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PubMed1997

Frequency resolution and spectral integration (critical band analysis) in single units of the cat primary auditory cortex.

Frequency resolution and spectral filtering in the cat primary auditory cortex (AI) were mapped by extracellular recordings of tone responses in white noise of various bandwidths. Single-tone excitatory tuning curves, critical bandwidths, and critical ratios were determined as a function of neuronal characteristic frequency and tone level. Single-tone excitatory tuning curves are inadequate measures of frequency resolution and spectral filtering in the AI, because their shapes (in most neurons) deviated substantially from the shapes of "tuning curves for complex sound analysis", the curves determined by the band limits of the critical bandwidths. Perceptual characteristics of spectral filtering (intensity independence and frequency dependence) were found in average critical bandwidths of neurons from the central and ventral AI. The highest frequency resolution (smallest critical bandwidths) reached by neurons in the central and ventral AI equaled the psychophysical frequency resolution. The dorsal AI is special, since most neurons there had response properties incompatible with psychophysical features of frequency resolution. Perceptual characteristics of critical ratios were not found in the average neuronal responses in any area of the AI. It seems that spectral integration in the way proposed to be the basis for the perception of tones in noise is not present at the level of the AI.

Acoustic Stimulation↗

PubMed2006

Varied growth, biomass and cellulose content in tobacco expressing yeast-derived invertases.

The effects of the expression of yeast-derived apoplastic (AI) and cytosolic (CI) invertases (EC 3.2.1.26) on biomass and structural carbohydrate accumulation in tobacco (Nicotiana tabacum L. cv. Xanthi) were evaluated. Transgenic tobacco plants expressing AI or CI under the control of either a tandem repeat of the Cauliflower Mosaic Virus 35S promoter (2X35S), or a promoter that drives xylem-localized expression (Petroselinum crispum 4-coumarate:CoA ligase promoter; 4CL) were generated. Yeast-derived invertase transcript levels, invertase protein, enzyme activity, growth parameters as well as both structural and soluble carbohydrates of stem tissue of all transformed lines were quantified. Transgenic tobacco lines expressing invertase under the control of 4CL displayed severe growth retardation with both yeast-derived isogenes. Similarly, several transformed lines expressing either AI or CI regulated by the 2X35S promoter were also shorter than wild-type (WT) plants. Despite the decreases in height, some transformed lines had significant increases in biomass. One line (2X35S::AI-1) had a biomass/height increase of 88% and an increase in stem diameter of over 40%, while a second line (2X35S::CI-5) had a biomass/height increase of 21%. A separate line (2X35S::AI-2) had a 36% increase in cellulose content, while two others (4CL::AI-2 and 4CL::AI-3) displayed significant decreases in cellulose content. The observed phenotypes can be in part explained by the levels of foreign invertase present, subcellular localization and the carbohydrate status of the tissues.

Biomass↗

PubMed2006

The prognostic value of circulating plasma DNA level and its allelic imbalance on chromosome 8p in patients with hepatocellular carcinoma.

PURPOSE: We demonstrated that chromosome 8p deletion is associated with metastasis of human hepatocellular carcinoma (HCC). This study assesses the value of circulating plasma DNA level and its allelic imbalance (AI) on chromosome 8p in the prediction of HCC prognosis. METHODS: Blood samples were collected from 79 patients with HCC before operation, 20 patients with liver cirrhosis, and 20 healthy volunteers. The HCC and adjacent non-tumor liver tissues were obtained from surgical specimens. Plasma DNA was extracted and quantified. Two microsatellite markers on chromosome 8p, D8S258 and D8S264, were selected and used in the AI analysis. RESULTS: The circulating plasma DNA level was found to closely associate with tumor size (P=0.008) and TNM stage (P=0.040), negatively associate with the 3-year disease-free survival (DFS) (P=0.017) and overall survival (OS) (P=0.001). AI at D8S258 in plasma DNA was significantly correlated with tumor differentiation (P=0.050), TNM stage (P=0.010), and vascular invasion (P=0.023), negatively correlated with the 3-year DFS (P=0.005) and OS (P=0.036). However, AI at D8S264 was only closely associated with 3-year DFS (P=0.014). Combined detection of AI at D8S258 and circulating plasma DNA level was independently associated with DFS (P=0.018) and OS (P=0.002) of patients with HCC. For patients with both AI at D8S258 and a higher level of plasma DNA, the 3-year DFS and 3-year OS rates were decreased remarkably (P=0.014 and 0.044). CONCLUSION: Combination of circulating plasma DNA level and AI at D8S258 might be an independent predictor for prognosis of HCC patients.

