Biomedical subjects

A Cittadini

Publications and source records attributed to A Cittadini.

At least 73 records · Page 4Linked to original sources

PubMed1997

Immunohistochemical analysis of p53 protein in transplant recipients with Kaposi's sarcoma.

PURPOSE: Kaposi's sarcoma (KS) is a proliferative process of suspected viral aetiology associated with immune deficiency. In transplanted patients, lesions regress on discontinuation of immunosuppressive therapy. The purpose of this work was to analyse the expression of the p53 oncosuppressor gene product, a proliferation regulator overexpressed in both malignant and non-malignant conditions, with the aim of better qualifying KS proliferation characteristics. METHODS: We analysed p53 expression in a group of transplanted, cyclosporin A-treated, KS patients by immunohistochemistry, utilizing the DO-7 (with and without the antigen retrieval pretreatment), and the PAb 240 monoclonal anti-p53 antibodies, the latter of which is able to detect a mutated epitope, and evaluating staining intensity and localization, whether cytoplasmic or nuclear. RESULTS: Seventy five percent of KS lesions from transplanted patients presented both nuclear and cytoplasmic positive p53 immunostaining with DO-7 antibody, thus demonstrating a presumably functional inactivation; one case also presented immunoreactivity with the PAb 240 antibody. CONCLUSIONS: On the basis of the results obtained and in the presence of lesion regression upon immunosuppression withdrawal, it may be concluded that KS in transplanted patients can be considered a non-malignant proliferative process, and that the cytoplasmic expression of p53 may stand for a functional inactivation pattern.

Female↗

PubMed1997

Growth hormone attenuates early left ventricular remodeling and improves cardiac function in rats with large myocardial infarction.

OBJECTIVES: We sought to investigate the cardiac effects of growth hormone (GH) administration during the early phase of pathologic remodeling in a rat model of large myocardial infarction (MI). BACKGROUND: Recent evidence suggests that exogenous administration of GH evokes a hypertrophic response and increases left ventricular (LV) function in vivo in rats with normal or chronically failing hearts. We hypothesized that these effects would attenuate ventricular remodeling early after MI. METHODS: Fifty-eight male rats underwent sham operation (n = 19) or had induced MI (n = 39). The day after the operation, the infarcted rats were randomized to receive 3 weeks of treatment with GH, 3 mg/kg body weight per day (n = 19) or placebo (n = 20). Echocardiography, catheterization and isolated whole heart preparations were used to define cardiac structure and function. RESULTS: Growth hormone caused hypertrophy of the noninfarcted myocardium in a concentric pattern, as noted by higher echocardiographic relative wall thickness at 3 weeks and by morphometric histologic examination. Left ventricular dilation was reduced in the GH-treated versus placebo group (echocardiographic LV diastolic diameter to body weight ratio 2.9 +/- 0.1 vs. 3.5 +/- 0.2 cm/kg; p < 0.05). In vivo and in vitro cardiac function was improved after GH treatment. Despite elevated insulin-like growth factor-1 (IGF-1) serum levels in GH-treated rats, myocardial IGF-I messenger ribonucleic acid was not different among the three groups, suggesting that an increase in its local expression does not appear necessary to yield the observed effects. CONCLUSIONS: These data demonstrate that early treatment of large MI with GH attenuates the early pathologic LV remodeling and improves LV function.

Animals↗

PubMed1997

Cardiac morphology and function in senescent rats: gender-related differences.

