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Biomedical subjects

S Giannini

Publications and source records attributed to S Giannini.

At least 91 records · Page 5Linked to original sources

Biomechanical, scanning electron microscopy, and microhardness analyses of the bone-pin interface in hydroxyapatite coated versus uncoated pins.

OBJECTIVE: To evaluate the bone-pin interface in hydroxyapatite coated versus uncoated pins. DESIGN: Eighty-four bicylindrical stainless steel external fixation pins were implanted in a test group of 14 sheep. One-half of the pins were coated with hydroxyapatite and the rest remained uncoated. INTERVENTION: Six coated pins were implanted in the left tibia of seven sheep, and six uncoated pins were implanted in the left tibia of the other seven sheep. In all sheep, the right tibia was left intact. During pin implantation, the final insertion torque was measured, and a linear external fixator was mounted on the pins. Then the medial tibial mid-diaphysis was exposed and a 5-mm resection osteotomy was performed. The sheep were killed six weeks after surgery. MAIN OUTCOME MEASURES: The extraction torque was measured on four pins removed from each sheep. Radiographic pin tract rarefaction was measured on all the pins. Two pins from each sheep were used for histologic, scanning electron microscopy (SEM), and microhardness analysis. Histomorphometric analysis was carried out on the SEM specimens at x 36 magnification. RESULTS: Radiographic pin tract rarefaction was significantly lower in the hydroxyapatite coated pins than in the uncoated pins (P < 0.001). Group average insertion torque was 960 +/- 959 N/mm in the hydroxyapatite coated pins, and 709 +/- 585 N/mm in the uncoated pins (p = not significant). Group average extraction torque was 1485 +/- 1308 N/mm and 298 +/- 373 N/mm, respectively (p = 0.0001). Histomorphometric analysis showed that the group average bone-pin contact was 50.7 +/- 16.9% in the hydroxyapatite coated pins and 27.6 +/- 7.1% in the uncoated pins (p < 0.01). Microhardness analysis showed that bone tissue close to the pins was softer than bone tissue far from them. CONCLUSION: Hydroxyapatite coating is an effective method of refining the bone-pin interface and may improve the clinical results of the external fixation technique.

Animals↗

Bone density and skeletal metabolism in patients with orthotopic ileal neobladder.

The interposition of a bowel segment as a bladder substitute into the urinary tract may result in impaired calcium metabolism. We studied 25 male patients (aged 45 to 77 yr) who had undergone a Vescica Ileale Padovana (VIP) reconstruction following cystectomy 29 to 75 mo before. Bone mineral density of the spine and femur was measured by dual x-ray absorptiometry. Blood and 24-h urine samples were analyzed for the main parameters of bone metabolism. Sixteen healthy men were enrolled as a control group. Although blood pH did not differ between patients and control subjects, VIP subjects showed lower levels of plasma HCO3- (P < 0.005) and higher serum chloride (P < 0.001). Bone alkaline phosphatase was higher (P < 0.001), and urine calcium, phosphate, and creatinine levels were lower in VIP patients (P < 0.01, P < 0.01, and P < 0.05, respectively). Bone mineral density at the femoral neck (P < 0.03) and Ward's triangle (P < 0.05) was decreased in VIP patients. When subdivided according to time since operation, patients who had the ileal neobladder implanted for a shorter period of time showed lower blood pH (P < 0.03) and urine calcium (P < 0.05) levels and higher urinary hydroxyproline (P < 0.02). Duration of the ileal neobladder was positively correlated with PTH (r = 0.46, P < 0.03) and blood pH (r = 0.47, P < 0.02). Furthermore, pH values were positively correlated with urine calcium (r = 0.48, P < 0.02). In conclusion, in patients with ileal neobladder, a mild metabolic acidosis is responsible for an increased bone turnover and lower bone mass. Moreover, a decrease over time in the absorption capacity of the ileal pouch might result in calcium malabsorption, which represents an additional risk factor for reduced bone mass in these patients.

Aged↗

High glucose level unmasks a genetic predisposition to enhanced extracellular matrix production in mesangial cells from the Milan normotensive strain.

