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Biomedical subjects

Francesco De Luca

Publications and source records attributed to Francesco De Luca.

13 recordsLinked to original sources
PubMed2006

Large surface mapping by a unilateral NMR scanner.

The nuclear magnetic resonance (NMR) surface scanner, which provides images of sample surfaces larger than the probe dimension, has been realized using a single-sided device. Although conditioned by distortion effects originated by convolution between the sensitive volume of the probe and the space structures to be imaged, the scanner is able to provide images with good spatial resolution. The images obtained by the surface scanner can be made sensitive to relaxation parameters, magnetization or molecular self-diffusion; also, the dimension perpendicular to the sample surface can be scanned by varying the depth from which the probe detects the sample signal. It may scan surfaces arbitrarily large and with some degree of curvature. This aspect, together with the noninvasive characteristic of the apparatus, indicates that the surface scanner could be used profitably in the field of cultural heritage, where it could provide NMR maps of frescos, paintings on wood, marble artifacts, books and others.

Equipment Design↗
PubMed2006

Inhibition of the proteasomal function in chondrocytes down-regulates growth plate chondrogenesis and longitudinal bone growth.

The proteasome is a large multiprotein complex that processes intracellular proteins functioning as cell cycle regulators and transcription factors. It has been shown that the chymotryptic component of the proteasome is an important regulator of osteoblast differentiation and bone formation, with inhibitors of the proteasome increasing osteoblast differentiation and bone formation. Yet, little is known about the effects of the proteasomal activity in the growth plate. In the present study, we cultured rat metatarsal bones in the presence of proteasome inhibitor I (PSI), a known inhibitor of the chymotrypsin-like activity of the 20S proteasome. PSI suppressed growth plate chondrocyte proliferation and hypertrophy/differentiation, and induced chondrocyte apoptosis. All these cellular effects led to reduced metatarsal linear growth. In cultured chondrocytes, PSI increased the expression of beta-catenin (a negative regulator of chondrogenesis) and reduced the DNA binding of nuclear factor kappaB, a transcription factor that stimulates growth plate chondrogenesis. In conclusion, our findings suggest that the proteasomal activity facilitates growth plate chondrogenesis and, in turn, longitudinal bone growth.

Animals↗
PubMed2006

Impaired growth plate chondrogenesis in children with chronic illnesses.

In mammals, statural growth is primarily accomplished by endochondral ossification, which takes place at the growth plate. Growth plate chondrocyte proliferation, hypertrophy/differentiation, apoptosis, and cartilage matrix synthesis all contribute to chondrogenesis or cartilage formation, a process tightly coupled to the simultaneous remodeling of the cartilage into bone at the metaphyseal border of the growth plate. Growth plate chondrogenesis is regulated by the complex interaction of molecular signals acting systemically as well locally within the growth plate. This network is often dysregulated during chronic illnesses, thus resulting in impaired growth plate chondrogenesis and, in turn, growth failure. The principal events responsible for altered growth plate chondrogenesis in chronic illness are inflammation, protein/calorie deprivation, uremia/metabolic acidosis, glucocorticoids, and impaired GH/IGF-I axis.

Acidosis↗
PubMed2006

Bladder hernia.

Bladder hernia is a rare condition, but crural herniation of the bladder into the scrotum is very rare. A case of bladder hernia presenting with urological symptoms is described. A 71-year-old man presented to the urological ward complaining for persistent frequency and nocturia associated with loss offorce and decrease of caliber of the urinary stream and the presence of a large mass of the right scrotum. An IVP (intra venous pyelography) showed a large herniation of the bladder through the right inguinal canal into the scrotum. An inguinal incision was made and a crural hernia was identified. The hernia sac, containing bowel and bladder, was dissectedfreefrom the spermatic cord and the testis and the hernia defect was repaired.

Aged↗
PubMed2005

Stanniocalcin 1 acts as a paracrine regulator of growth plate chondrogenesis.

