p53 and MDM2 expression in odontogenic cysts and tumours

OBJECTIVE: The aim of this report was to assess p53 and MDM2 expression in odontogenic cysts and tumours, as they are known to play important roles in cell proliferation and tumorigenesis. MATERIALS AND METHODS: The expression of p53 and MDM2 proteins was determined immunohistochemically in 51 formalin-fixed, paraffin embedded specimens of odontogenic cysts and tumours.RESULTS: No positivity to p53 was found in the cases studied. MDM2 expression in ameloblastoma was higher than in radicular cysts, but lower than that observed in odontogenic keratocysts. No difference was observed between MDM2 expression in radicular cyst and adenomatoid odontogenic tumour. The clear-cell odontogenic ameloblastoma presented strong immunoreaction to this antigen.CONCLUSIONS: The results suggest that MDM2 overexpression may be involved in the pathogenesis of some odontogenic lesions.     

Complete complex conjugate resolved heterodyne swept-source optical coherence tomography using a dispersive optical delay line

Swept-source optical coherence tomography (SSOCT) provides a substantial sensitivity advantage over its time-domain counterpart, but suffers from a reduced imaging depth range due to sensitivity falloff and complex conjugate ambiguity. Heterodyne complex conjugate-resolved SSOCT (HCCR-SSOCT) has been previously demonstrated as a technique to completely resolve the complex conjugate ambiguity, effectively doubling the falloff limited imaging depth, without the reduction in imaging speed associated with other CCR techniques. However, previous implementations of this technique have employed expensive and lossy optical modulators to provide the required differential phase modulation. In this paper, we demonstrate the use of a dispersive optical delay line (D-ODL) as the reference arm of an OCT system to realize HCCR-SSOCT. This technique maintains the existing advantages of HCCR-SSOCT in that it completely resolves the complex conjugate artifact and does not reduce imaging speed, while conferring the additional advantages of being low cost, maintaining system sensitivity and resolution, not requiring any additional signal processing, and working at all wavelengths and imaging speeds. The D-ODL also allows for hardware correction of unbalanced dispersion in the reference and sample arm, adding further flexibility to system design. We demonstrate the technique using an SSOCT system operating at 100kHz with a central wavelength of 1040nm. Falloff measurements performed using a standard OCT configuration and the proposed D-ODL demonstrate a doubling of the effective imaging range with no sensitivity or resolution penalty. Feasibility of the technique for in vivo imaging was demonstrated by imaging the ocular anterior segments of healthy human volunteers.     

SEAT-BELT SYNDROME REVISITED

This report describes a complex syndrome of injuries occurring in a young female who was a back seat passenger wearing a lap-belt restraint in a high-speed road traffic accident. As a consequence of the forced flexion distraction injury of her lumbar spine, she sustained a fracture-subluxation of the first lumbar vertebra in association with a jejunal perforation and extensive small intestinal mesenteric laceration. She also had a large traumatic hernia of the anterior abdominal wall, which was overlooked at primary laparotomy. This report highlights collectively the classical combination of injuries associated with the lap-belt syndrome and demonstrates the importance of carefully inspecting the anterior abdominal wall for deficiencies, because traumatic herniation may be easily overlooked.     

Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies

BACKGROUND: A wide variety of pathological conditions have been shown to result in cardiac remodelling and myocardial dysfunction. However, the mechanisms of transition from adaptive to maladaptive alterations, as well as those for changes in cardiac performance leading to heart failure, are poorly understood. OBSERVATIONS: Extensive studies have revealed a broad spectrum of progressive changes in subcellular structures and function, as well as in signal transduction and metabolism in the heart, among different cardiovascular disorders. The present review is focused on identifying the alterations in molecular and biochemical structure of myofibrils (myofibrillar remodelling) in hypertrophied and failing myocardium in different types of heart diseases. Numerous changes at the level of gene expression for both contractile and regulatory proteins have already been reported in failing hearts and heart diseases; these changes are potential precursors for heart failure such as cardiac hypertrophy and cardiomyopathies. Myofibrillar remodelling, as a consequence of proteolysis, oxidation, and phosphorylation of some functional groups in both contractile and regulatory proteins in hearts failing due to different etiologies, has also been described. CONCLUSIONS: Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractile and regulatory proteins are dependent on the type and stage of heart disease.     

Inhibitory profile of SEA0400 [2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline] assessed on the cardiac Na+-Ca2+ exchanger, NCX1.1

SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline) has recently been described as a potent and selective inhibitor of Na(+)-Ca(2+) exchange in cardiac, neuronal, and renal preparations. The inhibitory effects of SEA0400 were investigated on the cloned cardiac Na(+)-Ca(2+) exchanger, NCX1.1, expressed in Xenopus laevis oocytes to gain insight into its inhibitory mechanism. Na(+)-Ca(2+) exchange currents were measured using the giant excised patch technique using conditions to evaluate both inward and outward currents. SEA0400 inhibited outward Na(+)-Ca(2+) exchange currents with high affinity (IC(50) = 78 +/- 15 and 23 +/- 4 nM for peak and steady-state currents, respectively). Considerably less inhibitory potency (i.e., micromolar) was observed for inward currents. The inhibitory profile was reexamined after proteolytic treatment of excised patches with alpha-chymotrypsin, a procedure that eliminates ionic regulatory mechanisms. After this treatment, an IC(50) value of 1.2 +/- 0.6 microM was estimated for outward currents, whereas inward currents became almost insensitive to SEA0400. The inhibitory effects of SEA0400 on outward exchange currents were evident at both high and low concentrations of regulatory Ca(2+), although distinct features were noted. SEA0400 accelerated the inactivation rate of outward currents. Based on paired pulse experiments, SEA0400 altered the recovery of exchangers from the Na(+)(i)-dependent inactive state, particularly at higher regulatory Ca(2+)(i) concentrations. Finally, the inhibitory potency of SEA0400 was strongly dependent on the intracellular Na(+) concentration. Our data confirm that SEA0400 is the most potent inhibitor of the cardiac Na(+)-Ca(2+) exchanger described to date and provide a reasonable explanation for its apparent transport mode selectivity.