A growing body of evidence indicates that the individual genetic background plays a role in the pathogenesis of diabetic glomerular disease by either favoring or protecting against injury produced by hyperglycemia. Two genetically related rat strains, the Milan normotensive strain (MNS) and the Milan hypertensive strain (MHS) display different susceptibilities to develop glomerulosclerosis with age. Glomerular sclerosing lesions occur in the MNS rats, which remain normotensive throughout their entire life-span, but not in the MHS rats, despite the presence of arterial hypertension. Previous studies have reported that extracellular matrix production and cell proliferation increased with donor-aging in mesangial cells isolated from MNS rats, but not in those from MHS rats, thus suggesting the existence of an inherited defect in the regulation of cell and matrix turnover, which translates into an abnormal response to growth-promoting stimuli favoring the development of glomerulosclerosis. In the study presented here, it was hypothesized that, in addition to donor-aging, other independent risk factors for the development of glomerular disease, such as metabolic injury by hyperglycemia, would be able to trigger and/or precipitate the occurrence of these changes in mesangial cells from the susceptible normotensive strain, but not in those from the protected hypertensive strain. To test this hypothesis, mesangial cells obtained from these rat strains (before the onset of either glomerulosclerosis or hypertension) were used to assess the effects of prolonged (4 wk) exposure to high (30 mmol/L) versus normal (5.5 mmol/L) glucose concentrations on extracellular matrix and cytokine production and cell proliferation. The accumulation and/or gene expression of the matrix components fibronectin, laminin, and collagen IV, and of the cytokines insulin-like growth factor-I (IGF-I) and transforming growth factor-beta (TGF-beta) did not change under normal glucose and increased progressively in response to high glucose in both MNS and MHS cells. These increases, with the exception of the increment in TGF-beta gene expression, were significantly more pronounced in MNS cells than in MHS cells. In contrast, the proliferative response to serum was not affected by high glucose, but increased in MNS cells, and decreased, although not significantly, in MHS cells during the 4-wk period, thus mimicking the changes previously observed in these rat strains as a function of age. These results indicate that high glucose unmasks a genetic tendency to produce increasing amounts of extracellular matrix, not yet evident under normal glucose conditions, and suggest that a genetically determined propensity of mesangial cells to hyperrespond to chronic hyperglycemia may be implicated in the pathogenesis of diabetic glomerular disease.

Animals↗

Upregulation of mesangial growth factor and extracellular matrix synthesis by advanced glycation end products via a receptor-mediated mechanism.

Enhanced advanced glycosylation end product (AGE) formation has been shown to participate in the pathogenesis of diabetes-induced glomerular injury by mediating the increased extracellular matrix (ECM) deposition and altered cell growth and turnover leading to mesangial expansion. These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. Moreover, cells grown on BSA-AGE showed increased ECM protein and mRNA levels versus cells cultured on BSA, whereas cell proliferation was unchanged in human mesangial cells and slightly reduced in rat mesangial cells. Growing cells on BSA-AM did not affect any of the measured parameters. Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. The parallelism with increased ECM production raises the speculation that the enhanced synthesis of these growth factors resulting from advanced nonenzymatic glycation participates in the pathogenesis of hyperglycemia-induced mesangial expansion.

Animals↗

Calciotropic hormones and nephrolithiasis.

In recurrent calcium stone formers interfering factors or changes in receptor sensitivity may alter the interrelationships among calcium-regulating hormones, and hormonal behavior often does not fit with the theoretical assumptions. The vitamin D system appears to have the most important metabolic and clinical effects. Abnormal up-regulation of the synthesis of calcitriol and the consequent parathyroid hormone (PTH) suppression can induce hypercalciuria. Consequently, the hypocalciuric effect of thiazide would be caused by an enhanced response to PTH and by a reduction in 1,25(OH)2-vit D. A negative role of vitamin D on the skeleton has been observed in the presence of a negative calcium balance. Moreover, vitamin D also plays a role in urine oxalate excretion. PTH seems not to be directly stimulated in hypercalciuria and recurrent calcium nephrolithiasis, and patients with hyperparathyroidism and recurrent calcium nephrolithiasis show a similar degree of bone demineralization, irrespective of the presence of absence of the so-called 'primary hyperparathyroidism.' Calcitonin plays a contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to be strictly related to dietary calcium intake. A higher sensitivity of thyroid C cells, particularly in absorptive hypercalciuric patients, could be related to the pathogenesis of hypercalciuria and contribute to its persistence.

Calcitonin↗

Cytokine levels in osteoarthrosis patients undergoing mud bath therapy.