Adult↗

PubMed2002

Imbalance between apostain expression and proliferative index can predict survival in primary glioblastoma.

BACKGROUND: Cell proliferation and cell death are opposing processes in tumour growth, with tumour progression reflecting the balance between proliferating and apoptotic cells. The purpose of the present study is to verify the hypothesis that an imbalance between apoptosis and proliferation can predict survival in patients with primary glioblastoma. METHODS: After the immunohistochemical study of Apostain and MIB-1 expression, the index of apoptosis (AI), the index of proliferation (PI), and the ratio AI/PI was recorded for each tumour specimen, in a series of 32 primary glioblastomas. Studies of correlation between AI and PI, between AI and survival, between PI and survival, and between the ratio AI/PI and survival, were performed using the Spearman rank correlation test. Furthermore, a comparative study of survival was performed for subgroups of patients with ratio AI/PI greater or lesser than 1, using the log rank test. FINDINGS: In the present series, values of AI and PI showed a wide distribution, with a mean +/- SD of 8.16 +/- 7.2, and of 12.69 +/- 21.1, respectively. The values for the ratio AI/PI ranged between 0.01 and 6.03 (mean +/- SD: 1.44 +/- 1.60). Statistical study failed to obtain correlation between AI and PI. Survival of patients not correlated with AI neither with PI. The ratio between AI and PI did not correlate with survival either. Nevertheless, when survival for the subgroups of patients showing a ratio AI/PI greater or lesser than 1 was compared, a significant difference was found (p: 0.02). Survival ranged between 50 and 81 weeks (mean of 58.5 +/- 11.05 weeks) for the 12 cases showing a ratio AI/PI greater than 1, and it ranged between 8 and 85 weeks (mean: 38.20 +/- 25.37 weeks) for the 20 cases showing a ratio AI/PI lesser than 1. INTERPRETATION: Our present results suggest that a clear imbalance between cell proliferation and apoptosis can predict outcome in patients operated on for a primary glioblastoma.

Aged↗

PubMed2005

Risk of recurrence after surgical resection of small-sized invasive lung adenocarcinoma: analysis based on apoptotic index.

OBJECTIVE: It has been reported that small-sized invasive lung adenocarcinomas, i.e., those classified as type C through type F according to Noguchi's classification, may also recur even after complete resection. We evaluated the prognostic value of molecular biologic markers (apoptosis, Ki-67, p53, epidermal growth factor) and clinicopathological factors in patients with small-sized invasive lung adenocarcinomas. METHODS: The clinical records of all patients who had had a peripheral adenocarcinoma surgically resected between 1996 and 2002, and histologically diagnosed as type C through type F according to Noguchi's classification were retrospectively reviewed. The apoptotic index (AI) was determined by the triphosphate biotin nick end-labeling method and the expression of Ki-67, aberrant p53 protein and epidermal growth factor receptor was determined by immunohistochemical staining. RESULTS: Data from 28 patients who had been followed up for a mean period of 41.8 months (range: 16 to 89 months) were evaluated. During the follow-up period, recurrence was seen in 6 patients. The log-rank test showed that AI was a significant predictor of cancer recurrence. The 5-year disease-free survival rate of the 10 patients in the high AI group (AI > 0.3%) was 100%; while that of the 18 patients in the low AI group (AI < or = 0.3%) was 50.5% (p = 0.036). None of the other molecular biologic markers or clinicopathological factors were found to be a significant predictor of cancer recurrence. CONCLUSION: Peripheral small-sized invasive lung adenocarcinomas with a low AI carry an increased risk of distant metastases, indicating that adjuvant chemotherapy after complete resection might be needed.