OBJECTIVES: We sought to better understand the effects of aging and gender on left ventricular (LV) structure and function. BACKGROUND: Cardiovascular disease in older persons is associated with increased mortality and morbidity. The influence of gender on age-related cardiac changes is incompletely characterized. METHODS: We studied 34 senescent, male and female, normotensive Fischer rats with transthoracic Doppler echocardiography and morphometric and histopathologic analyses. RESULTS: Male rats were larger (396 +/- 31 g vs. 282 +/- 35 g), and LV mass in males was greater (1.04 +/- 0.22 g vs. 0.67 +/- 0.13 g). However, wall and chamber dimensions normalized to body weight revealed proportionately thicker anterior and posterior walls in females. Relative wall thickness ratio (2 [Diastolic posterior wall thickness]/Diastolic LV internal chamber diameter) was greater in females, but abnormal fractional shortening and diastolic filling (E/A ratio) patterns were more common in males. Significant mitral regurgitation (MR) was sevenfold more common among males (88% vs. 12%, p < 0.001). Histopathologic analysis showed that the cardiac myocytes were larger, and there was greater LV fibrosis in males (both p < 0.001). CONCLUSIONS: Gender-related morphologic and functional differences are important to consider in cardiovascular assessment. Very old rats show significant gender differences in LV size and function. Male rat hearts are larger, thinner and more fibrotic and have indexes of diminished performance. The high prevalence of MR in male rats may play a crucial role in these gender differences.

Aging↗

PubMed1997

New Y-TZP powders for medical grade zirconia.

There is interest in using zirconia for biomedical applications as ball heads for total hip prostheses. Two potential types are under discussion: partially stabilized zirconia (PSZ) and tetragonal zirconia polycrystals (TZP) materials. Because of its enhanced material properties, TZP stabilized with yttria is favourable. To eliminate high amounts of natural radioactive impurities, the precursors are purified. The kind of precursor and purification method determine the powder impurity level. The disadvantage of Y-TZP is that the hydrothermal decomposition reaction method is that it depends very strongly on the grain size and the distribution of the stabilizing yttria within the zirconia grains. Thermodynamical and kinetic investigations on high purity coprecipitated and yttria-coated zirconia powders show different behaviours. Y-TZP materials based on yttria-coated zirconia powders show excellent mechanical strength of more than 1000 MPa, a Weibull modulus of up to 20 a! nd a fracture toughness of 9 MPa radical m. The material properties of Y-TZP ceramics based on coprecipitated powders and prepared under the same conditions are less attractive. It is expected that materials based on yttria-coated zirconia will show enhanced properties compared to materials derived from coprecipitated powders. Therefore Y-TZP materials derived from yttria-coated powders are very attractive as medical grade zirconia.

Journal Article↗

PubMed1997

Detection of arrhythmogenic cellular magnesium depletion in hip surgery patients.

The use of high-dose magnesium infusions in critically ill and surgical patients is increasing. This practice is associated with considerable risk of toxicity, as no reliable criteria are currently available to detect significant intracellular magnesium depletion. We have evaluated, before and after surgery, 33 elderly patients with hip fracture, by 24-h Holter ECG monitoring, Doppler echocardiography and serum chemistry; lymphocyte magnesium was measured using atomic absorption spectrophotometry. The severity of ventricular arrhythmias increased, and serum and mononuclear magnesium concentrations decreased significantly after surgery. Decreases in either serum magnesium concentrations > 0.125 mmol litre-1 or cellular magnesium > 6 nmol mg-1, but not serum or lymphocyte absolute magnesium concentrations, were associated with postoperative development of repetitive arrhythmias. Variations in serum magnesium concentrations correlated with intracellular decreases, and yielded good accuracy in predicting the postoperative worsening of arrhythmias. Thus perioperative differences in serum magnesium concentrations reflected intracellular variations and allowed us to identify patients with clinically relevant cellular magnesium depletion.

Aged↗

PubMed1997

Growth hormone and heart performance. A novel mechanism of cardiac wall stress regulation in humans.