Osteoarthritis is an important rheumatic condition characterized by the progressive destruction of cartilage. The pathophysiologic phenomena leading to the pathologic changes in the joint appear to result from biomechanical factors and activation of final common pathways of tissue damage influencing chondrocyte homeostasis and a functional program. Several cytokines and growth factors are reported to be responsible for inflammation and cartilage degradation. Among these, IL-1 and TNF alpha have been suggested as important in promoting cartilage inflammation and tissue destruction, while IGF I has a protective influence on cartilage structure. Chondrocytes and their metabolism have gained interest as targets of drug intervention; the results of this study confirm that mud bath therapy is also able to influence chondrocyte activities. Our data suggest that mud bath therapy influences cytokines related to osteoarthrosis pathomechanism and maintenance, and encourage further investigations to evaluate possible synergism between pharmacological treatment and mud bath therapy.

Aged↗

The caa3 terminal oxidase of Bacillus stearothermophilus. Transient spectroscopy of electron transfer and ligand binding.

The thermophilic bacterium Bacillus stearothermophilus possesses a caa3-type terminal oxidase, which was previously purified (De Vrij, W., Heyne, R. I. R., and Konings, W. N. (1989) Eur. J. Biochem. 178, 763-770). We have carried out extensive kinetic experiments on the purified enzyme by stopped-flow time-resolved optical spectroscopy combined with singular value decomposition analysis. The results indicate a striking similarity of behavior between this enzyme and the electrostatic complex between mammalian cytochrome c and cytochrome c oxidase. CO binding to fully reduced caa3 occurs with a second order rate constant (k = 7.8 x 10(4)M-1 s-1) and an activation energy (E* = 6.1 kcal mol-1) similar to those reported for beef heart cytochrome c oxidase. Dithionite reduces cytochrome a with bimolecular kinetics, while cytochrome a3 (and CuB) is reduced via intramolecular electron transfer. When the fully reduced enzyme is mixed with O2, cytochrome a3, and cytochrome c are rapidly oxidized, whereas cytochrome a remains largely reduced in the first few milliseconds. When cyanide-bound caa3 is mixed with ascorbate plus TMPD, cytochrome c and cytochrome a are synchronously reduced; the value of the second order rate constant (k = 3 x 10(5) M-1 s-1 at 30 degrees C) suggests that cytochrome c is the electron entry site. Steady-state experiments indicate that cytochrome a has a redox potential higher than cytochrome c. The data from the reaction with O2 reveal a remarkable similarity in the kinetic, equilibrium, and optical properties of caa3 and the electrostatic complex cytochrome c/cytochrome c oxidase.

Animals↗

Platelet-activating factor enhances production of insulin-like growth factor binding proteins in a human adenocarcinoma cell line (HEC-1A)

We have recently demonstrated the existence of an autocrine growth loop driven by platelet-activating factor (PAF) in the human endometrial adenocarcinoma. cell line HEC-1A. To investigate a possible cooperation between PAF and the insulin-like growth factor (IGF) system in this cell line, the effect of PAF on insulin-like growth factor binding protein (IGFBP) production as well as binding and biological activities of IGF-I, IGFv-II, and the analog Des(1-3)IGF-I have been evaluated. Analysis of self- and cross-displacement curves of [125I]IGF-I binding to HEC-1A cells indicates the presence of a single class of binding sites, with affinity constants of 1-4 nM for IGF-I and IGF-II and 70 nM for Des(1- 3)IGF-I, which binds to IGFBPs with lower affinity. Insulin does not apparently bind to this binding site. Moreover, the addition of increasing concentrations of IGF-I leads to a paradoxical increase of binding. These results indicate a similarity of this binding site to IGFBPs. The presence of IGFBPs has been demonstrated by Western ligand blot analysis of HEC-1A conditioned medium which shows the presence of two bands of 32-34 and 40-45 kDa. By Western immunoblotting analysis, the two bands were respectively identified as IGFBP-2 and IGFBP-3. Incubation with PAF (1 microM) highly increases the release of the two IGFBPs from the cells. Such an effect is inhibited by the PAF receptor antagonist L659,989, by the PKC inhibitor sangivamycin, and by the tyrosine kinase inhibitor genistein. PAF also induces a time-dependent increase of mRNA expression for IGFBP-3, suggesting an effect on synthesis of this protein. IGF-I and IGF-II (0.1-100 nM) are almost ineffective in inducing [3H]thymidine incorporation, whereas a slight proliferative effect is observed with Des(1-3)IGF-I which also increases PAF synthesis. These data demonstrate a modulatory action of PAF on IGFBP secretion in HEC-1A cells and indicate that the IGF system plays a minor, if any, modulatory role on proliferation of this cell line.