Adenocarcinoma↗

PubMed2006

The "El Alamo" project (1990-1997): two consecutive hospital-based studies of breast cancer outcomes in Spain.

BACKGROUND: The "Alamo" project is a retrospective analysis of 14,854 patients diagnosed of breast cancer between 1990 and 1997 in 50 Spanish hospitals. METHODS: Alamo I (AI) consisted of 4,532 patients diagnosed with breast cancer between 1990 and 1993. Data were collected in 2000. Alamo II (AII) consisted of 10,322 patients diagnosed between 1994 and 1997. Data were collected in 2003. RESULTS: At presentation, there were (AI vs. AII) 17.6% vs. 24.3% at stage I; 55.5% vs. 53.1% at stage II; 18.7% vs. 15% at stage III; 7.2% vs. 5.9 at stage IV. Median age was 57 (AI) vs. 58 years (AII) and 65.9% vs. 67.2% (AI vs. AII) were post-menopausal. Firstline treatment for disease stages I, II and III was surgery in 91% of patients in both studies. Breast conserving surgery rate increased from 20.2% (AI) to 32.7% (AII). Adjuvant systemic treatments were administered to 87.6% (AI) and 92.8% (AII) of patients. Recurrence rate diminished from 36.6% (AI) to 22.5% (AII) and the 9-year survival rate increased from 63.2% (95% CI: 61.5-64.9) to 70.1% (95% CI: 68.5-71.8). CONCLUSION: Breast cancer outcomes in Spain have improved from 1990-1993 to 1994-1997, likely because of breast cancer screening program implementation and new therapies.

Adult↗

PubMed1991

Hypertrophy of nodules of Arantius and aortic insufficiency: pathophysiology and repair.

Aortic insufficiency (AI) due to fibrosis and thickening of the nodules of Arantius in the otherwise normal aortic valve was found in 11 adults (age range, 41 to 65 years) between 1976 and 1988. Nine had concomitant mitral stenosis; 2 had coronary artery disease. In 6 patients AI was graded 3+ or greater; in 5 it was less than 3+. Correction of AI and restoration of cuspid flexibility and apposition by shaving the hypertrophied nodules was accomplished in all, with postrepair AI graded as 1+ or less. There was one hospital death, a patient who had prior mitral operation. Mean follow-up was 68 +/- 56 months. Only 1 patient had late (6 years) recurrent serious (3+) AI. Nine continued to have 1+ or less AI, based on echocardiography or catheterization (n = 6) or on physical examination performed at a mean of 74 months. We conclude that thickening of the nodules of Arantius may cause AI. Long-term correction can be accomplished by sculpturing of the involved cusps.

Adult↗

PubMed1981

Prostacyclin (PGI2) release accompanying angiotensin conversion in rat mesenteric vasculature.

The relationship between angiotensin conversion and release of prostaglandins (PGs) were studied in isolated, perfused, mesenteric vasculature of rats. PGs in the mesenteric effluent were detected by bovine coronary artery and rat stomach strip, and by radioimmunoassay of 6-oxo-PGF1 alpha and PGE2. Angiotensin II (AII) was assayed simultaneously using rabbit aorta. Both angiotensin I (AI) and AII released a prostacyclin (PGI2)-like substance, but little PGE2 from the mesentery, AII being 5 times more potent. Indomethacin (2.8 micrometers) abolished angiotensin-induced release of PGI2. Of the AI (0.2--1.5 nmol) injected into the perfusion medium, 3--8% was converted to AII in passage through the mesentery. Captopril (4 micrometers), infused through the mesentery, inhibited AI-induced PGI2 release, but did not affect release induced by AII. Release of the PGI2-like substance by higher doses of AI (2--20 nmol) in the presence of captopril was always accompanied by concomitant contraction of rabbit aorta, indicating residual conversion of AI. Infusion of (Sar1, Ala8)AII (3--30 nM) through the mesentery abolished PGI2 release by both peptides. By choosing doses of AI and AII which produce equivalent amounts of AII in the mesenteric effluent, it appeared that AII generated locally in the mesenteric vasculature was a more effective stimulus for PGI2 generation than AII in the perfusion fluid. There is no evidence for intrinsic activity of AI, and release of the PGI2-like substance appears to be mediated through an AII receptor.