OBJECTIVES: This study was designed to assess systolic wall stress and ventricular function in patients with deranged growth hormone secretion, in an attempt to elucidate the mechanisms of growth hormone interaction with heart performance. DESIGN: A case-control study. SUBJECTS: Thirty patients with active acromegaly, free of diabetes mellitus and coronary artery disease, and 25 subjects with congenital growth hormone deficiency were studied. Twelve growth hormone-deficient subjects were reevaluated after 12 months of recombinant human growth hormone therapy. Two groups of 30 normal subjects each were used as controls for the acromegalic and growth hormone-deficient patients, respectively. RESULTS: In the acromegalics, end-systolic wall stress was reduced (-20%; P < 0.01) due to ventricular wall thickening (+ 26%; P < 0.001), whereas cardiac output was significantly increased (+ 20%; P < 0.01). The velocity of fibre shortening was unchanged. In growth hormone-deficient subjects, end-systolic wall stress was markedly increased (+ 38%; P < 0.001) due to a significant reduction of ventricular wall thickness (- 28%; P < 0.001), whereas cardiac output was significantly decreased (-44%; P < 0.001). Replacement therapy with recombinant human growth hormone produced a partial correction of wall thickness and stress. Consequently, systolic performance and cardiac output improved significantly. CONCLUSION: This study demonstrates that growth hormone plays a role in the control of cardiac wall stress and performance through a mechanism mediated by the effect of growth hormone on myocardial tissue growth. The data may have therapeutic implications in cardiac diseases that lead to heart failure.

Acromegaly↗

PubMed1997

Validation of different methods to compare isovolumic cardiac function in isolated hearts of varying sizes.

Functional comparison of isolated hearts with different sizes has been difficult because function varies at different ventricular volumes. To date, no standard volume has been established. To determine the most accurate experimental approach, we tested five different methods to standardize volume in control hearts with different sizes but similar papillary muscle function and in hearts with concentric hypertrophy: intracardiac balloon volume (VB) = 120 microliters (M1). VB at diastolic pressure = 10 mmHg (M2) or diastolic wall stress = 4 kdyn/cm2 (M3), V1 = 25 microliters/100 g body weight (M4) and VB = 50% of volume at peak developed pressure (Vmax; M5). Systolic and diastolic functions of control groups were different using M1 and comparable using M2 or M5. M3 and M4 showed borderline significant differences. We concluded that M5 and M2 were suitable to compare function among hearts of different sizes. If diastolic compliance is of interest, as in concentric hypertrophy, parameter-volume curves should be normalized by Vmax to compare function at corresponding points of the Frank-Starling curve (e.g., at 50% of Vmax, M5).

Aging↗

PubMed1997

Consequences of growth hormone deficiency on cardiac structure, function, and beta-adrenergic pathway: studies in mutant dwarf rats.

To evaluate GH's role in cardiac physiology and its interrelationship with the beta-adrenergic system, we studied GH-deficient dwarf (dw/dw) and control rats in 4 groups of 20 each: dwarf group receiving placebo, dwarf-GH group receiving 2 mg/kg GH, dwarf-GH-propranolol group receiving 2 mg/kg GH and 750 mg/liter propranolol, and a control group of Lewis rats receiving placebo. Dwarf rats showed reduced left ventricular weight and myocyte cross-sectional area, and impaired cardiac performance in vitro. Left ventricular pressure-volume curves showed a shift upward and leftward, indicating reduced distensibility. These abnormalities reversed after GH treatment regardless of concomitant propranolol administration. Although isoproterenol responsiveness was reduced in dwarf rats, there were no differences in beta-adrenergic receptor density, affinity, Na+,K+-adenosine triphosphatase activity, or adenylyl cyclase activity. In summary, myocyte size, cardiac structure, myocardial contractility, and distensibility are abnormal in GH deficiency. The effects of GH are not mediated by the beta-adrenergic pathway, which, in turn, is unaffected by changes in the GH-insulin-like growth factor I axis. Thus, GH plays a regulatory role in normal cardiac physiology that is independent of the beta-adrenergic system.

Adrenergic beta-Agonists↗

PubMed1997

Deregulated expression of p27(Kip1) in human breast cancers.