Adenocarcinoma↗

Increased activity of the insulin-like growth factor system in mesangial cells cultured in high glucose conditions. Relation to glucose-enhanced extracellular matrix production.

Recent evidence suggests that several growth factors participate in diabetic glomerular disease by mediating increased extracellular matrix accumulation and altered cell growth and turnover leading to mesangial expansion. Transforming growth factor (TGF)-beta has been demonstrated to be upregulated both in vivo and in vitro, whereas studies on the activity of the renal insulin-like growth factor (IGF) system in experimental diabetes have provided conflicting results. We investigated the effects of prolonged exposure (4 weeks) of cultured human and rat mesangial cells to high (30 mmol/l) glucose vs iso-osmolar mannitol or normal (5.5 mmol/l) glucose levels on: 1) the autocrine/paracrine activity of the IGF system (as assessed by measuring IGF-I and II, IGF-I and II receptors, and IGF binding proteins); and, in parallel, on 2) TGF-beta 1 gene expression; 3) matrix production; and 4) cell proliferation. High glucose levels progressively increased the medium content of IGF-I and the mRNA levels for IGF-I and IGF-II, increased IGF-I and IGF-II binding and IGF-I receptor gene expression, and reduced IGF binding protein production. TGF-beta 1 transcripts and matrix accumulation and gene expression were increased in parallel, whereas cell proliferation was reduced. Iso-osmolar mannitol did not affect any of the above parameters. These experiments demonstrated that high glucose levels induce enhanced mesangial IGF activity, together with enhanced TGF-beta 1 gene expression, increased matrix production, and reduced cell proliferation. It is possible that IGFs participate in mediating diabetes-induced changes in matrix turnover leading to mesangial expansion, by acting in a paracrine/autocrine fashion within the glomerulus.

Animals↗

Continuous and cyclical clodronate therapies and bone density in postmenopausal bone loss.

OBJECTIVE: To evaluate the effectiveness of different clodronate regimens in postmenopausal osteoporosis. METHODS: In groups of 20, 60 women were randomly assigned to one of three treatments: oral calcium, 1000 mg/day; oral calcium plus oral clodronate, 400 mg/day; oral calcium plus oral clodronate, 400 mg/day for 30 days, followed by a 60-day period of calcium supplement alone. This last regimen was repeated four times in the 12-month study period. RESULTS: Patients who received calcium alone showed a decline in spinal bone mass, both after 6 and 12 months (P < .03 and P < .005, respectively); femoral density in this group also decreased after 6 and 12 months (P < .002 and P < .05, respectively). On the other hand, both clodronate-treated groups had increased levels of lumbar bone mass compared with controls, both after 6 and 12 months of therapy. However, at the end of the study, patients treated with cyclical clodronate had higher spinal bone mass compared with those treated continuously (3.32 +/- 0.71 versus 0.43 +/- 0.89%, P < .02). After 6 months, femoral bone density was significantly higher both in subjects treated with clodronate, both cyclically and continuously (P < .01), compared with controls. Continuous clodronate treatment resulted in a clear fall in biochemical indices of bone resorption, together with a consequent decrease in osteocalcin at 6 (P < .02) and 12 months (P < .003) and a significant increase in parathyroid hormone after 12 months (P < .001) of therapy. CONCLUSION: One-year treatment with clodronate induces a gain in bone mass, especially in the spine. The continuous regimen does not result in any further benefit in lumbar bone density over the cyclical one, probably because of a greater suppression of bone turnover.

Absorptiometry, Photon↗

Long-term results of spine surgery in Duchenne muscular dystrophy.

We report the long-term orthopaedic and functional results of segmental spinal instrumentation and fusion in 30 Duchenne patients. Twenty-nine had a mean 59% correction of scoliosis with post-operative immobilization in a brace of only three months on average and with a very limited loss of correction over time. One died after cardiac arrest. The mean vital capacity preoperatively was 57 +/- 17% with a decrease to 34 +/- 13% at 3.9 +/- 2 yr after surgery. The sitting position, aesthetic improvement and the quality of life after spinal fusion have been positively evaluated by the large majority of the patients and their parents. Head control was lost in the 14 patients who developed a more severe extension contracture of the neck measured as a significantly longer chin-sternum distance. More than 90% would have the operation or would give their consent again for their son having the operation.