Angiotensin I↗

PubMed1991

Angiotensin I conversion and coronary constriction by angiotensin II in ischemic and hypoxic isolated rat hearts.

Dose-response curves of angiotensin I (AI, 1.0-1000.0 pmol) and angiotensin II (AII, 1.25-1250.00 pmol) were obtained in isolated rat hearts subjected to control conditions, mild hypoxia (PO2 = 145 mm Hg), reoxygenation, ischemic (perfusion pressure = 35 mm Hg) and reperfusion. Both AI and AII caused dose-dependent coronary flow (CF) of 26 +/- 3 and 27 +/- 2%, respectively. The effects of both AI and AII were substantially attenuated during hypoxia, but were fully restored upon reoxygenation. During ischemia, the effect of AII was unaltered while the effect of AI was enhanced compared to the control (P less than 0.05). This enhancement was reversible on reperfusion. Cardiac conversion of AI, calculated from ED50 values for AI and AII, was significantly increased during ischemia (P less than 0.05). Infusion of saralasin (0.5-5.0 micrograms/min) did not increase CF in any of the groups. We conclude that (1) the coronary vasoconstrictive effect of AII is preserved in ischemia but attenuated in hypoxia and (2) cardiac conversion of AI to AII is enhanced in hearts injured by ischemia.

Angiotensin I↗

PubMed1985

A cardiac specific analog of angiotensin I potentiated by converting enzyme inhibition.

[1-Sarcosine, 7-Alanine] angiotensin I [( 1-Sar, 7-Ala] AI) and closely related analogs were tested for inotropic activity in the isolated cat heart, and for pressor activity in the intact conscious sheep both before and during converting enzyme inhibition (CEI). [1-Sar, 7-Ala] AI exhibited potent inotropic activity but was only weakly pressor. [1-Sar] AI, [1-Sar, 5-Val] AI, [1-Sar, 7-alpha MeAla] AI [1-Sar, 5-Val, 7-NMeAla] AI and [1-Sar, 5-Val, 7-Sar] were all potent agonists in both preparations. The action of [1-Sar, 7-Ala] AI was potentiated by CEI in both the isolated heart and the intact sheep. The activity of the remaining analogs was either partially or completely blocked by CEI. The activity of all analogs was inhibited by AII receptor blockade. These data indicate that the nature of the substitution in position 7 determines the affinity of the analog for converting enzyme. The [7-Ala] substitution appears to decrease the effect of the analog upon vascular receptors.

Angiotensin I↗

PubMedDate not supplied

Initial subsensitivity to anxiolytic treatments on conflict behavior in rats: parametric studies across drug classes.

In conflict paradigms, benzodiazepines (BZs) often exhibit maximal anticonflict effects only after three to four BZ exposures (anxiolytic initial subsensitivity; AIS). The present experiments examined 1) whether AIS occurs with non-BZ anxiolytics and 2) whether prior exposure to non-BZs prevents the occurrence of BZ AIS. Female rats were trained to stable responding levels on a repeated-measures punished drinking paradigm. In Experiment 1, dose-response curves for the effects of the BZs chlordiazepoxide and diazepam, the barbiturates (BBs) pentobarbital and amobarbital, and the non-BZ, non-BB agent carbamazepine were determined in five groups of rats (one group/drug); dose-response curves were determined on two occasions for each drug. There was an AIS with both BZs, with the anticonflict effect being significantly greater for dose-response determination #2. There was no AIS with the BBs (robust and dose-dependent increases in punished responding on both determinations) or with carbamazepine (weak anticonflict effect on both determinations). In Experiment 2, the rats from Experiment 1 received a single-dose challenge with chlordiazepoxide (10 mg/kg). This challenge resulted in a robust anticonflict effect in subjects with a history of repeated BZ treatment; in contrast, subjects with a history of repeated BB or carbamazepine treatment exhibited smaller anticonflict responses. These data suggest that 1) the AIS does not occur with non-BZ anxiolytics and 2) the BZ AIS cannot be prevented by repeated exposure to non-BZs.