Protein complexes composed of cyclins and cyclin-dependent kinases control the orderly progression of mammalian cells through the cell cycle. The p27(Kip1) protein belongs to a family of cyclin-dependent kinase-inhibitory proteins that are negative regulators of cell cycle progression and have been proposed as candidate tumor suppressor genes. However, the p27(Kip1) gene is only rarely mutated in human primary breast carcinomas and breast cancer cell lines. To further address the role of p27(Kip1) in the development of human tumors, we determined by Western blot analysis the levels of expression of the p27(Kip1) protein in a series of human cancer cell lines and found that this protein is expressed at high levels in many of these cell lines, even during exponential growth. The levels of p27(Kip1) were significantly associated with the levels of cyclins D1 and E. In contrast to the high level of p27(Kip1) in breast cancer cell lines, three cell lines established from normal mammary epithelium expressed low levels of this protein. Cell synchronization studies demonstrated deregulation of the expression of p27(Kip1) throughout the cell cycle in two breast cancer cell lines but normal regulation in a normal mammary epithelial cell line. Immunohistochemical studies on p27(Kip1) expression in 52 primary human breast cancers indicated that this protein was also expressed at relatively high levels in 44% of the tumor samples, but it was barely detectable or undetectable in the remaining 56% of the samples. Additional studies are required to determine why some breast cancer cells express relatively high levels of p27(Kip1) despite its known role as an inhibitor of cell cycle progression.

Biomarkers, Tumor↗

PubMed1996

Regulation of intracellular magnesium in ascites cells: involvement of different regulatory pathways.

Extracellular ATP causes 40% stimulation of Mg2+ efflux from Ehrlich ascites tumor cells (EATC) incubated under 0-trans conditions. ATP also causes a threefold increase of arachidonic acid (AA) metabolite release from [3H]AA-preloaded EATC, indicating that, under these experimental conditions, it induces phospholipase A2 (PLA2) activation. ATP-induced Mg2+ efflux can be prevented by cyclooxygenase inhibition with indomethacin or lysine acetylsalicylate, but not by 5-lipooxygenase inhibition with BWA4C. Mg2+ efflux is also directly stimulated by exogenous AA in a concentration-dependent manner. This phenomenon involves PKA as it is virtually abolished by the specific inhibitor 8-bromoadenosine-3',5'-cyclic monophosphothioate. While stimulating Mg2+ efflux, exogenous AA also increases cAMP content of EATC and this effect can be prevented by cyclooxygenase inhibition. Measurements in mag-fura-2-loaded EATC reveal that stimulation of Mg2+ efflux does not correlate with significant fluctuations of [Mg2+]i. This suggests that Mg2+ efflux is compensated for by mobilization of bound Mg2+, leaving [Mg2+]i unaltered. Altogether these data indicate that Mg2+ efflux can be modulated by extracellular stimuli capable of activating PLA2. This modulation is triggered by cyclooxygenase products which, by activating adenylcyclase, determine an elevation of cAMP. This intracellular messenger upregulates Na-dependent Mg2+ efflux.

Adenosine Triphosphate↗

PubMed1996

Chronic growth hormone treatment in normal rats reduces post-prandial skeletal muscle plasma membrane GLUT1 content, but not glucose transport or GLUT4 expression and localization.