During embryogenesis, the expression of mammalian stanniocalcin (STC1) in the appendicular skeleton suggests its involvement in the regulation of longitudinal bone growth. Such a role is further supported by the presence of dwarfism in mice overexpressing STC1. Yet, the STC 1 inhibitory effect on growth may be related to both postnatal metabolic abnormalities and prenatal defective bone formation. In our study, we used an organ culture system to evaluate the effects of STC on growth plate chondrogenesis, which is the primary determinant of longitudinal bone growth. Fetal rat metatarsal bones were cultured in the presence of recombinant human STC (rhSTC). After 3 days, rhSTC suppressed metatarsal growth, growth plate chondrocyte proliferation and hypertrophy/differentiation, and extracellular matrix synthesis. In addition, rhSTC increased the number of apoptotic chondrocytes in the growth plate. In cultured chondrocytes, rhSTC increased phosphate uptake, reduced chondrocyte proliferation and matrix synthesis, and induced apoptosis. All these effects were reversed by culturing chondrocytes with rhSTC and phosphonoformic acid, an inhibitor of phosphate transport. The rhSTC-mediated inhibition of metatarsal growth and growth plate chondrocyte proliferation and hypertrophy/differentiation was abolished by culturing metatarsals with rhSTC and phosphonoformic acid. Taken together, our findings indicate that STC1 inhibits longitudinal bone growth directly at the growth plate. Such growth inhibition, likely mediated by an increased chondrocyte phosphate uptake, results from suppressed chondrocyte proliferation, hypertrophy/differentiation, and matrix synthesis and by increased apoptosis. Last, the expression of both STC1 and its binding site in the growth plate would support an autocrine/paracrine role for this growth factor in the regulation of growth plate chondrogenesis.

Animals↗
PubMed2005

Endocrine regulation of the growth plate.

Longitudinal bone growth occurs at the growth plate by endochondral ossification. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue. This process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin. Many of these signals regulate growth plate function, both by acting locally on growth plate chondrocytes and also indirectly by modulating other endocrine signals in the network. Some of the local effects of hormones are mediated by changes in paracrine factors that control chondrocyte proliferation and differentiation. Many human skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate. This review provides an overview of the endocrine signals that regulate longitudinal bone growth, their interactions, and the mechanisms by which they affect growth plate chondrogenesis.

Androgens↗
PubMed2005

Bayesian analysis of in vivo dynamic 13C-edited 1H images.

We propose an application of a Bayesian methodology to dynamic MR images of protons J-coupled to 13C nuclei for monitoring the in vivo 13C-glucose uptake of mouse brain. The very low population of these protons and the random noise make the analysis of these images extremely difficult. The proposed method restores the images and provides an "activation" map of the mouse brain by means of a hypothesis testing procedure. The restoration step is performed in the Bayesian framework so that among the other advantages of a stochastic approach, it is possible to model spatial and temporal information about neighboring pixels. This leads to a restoration procedure able to reduce the noise level while preserving the information about the edges of signal areas. Based on the restored images, the testing procedure provides us with a reliable map of pixels characterized by the 13C-glucose uptake.

Animals↗
PubMed2004

Effects of valproic acid on longitudinal bone growth.

Valproic acid is widely used in the treatment of children with epilepsy. Evidence indicates that valproic acid has teratogenic effects on the skeletal system. In addition, the use of valproic acid in children has been associated with short stature. Thus, we hypothesized that valproic acid could also affect bone growth after skeletal morphogenesis is completed. To test this hypothesis, we cultured fetal rat metatarsal bones in the presence of valproic acid. Valproic acid markedly suppressed metatarsal longitudinal growth. To determine the underlying mechanisms, we studied cell proliferation and hypertrophy in the growth plate, the site where bone growth takes place. At the end of the culture period, valproic acid-treated bones exhibited narrow growth plate proliferative and hypertrophic zones and an expanded ossification center. In addition, valproic acid suppressed chondrocyte proliferation in the metatarsal rudiments. Our results suggest that valproic acid suppresses longitudinal bone growth by inhibiting cartilage formation and accelerating ossification of the growth plate. These findings warrant a prospective study on the effects of valproic acid on growth in children treated with valproic acid.

Animals↗
PubMed2004

Intracardiac echocardiography using the AcuNav ultrasound catheter during percutaneous closure of multiple atrial septal defects.

