultrahigh fields, where conventional RF coil designs present difficulties and limitations. To demonstrate this concept, we successfully designed and fabricated a 400-MHz RF coil for rat imaging using a second-harmonic resonant microstrip transmission line. This coil has a high Q-factor, reduces coil-cable interactions without the use of a matching balun, and has a broad range for tuning the coil's resonant frequency at the loaded condition. This work demonstrates that the use of higher-order harmonics in a transmission-line resonator provides an alternative, efficient approach to the design of large and high-frequency RF coils.

Animals↗

PubMed2005

Influence of gradient acoustic noise on fMRI response in the human visual cortex.

A paired-stimuli paradigm combined with fMRI was utilized to study the effect of gradient acoustic noise on fMRI response in the human primary visual cortex (V1) in terms of the auditory-visual cross-modal neural interaction. The gradient noise generated during the fMRI acquisition was used as the primary stimulus, and a single flashing light was used as the secondary stimulus. An interstimulus interval (ISI) separated the two. Six tasks were designed with different ISIs ranging from 50 to 700 ms. Both BOLD signal intensity and the number of activated pixels in V1 were analyzed and examined, and they showed a significant reduction when the gradient noise preceded the flashing light by approximately 300 ms. These results indicate that the gradient acoustic noise generated during fMRI acquisitions does interfere with neural behavior and the BOLD signal in the human visual cortex. This interference is modulated by the delay between the gradient noise and visual stimulation, and it can be studied quantitatively when the stimulation paradigm is designed appropriately. This study provides evidence of the auditory-visual interaction during fMRI studies, and the results should have an impact on fMRI applications.

Acoustics↗

PubMed2005

In vivo 17O NMR approaches for brain study at high field.

17O is the only stable oxygen isotope that can be detected by NMR. The quadrupolar moment of 17O spin (I = 5/2) can interact with local electric field gradients, resulting in extremely short T1 and T2 relaxation times which are in the range of several milliseconds. One unique NMR property of 17O spin is the independence of 17O relaxation times on the magnetic field strength, and this makes it possible to achieve a large sensitivity gain for in vivo 17O NMR applications at high fields. In vivo 17O NMR has two major applications for studying brain function and cerebral bioenergetics. The first application is to measure the cerebral blood flow (CBF) through monitoring the washout of inert H2 17O tracer in the brain tissue following an intravascular bolus injection of the 17O-labeled water. The second application, perhaps the most important one, is to determine the cerebral metabolic rate of oxygen utilization (CMRO2) through monitoring the dynamic changes of metabolically generated H2 17O from inhaled 17O-labeled oxygen gas in the brain tissue. One great merit of in vivo 17O NMR for the determination of CMRO2 is that only the metabolic H2 17O is detectable. This merit dramatically simplifies both CMRO2 measurement and quantification compared to other established methods. There are two major NMR approaches for monitoring H2 17O in vivo, namely direct approach by using 17O NMR detection (referred as direct in vivo 17O NMR approach) and indirect approach by using 1H NMR detection for measuring the changes in T2- or T1rho-weighted proton NMR signals caused by the 17O-1H scalar coupling and proton chemical exchange (referred as indirect in vivo 17O NMR approach). Both approaches are suitable for CBF measurements. However, recent studies indicated that the direct in vivo 17O NMR approach at high/ultrahigh fields appears to offer significant advantages for quantifying and imaging CMRO2. New developments have further demonstrated the feasibility for establishing a completely noninvasive in vivo 17O NMR approach for imaging CMRO2 in a rat brain during a brief 17O2 inhalation. This approach should be promising for studying the central role of oxidative metabolism in brain function and neurological diseases. Finally, the similar approach could potentially be applied to image CMRO2 noninvasively in human brain.

Animals↗

PubMed2005

Chronic toxicity and responses of several important enzymes in Daphnia magna on exposure to sublethal microcystin-LR.

In the current study, the toxicological mechanisms of microcystin-LR and its disadvantageous effects on Daphnia magna were examined. Survival rate, number of newborn, activity of several important enzymes [glutathione S-transferase (GST), lactate dehydrogenase (LDH), phosphatases, and glutathione], accumulated microcystins, and ultrastructural changes in different organs of Daphnia were monitored over the course of 21-day chronic tests. The results indicated that low concentrations of dissolved microcystin had no harmful effect on Daphnia. On the contrary, stimulatory effects were detected. In the presence of toxin at high dosage and for long-term exposure, GST and glutathione levels decreased significantly. The decreased enzyme activity in the antioxidant system probably was caused by detoxification reactions with toxins. And these processes of detoxification at the beginning of chronic tests may enable phosphatases in Daphnia magna to withstand inhibition by the toxins. At the same time, we also found that the LDH activity in test animals increased with exposure to microcystin-LR, indicating that adverse effects occurred in Daphnia. With microcystin given at a higher dosage or for a longer exposure, the effect on Daphnia magna was fatal. In the meantime, microcystin began to accumulate in Daphnia magna, and phosphatase activity started to be inhibited. From the ultrastructure results of cells in D. magna, we obtained new information: the alimentary canal may be the target organ affected by exposure of microcystins to D. magna. The results of the current study also suggested that the oxidative damage and PPI (protein phosphatase inhibition) mechanisms of vertebrates also are adapted to Daphnia.