Whether skeletal muscle glucose transport system is impaired in the basal, post-prandial state during chronic growth hormone treatment is unknown. The current study was designed to determine whether 4 weeks of human growth hormone (hGH) treatment (3.5 mg/kg per day) would impair glucose transport and/or the number of glucose transporters in plasma membrane vesicles isolated from hindlimb skeletal muscle of Sprague-Dawley rats under basal, post-prandial conditions. hGH treatment was shown to have no effect on glucose influx (Vmax or K(m)) determined under equilibrium exchange conditions in isolated plasma membrane vesicles. Plasma membrane glucose transporter number (Ro) measured by cytochalasin B binding was also unchanged by hGH treatment. Consequently, glucose transporter turnover number (Vmax/Ro), a measure of average glucose transporter intrinsic activity, was similar in hGH-treated and control rats. hGH did not change GLUT4 protein content in whole muscle or in the plasma membrane, and muscle content of GLUT4 mRNA also was unchanged. In contrast, GLUT1 protein content in the plasma membrane fraction was significantly reduced by hGH treatment. This was associated with a modest, although not significant, decrease in muscle content of GLUT1 mRNA. In conclusion, high-dose hGH treatment for 4 weeks did not alter post-prandial skeletal muscle glucose transport activity. Neither the muscle level nor the intracellular localization of GLUT4 was changed by the hormone treatment. On the contrary, the basal post-prandial level of GLUT1 in the plasma membrane was reduced by hGH. The mRNA data suggest that this reduction might result from a decrease in the synthesis of GLUT1.

Animals↗

PubMed1996

Differential cardiac effects of growth hormone and insulin-like growth factor-1 in the rat. A combined in vivo and in vitro evaluation.

BACKGROUND: Despite their increasing clinical use and recent evidence that growth hormone (GH) and insulin-like growth factor-1 (IGF-1) target the heart, there has been no systematic investigation of the effects of GH and IGF-1 on the cardiovascular system. METHODS AND RESULTS: Sixty normal but growing adult female rats were randomized to receive 4 weeks of treatment with GH (3.5 mg.kg-1.d-1), IGF-1 (3 mg.kg-1.d-1), a combination of the two, or placebo. Transthoracic echocardiograms were performed at baseline and at 2 weeks and 4 weeks of treatment. After the final echocardiography, rats underwent either closed-chest left ventricular (LV) catheterization or Langendorff perfusion studies. Myocyte diameter and interstitial tissue fraction were assessed by morphometric histology. Echocardiographic and ex vivo data demonstrated a LV hypertrophic response in all three groups of treated animals that was most marked in the GH group, which alone exhibited a concentric growth pattern (relative wall thickness, 0.52 versus 0.42 to 0.44 in the other groups; P < .001). At 4 weeks, cardiac index was significantly higher and total systemic vascular resistance was lower in all groups of treated animals than in control animals (both P < .001), whereas arterial blood pressure did not differ significantly. All indexes of in vivo and in vitro cardiac function were higher in GH- and IGF-1-treated rats than in control animals, whereas combination therapy yielded a blunted effect. Myocyte diameter was increased in all three treated groups without an increase in interstitial tissue. CONCLUSIONS: Exogenous administration of GH and IGF-1 in the normal adult rat induces a cardiac hypertrophic response without development of significant fibrosis. Cardiac performance is increased both in vivo and in the isolated heart.

Animals↗

PubMed1996

Detection of oncogene mutation from neoplastic colonic cells exfoliated in feces.

PURPOSE: Best chances of a cure from colorectal cancer are obtained before metastatic spread. Lack of specific tests allowing early diagnosis of the tumor accounts for investigation of gene alterations involved in carcinogenesis by a noninvasive method. In the present study, K-ras codons 12 and 13 mutations were studied in neoplastic cells shed from the bowel into the stool and those contained in the tumor and normal mucosa. Moreover, healthy patients and a few others with precancerous conditions were examined. METHODS: Stool, tumor, and mucosa samples were taken from 25 patients with colorectal adenocarcinoma. Stool and mucosa samples were obtained from 11 healthy patients, and stool, pathologic bowel tissue, and normal mucosa samples were obtained from 3 patients with adenoma (1) or ulcerative colitis (2). Polymerase chain reaction amplification and restriction enzyme analysis were performed. RESULTS: K-ras codon 12 mutations were detected in both tumor and stool samples of 10 cancer patients, and no gene alterations were observed in 14 patients. In one patient with a tumor, a mutation was shown in only the tumor tissue. The agreement rate in tumor and stool analysis was 96 percent. A normal pattern of K-ras codons 12 and 13 was observed in the bowel mucosa. All stool and mucosa samples from healthy patients were not altered in K-ras. Agreement was registered between samples taken from patients with preneoplastic lesions. CONCLUSIONS: These preliminary findings show a high rate of accuracy in the investigation of K-ras alterations in the colorectal cells shed into the feces, suggesting that such an approach could be used to study other gene alterations and, prospectively, to identify early colorectal cancers.