Animals↗

PubMed1993

A field investigation of the effects of bovine viral diarrhea virus infection around the time of insemination on the reproductive performance of cattle.

During a study of methods of synchronizing estrus in Bos indicus cattle, blood was collected from 169 heifers and 38 cows 2 to 3 days prior to artificial insemination (AI), and then again at Day 51 and Day 210 after AI to determine the incidence of infection with bovine viral diarrhea (BVD) virus. Prior to insemination 53 and 68% of the cows and heifers, respectively, were seronegative to the BVD virus. At Day 51 after AI, 70 and 32% of the seronegative cows and heifers, respectively, had seroconverted; but between Day 51 and Day 210, only 17 and 3% of the seronegative cows and heifers, respectively, had seroconverted. The Day- 51 pregnancy rate of cows which were immune (seropositive) to BVD virus infection at the time of AI was similar to the rate of the cows which became infected around the time of AI. However, the pregnancy rate of the immune heifers (44%, n=54) was significantly (P=0.04) greater than the rate of the heifers which became infected around the time of AI (24%, n=37). It was concluded that infection of susceptible females with BVD virus around the time of AI may significantly lower the pregnancy rate.

Journal Article↗

PubMed1986

Characterization of high-density lipoprotein binding and cholesterol efflux in cultured mouse adipose cells.

Binding of high-density lipoproteins to cultured mouse Ob1771 adipose cells was studied, using labeled human HDL3, mouse HDL and apolipoprotein AI- or AII-containing liposomes. In each case, saturation curves were obtained, yielding linear Scatchard plots. The Kd values were found to be respectively 18, 42, 30 and 3.4 micrograms/ml, whereas the maximal binding capacities were found to be 160, 100, 90 and 21 ng/mg of cell protein. Apoprotein AI not inserted into liposomes did not bind. The binding of 125I-HDL3 was competitively inhibited by apolipoprotein AI-containing liposomes greater than mouse HDL greater than HDL3. The binding of 125I-labeled apolipoprotein AI- and 125I-labeled apolipoprotein AII-containing liposomes was competitively inhibited by HDL3, apolipoprotein AI- and apolipoprotein AII-containing liposomes. Dimyristoylphosphatidylcholine liposomes containing or not cholesterol did not interfere with the binding of labeled HDL3 or apolipoprotein-containing liposomes. Binding studies on crude membranes of Ob1771 adipose cells revealed the presence of intracellular binding sites for LDL and HDL3. Thus, adipose cells have specific binding sites for apolipoprotein E-free HDL and apolipoprotein AI (or AII) is the ligand for these binding sites. Long-term exposure of adipose cells to LDL cholesterol as a function of LDL concentration led to an accumulation of cellular unesterified cholesterol. This process was saturable and reversible as a function of time and concentration by exposure to HDL3 or apolipoprotein AI-containing liposomes, whereas apolipoprotein AII-containing liposomes did not promote any cholesterol efflux. Since long-term exposure of adipose cells to LDL and HDL3 did not affect the number of apolipoprotein B,E receptors and apolipoprotein E-free binding sites, respectively, it appears that adipose cells do not show efficient cholesterol homeostasis and thus could accumulate or mobilize unesterified cholesterol.

Adipose Tissue↗

PubMed1984

Prostaglandins and the contractile effect of angiotensin I and II in the uterus isolated from ovariectomized rats. Influences of indomethacin and 17-beta estradiol.