Adaptation, Physiological↗

PubMed2005

Effects of microcystins on and toxin degradation by Poterioochromonas sp.

A Chrysophyceae species, Poterioochromonas sp., was isolated from Microcystis cultures. This species can efficiently prey on Microcystis and can grow faster phagotrophically than autotrophically. The growth of Poterioochromonas sp. was stimulated in the presence of microcystin-LR and microcystin-RR (in concentrations ranging from 0.1 to 4 mg/L). The growth rate of Poterioochromonas was 4-5 times higher than the control, indicating the toxins serve as growth stimuli for this organism. A subculture of toxin-treated cells, however, showed low cellular viability, suggesting that growth enhancement by microcystins was not a normal process. The antioxidant enzymatic activity of Poterioochromonas sp. was screened for toxicology analysis. Glutathione, malondialdehyde, and superoxide dismutase (SOD) content was up-regulated within 8 h of exposure to microcystin-LR (500 microg/L). A high level of SOD activity during exposure to the toxin indicated that SOD was involved in decreasing oxidative stress caused by microcystin-LR. Simultaneously with growth, Poterioochromonas was able to degrade microcystin-LR even, at a toxin concentration of 4 mg/L. This putative degradation mechanism in Poterioochromonas is explored further and discussed in this article. Our findings may shed light on understanding the role of Poterioochromonas in the aquatic ecosystem, in particular, as a grazer of toxic cyanobacteria and a biodegrader for microcystins.

Biodegradation, Environmental↗

PubMed2005

Effects of total flavonoids of Hippophae rhamnoides L. on intracellular free calcium in cultured vascular smooth muscle cells of spontaneously hypertensive rats and Wistar-Kyoto rats.

OBJECTIVE: To explore the effects of total flavonoids of Hippophae rhamnoides L. (TFH), quercetin (Que) and isorhamnetin (Isor) on the intracellular free calcium ([Ca(2+)](i)) in vascular smooth muscle cells (VSMC) of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). METHODS: Fluo 3-acetoxymethylester (Fluo-3/AM) was used to observe the effects of TFH (100 mg/L) and its essential monomers, namely Que (10(-4) mol/L) and Isor (10(-4) mol/L) on changes of [Ca(2+)](i) in cultured SHR and WKY VSMC (abbr. to Ca-SHR & Ca-WKY) following exposure to high K(+), norepinephrine (NE) and angiotensin II (Ang II), and to compare with the effects of verapamil (Ver). RESULTS: (1) TFH, Que and Isor had inhibitory effects on resting Ca-SHR (P < 0.05), but had no significant effects on Ca-WKY (P > 0.05). (2) High K(+) could increase Ca-SHR more significantly than Ca-WKY (P < 0.05); TFH, Que and Isor could inhibit the elevation of [Ca(2+)](i) induced by high K(+)-depolarization, with the effects similar to that of Ver, and the effect on Ca-SHR was more significant than that on Ca-WKY (P < 0.05). (3) NE and Ang II could increase Ca-SHR more significantly than Ca-WKY (P < 0.05), TFH, Que and Isor had remarkably inhibitory effect on the elevation of Ca-SHR and Ca-WKY induced by NE or Ang II. (4) In the absence of extracellular Ca(2+), TFH, Que and Isor also had certain inhibitory effect on Ca-SHR and Ca-WKY induced by NE, and the effect on the former was more significant than that on the latter (P < 0.05). CONCLUSION: TFH, Que and Isor might decrease the levels of [Ca(2+)](i) in VSMCs by blocking both voltage-dependent calcium channels (VDC) and receptor-operated calcium channels (ROC) in physiological or pathological state, which may be one of the important mechanisms of their hypotensive and protective effects on target organs in patients with hypertension.

Angiotensin II↗

PubMed2005

Real time in vivo non-invasive optical imaging using near-infrared fluorescent quantum dots.