Transesophageal echocardiography is routinely used in catheterization laboratories to guide the percutaneous closure of ostium secundum atrial septal defects. The patient is under general anesthesia, and the interatrial septum anatomy is usually well defined. Multiple atrial septal defects are, in some cases, a challenge for both the interventional echocardiographer and the interventional cardiologist, when trying to evaluate the anatomy of the defects, the strategy of closure and the correct choice of the device. We describe the usefulness of a new phased-array ultrasound-tipped catheter for intracardiac echocardiography in a case of percutaneous closure of multiple ostium secundum atrial septal defects.

Adolescent↗
PubMed2003

Role of cholesterol in the regulation of growth plate chondrogenesis and longitudinal bone growth.

Inborn errors of cholesterol synthesis are associated with multiple systemic abnormalities, including skeletal malformations. The regulatory role of cholesterol during embryogenesis appears to be mediated by Shh, a signaling molecule in which activity depends on molecular events involving cholesterol. Based on this evidence, we hypothesized that cholesterol, by modifying the activity of Ihh (another of the Hedgehog family proteins) in the growth plate, regulates longitudinal bone growth. To test this hypothesis, we treated rats with AY 9944, an inhibitor of the final reaction of cholesterol synthesis. After 3 weeks, AY 9944 reduced the cumulative growth, tibial growth, and the tibial growth plate height of the rats. To determine whether cholesterol deficiency affects bone growth directly at the growth plate, we then cultured fetal rat metatarsal bones in the presence of AY 9944. After 4 days, AY 9944 suppressed metatarsal growth and growth plate chondrocyte proliferation and hypertrophy. The inhibitory effect on chondrocyte hypertrophy was confirmed by the AY 9944-mediated decreased expression of collagen X. Lastly, AY 9944 decreased the expression of Ihh in the metatarsal growth plate. We conclude that reduced cholesterol synthesis in the growth plate, possibly by altering the normal activity of Ihh, results in suppressed longitudinal bone growth and growth plate chondrogenesis.

Animals↗
PubMed2003

Effects of Ca2+ sensing receptor activation in the growth plate.

The Ca2+-sensing receptor (CaR) is a G protein-coupled receptor expressed in many mammalian tissues, including the long bone's growth plate. CaR knockout mice exhibit growth retardation, suggesting that CaR may promote skeletal growth. However, the complex phenotype of these knockout mice, which includes hyperparathyroidism, hypercalcemia, and hypophosphatemia, may confound the effects of CaR activation. To determine whether CaR regulates growth plate chondrogenesis and longitudinal bone growth, we chose an organ culture model. Fetal rat metatarsal bones (dpc 20) were cultured in serum-free medium for 7 days in the presence or absence of NPS-R-568, a CaR agonist. The addition of 10 nM NPS-R-568 increased the cumulative longitudinal growth of the metatarsal explants. To explore the underlying mechanisms, we then assessed the effects of NPS-R-568 on growth plate chondrocyte hypertrophy/differentiation and chondrocyte proliferation. After 7 days in culture, NPS-R-568 increased the height of the growth plate hypertrophic zone and the expression of collagen X, a marker of growth plate chondrocyte differentiation (assessed by immunohistochemistry). NPS-R-568 also induced a significant increase of the height of the growth plate proliferative zone and of the total thymidine incorporation in the metatarsal bone. In conclusion, our findings suggest that the activation of CaR in the growth plate accelerates longitudinal bone growth by stimulating growth plate chondrogenesis.

Animals↗
PubMed2002

Transcatheter treatment of muscular ventricular septal defect and pulmonary valvar stenosis in an infant.

An 11-month-old, 8 kg girl with muscular ventricular septal defect and pulmonary valvar stenosis had successful transcatheter treatment of both anomalies. The stenotic pulmonary valve was dilated first by balloon catheter, then the VSD was approached and closed using a 6 mm Amplatzer VSD occluder device. Due to technological improvements, transcatheter techniques are more and more the procedure of choice in a larger number of congenital heart diseases in younger and younger patients.

Catheterization↗