Aged↗

PubMed1996

Prognostic significance of cytoplasmic p53 overexpression in colorectal cancer. An immunohistochemical analysis.

p53 overexpression was studied by immunohistochemistry in 96 consecutive colorectal cancer patients, subdividing positive specimens according to two staining patterns: cytoplasmic or nuclear. Forty-seven per cent of the cases were p53 positive, a significant correlation being found with Dukes' stage (P = 0.0036). A prevalence of nuclear staining was observed in Dukes' B and cytoplasmic in Dukes' D stages. After 36 months, 23% of the patients had a recurrence, and 45% were p53 positive, all Dukes' C-D stage with cytoplasmic staining. The Kaplan-Meier curve showed a significant correlation between p53 cytoplasmic staining and disease-free survival period (P = 0.002). With respect to disease-free survival, the Cox proportional hazard regression test, comparing p53 positivity with Dukes' stage, showed the latter to be the most significant variable. In our series of patients, advanced Dukes' stage tumours were localised in the right colon, where a higher percentage of p53 positivity (67% versus 40% of the left side), as well as a higher frequency of cytoplasmic staining was observed. In conclusion, from the data obtained, a strong correlation between p53 cytoplasmic staining and patient prognosis is clearly indicated.

Adult↗

PubMed1996

Immunohistochemical quantitation of 4-aminobiphenyl-DNA adducts and p53 nuclear overexpression in T1 bladder cancer of smokers and nonsmokers.

An immunoperoxidase method, using a monoclonal antibody which recognizes 4-aminobiphenyl (4-ABP)-DNA adducts, was developed for the detection and quantitation of DNA damage in bladder tissue and applied to stored paraffin blocks of transurethral resection specimens of 46 patients with T1 bladder cancer. Mean relative staining intensity for 4-ABP-DNA adducts was significantly higher in current smokers (275 +/- 81, n = 24) compared to nonsmokers (113 +/- 71, n = 22) (P < 0.0001). There was a linear relationship between mean levels of relative staining and number of cigarettes smoked with lower levels in the 1-19 cig/day group (205 +/- 30, n = 5), compared to the 20-40 (289 +/- 40, n = 7) and the >40 cig/day group (351 +/- 57, n = 3)(P < 0.001). Nuclear overexpression of p53, analyzed by immunoperoxidase staining, was observed in 27 (59%) of the 45 stage T1 tumors analyzed. There was a significant correlation between p53 overexpression and recurrence of disease (odds ratio = 12.3, P < 0.01). Nuclear staining of p53 was also correlated with smoking status, cig/day and 4-ABP-DNA adducts. This work demonstrates that the immunohistochemical method has sufficient sensitivity for detection of 4-ABP-DNA adducts in human bladder samples. The method has several advantages including small sample size, the possibility of retrospective analysis of stored paraffin blocks, the ability to analyze binding in specific cell types, and a relatively low cost.

Aged↗

PubMed1996

Exogenously administered growth hormone and insulin-like growth factor-I alter intracellular Ca2+ handling and enhance cardiac performance. In vitro evaluation in the isolated isovolumic buffer-perfused rat heart.