Adolescent↗

Insulin-like growth factor (IGF) system components in human prostatic cancer cell-lines: LNCaP, DU145, and PC-3 cells.

BACKGROUND: Evidence has been accumulating that in many tumors, insulin-like growth factors (IGFs) promote cancer cell growth in an autocrine/paracrine manner via the IGF-I receptor. In an effort to understand the role of IGFs in prostate cancer cell growth, we characterized the IGF system components produced by human prostatic cancer cell-lines, LNCaP, DU145, and PC-3, grown in serum-free medium. METHODS: IGFs, their receptors, and IGF binding proteins (IGFBPs) produced by the three human prostate cell lines were characterized by reverse transcriptase-polymerase chain reaction (RT-PCR), radioimmunoassay (RIA), Western ligand blot, Western immunoblot, and Northern blot analyses. RESULTS: mRNA for IGF-II and receptors for IGF-I and IGF-II were detected in all three cell-lines by RT-PCR. In contrast to the published study, only LNCaP cells expressed a trace amount of IGF-I mRNA. RIA on conditioned media collected from these cells revealed that all three cell-lines produced measurable IGF-II but not IGF-I. Western Ligand blot, Western immunoblot, and Northern blot analyses revealed that LNCaP, DU145, and PC-3 cells expressed IGFBP-2, IGFBP-2/-3/-4/-6, and IGFBP-2/-3/-4/-5/-6, respectively. IGF-II stimulated [3H]thymidine incorporation into DNA in DU145 and PC-3 cells significantly although the effect was small. DNA synthesis in PC-3 cells but not in LNCaP and DU145 cells was significantly inhibited by the IGF-I receptor-specific monoclonal antibody. CONCLUSION: Theses results suggest potentially important roles of IGFs and IGFBPs in prostate cancer cell growth, and that in particular, IGF-II may play a critical role in prostate cancer cell growth.

Antibodies, Monoclonal↗

Long-term efficacy and tolerability of simvastatin in a large cohort of elderly hypercholesterolemic patients.

The long-term efficacy and tolerability of simvastatin, a 3-hydroxy-3-methylglutaryl-co-enzyme A (HMG-CoA) reductase inhibitor, was assessed during a 24-month follow-up period in 168 elderly hypercholesterolemic patients. After completing a 4 week double blind dose ranging study with simvastatin, 47 males and 122 females over 62 years of age with type II hyperlipidemia, a total cholesterol level above 6.5 mmol/l and clinically manifest cardiovascular disease were included in this extended study. A total of 159 patients completed the 12-month follow-up period and 141 patients were monitored over the full 24 months. All patients were started on 10 mg simvastatin once daily and the dosage was increased until the target levels of low density lipoprotein (LDL) cholesterol between 2.3 mmol/l (90 mg/dl) and 3.6 mmol/l (140 mg/dl) were reached. Fifty percent of patients reached the targeted LDL cholesterol goal of < 3.6 mmol/l (140 mg/dl) during the study. At study completion, 65 patients (39%) were taking 40 mg simvastatin per day, 56 patients (33%) 20 mg, 42 patients (25%) 10 mg and 5 patients (3%) only used 5 mg per day. Sixteen patients (9%) received concomitant lipid lowering therapy. Over 2 years, the mean decrease in LDL cholesterol ranged from 36% to 38%, the median decrease in triglycerides was 12% to 19% and the mean increase in high density lipoprotein (HDL) cholesterol ranged from 9% to 10%, respectively. Seven patients discontinued simvastatin because of adverse clinical or laboratory events, but only in two (1.1%) was this considered to be drug-related. Side-effects were mild and most frequently gastrointestinal in nature. Mean changes in asparate aminotransferase (AST) were not significantly different from zero and mean changes in alanine aminotransferase (ALT) and creatine phosphokinase (CPK) showed a small increase. We conclude that simvastatin is an efficacious and well-tolerated treatment for hypercholesterolemia in elderly individuals for extended periods.

Aged↗

Resorbable device for fracture fixation: in vivo degradation and mechanical behaviour.