RATIONALE AND OBJECTIVE: Deep-tissue optical imaging is of particular interest, as the equipment costs are lower than for competing technologies such as MRI. For this purpose, the development of novel contrast agents with near-infrared (NIR) fluorescence is especially important. We report on the use of NIR semiconductor nanocrystals in deep-tissue in vivo optical imaging. MATERIALS AND METHODS: Semiconductor nanocrystals of CdMnTe/Hg were grown in aqueous solution and then coated with bovine serum albumin (BSA). The nanocrystals were approximately 5 nm in diameter and have a broad fluorescence peak in the NIR (770 nm). Nanocrystals were injected either subcutaneously or intravenously into athymic NCR NU/NU and C3H/HENCR MTV mice and then excited with a spatially broad 633 nm source; the resulting fluorescence was captured with a sensitive CCD camera. RESULTS: We have demonstrated that the nanocrystals are a useful angiographic contrast agent for vessels surrounding and penetrating a murine squamous cell carcinoma in a C3H mouse. Preliminary assessment of the depth of penetration for excitation and emission was done by imaging a beating mouse heart, both through an intact thorax and after a thoracotomy. The temporal resolution associated with imaging the nanocrystals in circulation has been addressed, and the blood clearance for this contrast agent has also been measured. CONCLUSIONS: There was no significant photobleaching or degradation of the nanocrystals after an hour of continuous excitation. The stability of the nanocrystals together with the time resolution of the optical detection makes them particularly attractive candidates for pharmacokinetic imaging studies.

Animals↗

PubMed2005

Vascular abnormalities in asymptomatic, healthy young adult smokers without other major cardiovascular risk factors: the Bogalusa Heart Study.

Cigarette smoking, an established cardiovascular (CV) disease risk factor, is known to impair pulsatile arterial function in middle-aged and older adults. However, information is scant in healthy young adults for whom smoking is the only CV risk factor, at current guidelines. Nonsmokers (n = 145) and smokers (n = 142) aged on average 36 years were selected for not having obesity, hypertension, dyslipidemia, diabetes, or clinically manifest CV disease. Pulsatile arterial function was measured in terms of large artery compliance (C1), small artery compliance (C2), and systemic vascular resistance (SVR) by noninvasively recorded radial artery waveforms. Smokers versus nonsmokers had significantly lower measures of adiposity and LDL-cholesterol; and higher systolic blood pressure and triglycerides. In addition, smokers versus nonsmokers had lower C2 (5.09 v 6.63 mL/mm Hg x 100, P = .0009) and higher SVR (1399.0 v 1325.5 dyn . sec . cm(-5), P = .006), after adjustment for race, sex, and age. Decreases in C2 (P for trend = .001) and increases in SVR (P for trend = .01) were noted with increasing years of smoking. Multivariate analysis revealed that duration of smoking was associated adversely with C2 (P = .004), independent of race, sex, age, systolic and diastolic blood pressures, HDL-cholesterol, triglycerides, glucose, and insulin. The odds of having adverse C2 (bottom 10 percentile) and SVR (top 10 percentile) were, respectively, 2.9 (P = .01) and 2.6 (P = .07) times higher in smokers versus nonsmokers. The observed deleterious effects of cigarette smoking on arterial wall dynamics in otherwise healthy young adults underscore the need for aggressive early prevention and intervention strategies to control smoking behavior.

Adult↗

PubMed2005

Distribution and correlates of arterial compliance measures in asymptomatic young adults: the Bogalusa Heart Study.

BACKGROUND: Impaired arterial compliance is an independent predictor of early vascular damage and related adverse cardiovascular (CV) outcome. Information is scant on the distributions and correlates of measures of arterial pulsatile function in a community-based, biracial cohort of young adults. METHODS: In 800 African American and white subjects aged 18 to 44 years, pulsatile arterial function was assessed in terms of large artery (capacitive) compliance, small artery (oscillatory) compliance, systemic vascular resistance, and vascular impedance by noninvasive radial artery pressure pulse contour analysis. RESULTS: African Americans versus whites and women versus men had lower large and small artery compliances and higher systemic vascular resistance and vascular impedance (P < .001). In multiple regression analysis, mean arterial pressure, body mass index (BMI), insulin levels, and age were correlated inversely and body surface area positively with large artery compliance and accounted for 39.2% of the variance; mean arterial pressure, female gender, age, and triglyceride levels inversely and cardiac output positively with small artery compliance and explained 56.4% of the variance; mean arterial pressure and age positively and cardiac output inversely with systemic vascular resistance and accounted for 91.4% of variance; and mean arterial pressure and BMI positively and cardiac output and body surface area inversely with vascular impedance and contributed to 37.6% of the variance. CONCLUSIONS: The observed deleterious impact of traditional CV risk factors on the arterial wall dynamics in asymptomatic young adults has important implications for preventive cardiology. Noninvasive pulsatile arterial function assessment may be helpful for evaluation of early vascular damage in a high-risk young population group.

Adolescent↗