It has been proposed that chronic treatment with growth hormone (GH) or insulin-like growth factor-I (IGF-I) in the rat may enhance cardiac function in vivo. To confirm these findings and elucidate the mechanisms by which cardiac function is modulated, we studied isolated buffer-perfused rat hearts after 4 weeks of treatment with high doses of GH and IGF-I alone or in combination. Mechanical parameters were measured at 50% of the intracardiac balloon volume at which maximal developed pressure (DevP) occurred. EC50 of the force-Ca2+ relationship and maximal Ca(2+)-activated systolic wall stress (max sigma s) were assessed by increasing Ca2+ in the perfusate in a stepwise fashion and plotting systolic wall stress (sigma s) versus intracellular peak systolic Ca2+, measured by the aequorin bioluminescence method. We found a marked increase of systolic pressure (Ps), DevP, and (+dP/dt)/DevP in the treated groups compared with the control group. The combination group showed a blunted effect. sigma s was increased in all treated groups for a perfusate Ca2+ concentration of > 1.5 mmol/L. The enhanced systolic performance can be explained by an increase of the overall Ca2+ responsiveness due to an increased maximal response to Ca2+ even though the EC50 of the Ca(2+)-dose response was also slightly increased. Ps was further enhanced by an increase of the relative wall thickness induced by the treatment. Diastolic pressure, diastolic Ca2+, and the amplitude and time course of the Ca2+ transient were not influenced by any treatment protocol. All treatments caused increases of body and heart weight. These data support the hypothesis that both IGF-I and GH directly affect cardiac performance by altering cardiac geometry as well as by enhancing max sigma s.

Animals↗

PubMed1995

Treatment with growth hormone and IGF-I in growing rats increases bone mineral content but not bone mineral density.

Human growth hormone (hGH) and insulin-like growth factor I (IGF-I) both stimulate bone formation and have been proposed as therapeutic agents for osteoporosis. We examined the effect of hGH and IGF-I alone and in combination on bone size, bone mineral content (BMC), and bone mineral density (BMD) in 10- to 12-week old growing female Sprague-Dawley rats. Sixty rats were assigned to treatment with either placebo, hGH, IGF-I, or both for 4 weeks. After 4 weeks, the right femurs and tibias were excised, and ex vivo BMC and the area of the tibia and femur were measured by dual-energy X-ray absorptiometry (DXA); volume of these bones was measured by Archimedes' principle. In addition, proximal tibial bone density was measured directly by peripheral quantitative computerized tomography (pQCT). Bone length, area, and volume in all treated groups was greater than controls. Areal bone density by DXA (BMC/area) was higher in IGF-treated rats and lower in GH-treated rats than in controls. Volumetric bone density (BMC/volume) was lower in treated groups than in controls. Measurements by pQCT confirmed that true bone density was lower in all treated groups than in controls. We conclude that treatment with hGH or IGF-I increased bone size and mineral content but decreased bone density in growing rats. Because areal correction of BMC did not adequately correct for the increased bone volume in IGF-treated rats, results of areal bone density by DXA should be interpreted with caution when treatment causes a disparity in bone size between groups.

Animals↗

PubMed1995

Optimal determination of right ventricular filling dynamics in systemic hypertension.

To determine the optimal method of normalizing peak filling rate (PFR) determinations and apply it to the assessment of right ventricular (RV) and left ventricular (LV) filling characteristics and their interactions, 41 subjects with hypertension and 40 matched normals underwent echo-Doppler and nuclear study. Conventional normalization of PFR to end-diastolic volume (EDV) yielded poor correlations between nuclear- and echo-derived PFR (RV, r = 0.34; LV, r = 0.42), whereas nuclear and echo PFR normalized to stroke volume (SV) were closely correlated (RV, r = 0.87; LV, r = 0.92). Further, use of PFR normalized to SV revealed to close relation between RV and LV filling characteristics. Multivariate analysis confirmed that, in contrast to normalization to EDV or early to late filling-velocity ratios (E/A), peak filling rate normalized to SV was independent of ejection fraction and heart rate. In addition, RV filling impairment was related to LV filling impairment, and the effects of hypertension eliminated the independent influence of age on both LV and RV filling. In conclusion, normalization of PFR to SV may be preferable to use of EDV or E/A in evaluating RV and LV filling dynamics.

Adult↗