The availability of a high molecular weight poly(L-lactide), with supposed good mechanical properties, encouraged us to carry out an in vivo experimental study to evaluate the degradation rate and accompanying loss of strength during interaction with bone. Small cylindrical PLLA rods were manufactured by compression moulding. Thirty-six male New Zealand rabbits (b.w. 3 kg), randomly divided into six groups of six animals each, were submitted to implantation of the rods under general anaesthesia (phi 3 x 7 mm rods in the lateral condylic region of the right femur and phi 3 x 50 mm rods in the intracondylic channel of the left femur). The animals were then sacrificed at the end of each experimental time (4, 8, 12, 24, 52, 64 weeks), hence the femurs were explanted. Histology showed no inflammatory cells with fragmentation or resorption of bone trabeculae. Mechanical studies showed a decrease in mechanical properties and flexional stiffness, and the absence of evident material resorption. Finally, the properties of this newly developed resorbable device, when confirmed, seem to justify future clinical introduction of this synthetic material.

Animals↗

Short cycles of very low calorie diet in the therapy of obese type II diabetes mellitus.

Very Low Calorie Diet (VLCD) is known to induce not only weight loss, but also an improvement of metabolic control, in obese type II diabetics. In order to evaluate the therapeutical efficacy of cycles of VLCD shorter than those previously described, 29 obese type II diabetics and 31 obese nondiabetic subjects were entered as inpatients and prescribed a 450 kcal/day diet for 15 days. Metabolic results obtained were similar to those achieved with longer cycles of VLCD, showing that 15 days are sufficient to induce a BMI decrease in diabetic (BMI from 35.3 +/- 4.8 to 33.3 +/- 4.6 after VLCD) and nondiabetic patients (BMI from 40.5 +/- 7.4 to 38.1 +/- 7.2 after VLCD), a desired fall of blood glucose levels and the decrease of daily insulin needs in insulin-treated patients. Glucagon tests were performed before and after VLCD in order to study possible modifications of insulin secretion. Although we did not observe any significant increase of C-peptide basal or peak levels (nM/ml) either in diabetic (basal levels before VLDC: 1.2 +/- 0.4 and peak levels 2.4 +/- 0.7; basal after VLCD 1.23 +/- 0.6 and peak 2.6 +/- 0.7) and nondiabetic patients (basal levels before VLDC 1.0 +/- 0.3 and peak levels 2.5 +/- 0.4; basal after VLCD 0.9 +/- 0.3 and peak 2.4 +/- 0.6). The rise of the C-peptide/glycemia ratio is an index of an improvement of insulin biological activity, which could be partly responsible for the therapeutical effects of VLCD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Bone density and mineral metabolism in thyroidectomized patients treated with long-term L-thyroxine.

1. A decreased bone mass has been reported in patients with endogenous hyperthyroidism, but the effect on bone density and mineral metabolism of thyroxine administration in thyroidectomized patients is still controversial. To further contribute to this debate, we studied 25 women thyroidectomized for thyroid cancer on long-term treatment with thyroid-stimulating hormone-suppressive doses of L-thyroxine. Twenty-one sex- and age-matched normal subjects were also studied as a control group. 2. The bone density of the spine and serum calcitonin, calcitriol and parathyroid hormone concentrations were not different when the whole patient group was compared with the control subjects, nor when the patients and control subjects were compared according to their menopausal status. However, post-menopausal thyroidectomized patients showed significantly lower bone mass (P < 0.001) than premenopausal patients. 3. L-Thyroxine-treated patients showed significantly higher levels of bone alkaline phosphatase and urine hydroxyproline excretion than control subjects (P < 0.003 and P < 0.001, respectively). These differences were still present when patients and control subjects were analysed according to their menopausal status. However, bone alkaline phosphatase was significantly higher in postmenopausal than in premenopausal women only in L-thyroxine-treated patients (P < 0.05). In postmenopausal L-thyroxine-treated patients a negative correlation between time since menopause and bone mass (P < 0.05) and a positive correlation between bone alkaline phosphatase and hydroxyproline excretion (P < 0.03) were also found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Surgical repair of achilles tendon ruptures using polypropylene braid augmentation.

Surgical repair in fresh rupture of the Achilles tendon should be considered in active patients and athletes to restore their preinjury level of activity. Fifteen cases of Achilles tendon rupture underwent surgical repair using interpositional augmentation. This technique provides an immediate mechanical strength of the repair, avoiding the need for a postoperative plaster cast and allowing immediate motion of the ankle. No wound infection, scar adherence of the skin to the tendon, or rerupture of the tendon is present in this series. All patients were subjectively satisfied with the results and returned to their preinjury level of activity. Objectively, isokinetic assessment revealed no significant difference, as per t-test evaluation (P < .05), between the operated leg and the controlateral one.

Achilles Tendon↗