The purpose of the present study was to explore whether, the stimulating contractile action of angiotensin II (AII) or of angiotensin I (AI), in uterine strips isolated from rats, either spayed or spayed and injected with 17-beta estradiol, was somehow linked to tissue generated prostaglandins (PGs). Indomethacin (10(-6)M), shifted to the left the dose-response curve for AII in preparations from ovariectomized animals; augmenting both, the efficacy and the potency of the agonist. Dose-response curves for AII were also explored in the presence of subthreshold concentrations of several exogenous PGs. PGE2 (10(-9) M) completely abolished the influence of indomethacin on the curve for AII; PGD2 (10(-9) M) did not evoke effects and PGF2 alpha (10(-9) M) only altered the threshold dose, the rest of the curve remaining similar to that obtained with indomethacin alone. The cumulative dose-response curve for AI, in strips isolated from ovariectomized rats, was comparable to that for AII and, the presence of indomethacin, only reduced the concentration for the threshold action of AI, in comparison to controls. Captopril (100 ng/ml), shifted to the right the dose-response curve for AI and indomethacin failed to alter the effects of AI in the presence of captopril. In strips isolated from ovariectomized rats, injected with 17-beta estradiol, the low concentration points of the dose-response curve for AII were shifted to the left of those for the agonist in control preparations from spayed rats not treated with estradiol. Furthermore, indomethacin failed to alter the responses to AII in strips from spayed animals injected with 17-beta estradiol. The foregoing results document that an inhibitor of tissue PGs synthesis, namely indomethacin, is able to modify the dose-response curve for AII, rather than that for AI, in the uterus from ovariectomized rats, but not in preparations from spayed animals treated with estradiol. This, as well as the effect of a subthreshold dose of PGs, suggest that a minimum of PGE2 is required for the contractile influence of AII and not for that of AI. Moreover, the absence of estrogen dominance appears, as well, as a crucial factor for the action of AII.

Angiotensin I↗

PubMed1992

The effects of sulphur gas and elemental sulphur dust deposition on Pinus contorta x Pinus banksiana: cell walls and water relations.

The bulk modulus of elasticity (E) for Pinus contorta (lodgepole pine) x Pinus banksiana (jack pine) hybrids was compared between a site (AI) close to a sour gas processing plant and a control site (AV). The mean bulk modulus of elasticity for branches from AI was 47.5 MPa vs 18.5 MPa for the control site (AV). Site AI had been exposed to S-gas emissions and large amounts of elemental S deposition and had an acidic soil (pH 4.0 at 10 cm depth). During 1981 the needles at AI had more aluminum and iron compared to those at AV (900 ppm vs 390 ppm AI in the 3-year-old needles). Mean leader growth was measured over a 3-year period and was observed to be greater at AI than AV (46+/-7 cm vs 29+/-9 cm for 1988). Histochemically, the needles at AI had higher phenol and lignin content than AV. These results suggest that the S-gas fumigation, S-dust deposition, plus increased concentrations of soluble aluminum and iron had altered the cell wall elastic properties resulting in altered water relations. The implications of this on leaf diffusive resistance and photosynthesis are discussed.

Journal Article↗

PubMed1990

Loss of androgen dependence is associated with an increase in tumorigenic stem cells and resistance to cell-death genes.

Complete remissions of the androgen-dependent Shionogi mouse mammary carcinoma are observed after androgen withdrawal but invariably the disease recurs and is refractory to further hormonal manipulations. To determine the proportions of androgen-dependent (AD) and -independent (AI) tumorigenic stem cells in parent and recurrent tumors an in vivo limiting dilution assay was developed. There was a marked enrichment of stem cells in the recurrent tumors (1/200 tumor cells) relative to the parent tumors (1/4000 tumor cells) when assayed in male hosts. By assaying tumor takes in female mice, the proportion of AI stem cells was found to be 1/370,000 tumor cells in the parent vs 1/800 tumor cells in the recurrent carcinoma; a 500-fold increase in AI stem cells resulting from androgen-withdrawal. Unexpectedly, no enrichment of AI stem cells was evident in regressing parent tumors; rather, the proportion of such cells was very small (1/2,200,000 tumor cells). This finding implies that the AI cells which survive androgen withdrawal may result from the ability of small number of initially AD stem cells to adapt to an altered hormonal environment. This adaptive process was further defined in terms of the disappearance of androgen receptors from the nucleus and the expression of androgen-repressed genes including the proto-oncogenes, c-fos and c-myc, and the cell death gene, TRPM-2; all of which are constitutively active in recurrent AI tumor cells. Overall, our results indicate: (1) the tumor mass consists mainly of differentiated cells; (2) stem cells initially are AD but at most the killing effect of androgen-withdrawal will be limited to 2-3 logarithms before compensatory adaptive mechanisms supervene; and (3) progression of stem cells to an AI state, in which they are resistant to the killing effects of cell death genes, might be prevented by the inhibition of androgen-repressed adaptive mechanisms which come into play when androgens are withdrawn.

Androgens↗

PubMed2005

Tooth movement and cytokines in gingival crevicular fluid and whole blood in growing and adult subjects.

INTRODUCTION: Tooth movement has been studied largely with respect to the force required for tipping when pressure distribution varies along the length of the periodontal ligament. But important factors for effective canine translation include the nature and magnitude of applied stress and the patient's cell biology. The purpose of this research was to test 3 hypotheses: (1) the velocity of tooth translation (v(t)) is related to applied stress and growth status, (2) a threshold of stress accounts for the lag phase, and (3) v(t) is correlated with the ratio (AI) of 2 cytokines (IL-1beta, IL-1RA) measured in gingival crevicular fluid (GCF) and stimulated whole blood (SWB). METHODS: Continuous maxillary canine retraction stresses of 13 kPa and 4, 26, or 52 kPa were applied bilaterally in 6 growing and 4 adult subjects for 84 days. Dental models and GCF samples were collected at 1- to 14-day intervals. Cytokines were measured in GCF and SWB cell cultures. RESULTS: V(t) was positively related to stress and was higher in growing subjects (P = .001). It was also related to AI(GCF) in growers (R2= 0.56) and nongrowers (R2= 0.72). Canines moved with 52 kPa showed a lag phase, and postlag phase AI(GCF) was twice that of lag phase AI(GCF). Mean v(t) and associated AI(GCF) during the postlag phase were nearly double the values for canines moved with 13 and 26 kPa. SWB production of cytokines was dose-dependent. For growing subjects, SWB IL-1RA was correlated with v(t) (R = 0.70-0.72), and AI(SWB) and IL-1beta concentrations were correlated with AI(GCF) (R = 0.73-0.78). CONCLUSIONS: V(t) varied with growth status and stresses < or = 52 kPa; stresses of < 52 kPa showed no lag phase; and equivalent stresses yielded subject-dependent differences in v(t), which correlated with cytokines in GCF and SWB.

Adolescent↗

PubMed2006

Enhanced radial late systolic pressure augmentation in hypertensive patients with left ventricular hypertrophy.

BACKGROUND: Wave reflection augments central blood pressure (BP) in late systole, thus increasing cardiac afterload. We examined the relationship between late systolic pressure augmentation in the peripheral radial artery pulse wave and the existence of left ventricular hypertrophy (LVH) in hypertension. METHODS: Brachial BP, radial augmentation index (AI(r)), and carotid-femoral pulse wave velocity (PWV(cf)) were determined in 77 untreated hypertensive patients aged 56 +/- 10 years. Cardiac structure and function were assessed by ultrasound, and LVH was defined based on the LV mass index (LVMI). Using multivariate analysis, patient characteristics were compared between those with (+) and without (-) LVH. RESULTS: The LVMI was correlated independently and positively with AI(r) (beta = 0.33, P = .004) and the brachial mean arterial pressure (MAP; beta = 0.25, P = .03). The ratio of early to atrial peak velocities (E/A ratio) of the diastolic transmitral flow tended to be correlated negatively with the AI(r). The LVH (+) group had a significantly higher AI(r) than the LVH (-) group [LVH (+), 97% v LVH (-), 89%, P = .003]; this difference remained significant even after adjustment for age, gender, MAP, and heart rate. The adjusted relative risk of LVH was 1.99 for each 10% AI(r) increase (P = .005). In contrast, LVMI was not correlated with the PWV(cf), and the PWV(cf) was not different between the LVH (+) and LVH (-) groups. Moreover, there was no significant correlation between PWV(cf) and AI(r). CONCLUSIONS: These results suggest that the peripheral AI(r) measurement is clinically useful in predicting LVH. Enhanced wave reflection may be related to the development of LVH in hypertensive patients.

Adult↗