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Energy‐dispersive inelastic X‐ray scattering (EDIXS) and Fourier transform infrared spectroscopy (FTIR) were used to study hard dental tissues like dentine, enamel, and cementum in several human dental pieces of adult individuals. Analysis of linear paths crossing different interfaces were carried out. These different techniques provide specific information that allows a combined interpretation of the results as well as a comparison of performances of both methodologies. The EDIXS analysis was focused on the calcium absorption edge because this major element has a fundamental role in the formation of the calcium phosphate structure. Regarding FTIR, the investigation focused on the study of ν1, ν3, and ν4 vibrational modes of hydroxyapatite. The ν1, ν3, and ν4 vibrational modes of hydroxyapatite are related to the vibrations of the phosphate (PO43‐) ion. Specifically, ν1 corresponds to the symmetric stretching vibration, ν3 is the asymmetric stretching vibration, and ν4 is the bending vibration of the phosphate ion. The results allowed us to infer a correlation between the variations observed in EDIXS and the ν3 vibrational mode measured with FTIR. This correlation between inelastic X‐ray scattering and FTIR spectroscopy offers a more comprehensive characterization of hydroxyapatite parameters. Furthermore, it establishes a complementary technique for the structural characterization of dental tissues. [ABSTRACT FROM AUTHOR]

We compared the prevalence of levofloxacin (LVX) resistance with that of ofloxacin (OFX) and moxifloxacin (MFX) among multidrug resistant (MDR) MTB clinical isolates collected in Medellin, Colombia, between 2004 and 2009 and aimed at unraveling the underlying molecular mechanisms that explain the correlation between QRDR-A mutations and LVX resistance phenotype. We tested 104 MDR isolates for their susceptibility to OFX, MFX, and LVX. Resistance to OFX was encountered in 10 (9.6%) of the isolates among which 8 (7.7%) were also resistant to LVX and 6 (5.7%) to MFX. Four isolates resistant to the 3 FQ were harboring the Asp94Gly substitution, whilst 2 other isolates resistant to OFX and LVX presented the Ala90Val mutation. No mutations were found in the QRDR-B region. The molecular modeling of the interaction between LVXand the DNA-DNAgyrase complex indicates that the loss of an acetyl group in the Asp94Gly mutation removes the acid base interaction with LVX necessary for the quinolone activity. The Ala90Val mutation that substitutes a methyl for an isopropyl group induces a steric modification that blocks the LVX access to the gyrase catalytic site. [ABSTRACT FROM AUTHOR]

Aims The fast transient outward current, Ito,fast, is the most extensively studied cardiac K+ current in diabetic animals. Two hypotheses have been proposed to explain how type-1 diabetes reduces this current in cardiac muscle. The first one is a deficiency in channel expression due to a defect in the trophic effect of insulin. The second one proposes flawed glucose metabolism as the cause of the reduced Ito,fast. Moreover, little information exists about the effects and possible mechanisms of diabetes on the other repolarizing currents of the human heart: Ito,slow, IKr, IKs, IKur, IKslow and IK1. Methods We recorded cardiac action potentials and K+ currents in ventricular cells isolated from control and streptozotocin- or alloxan-induced diabetic mice and rabbits. Channel protein expression was determined by immunofluorescence. Results Diabetes reduces the amplitude of Ito,fast, Ito,slow and IKslow, in ventricular myocytes from mouse and rabbit, with no effect on Iss, IKr or IK1. The absence of changes in the biophysical properties of the currents and the immunofluorescence experiments confirmed the reduction in channel protein synthesis. Six-hour incubation of myocytes with insulin or pyruvate recovered current amplitudes and fluorescent staining. The activation of AMP- K reduced the same K+ currents in healthy myocytes and prevented the pyruvate-induced current recovery. Conclusion Diabetes reduces K+ current densities in ventricular myocytes due to a defect in channel protein synthesis. Activation of AMP- K secondary to deterioration in the metabolic status of the cells is responsible for K+ channel reductions. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the expression of IGF-1 receptors and insulin receptors on the minor salivary gland (MSG) tissues of patients diagnosed with Sjögren's syndrome (SS) and normal salivary gland tissue surrounding mucoceles. SUBJECTS AND METHODS: Five MSG tissue sections from SS and seven from mucocele patients were stained immunohistochemically using antibody to IGF-1 receptor and insulin receptor in a horse radish peroxidase and DAB system. RESULTS: The expression of the insulin receptor was increased in the SS sections compared with controls, while the insulin-like growth factor-1 receptor was more intensely expressed in the controls. CONCLUSION: The presence of differential expression of receptors for IGF and insulin might suggest a possible role of these growth factors in the pathogenesis of SS. [ABSTRACT FROM AUTHOR]

Background: Transforming growth factor beta 1 (TGF-β1) is a pleiotropic cytokine that activates hepatic stellate cell (HSC) proliferation, but inhibits parenchymal cell proliferation. Therefore, we hypothesize that TGF-β1 regulates HSC proliferation and elucidated its molecular action., Methods: In order to elucidate the molecular mechanism whereby TGF-β1 up-regulates platelet derived growth factor beta (PDGF-β) receptor mRNA and induces a delayed proliferation of HSC, we used proliferation and apoptosis assays as well as RT-PCR, Western blot analysis, immunostaining, and flow cytometry in mouse and rat HSC., Results: We show that TGF-β1 markedly induces the proliferation of mouse HSC in culture with concomitant 2.1-fold (p < 0.001) stimulation in [(3) H]-thymidine incorporation into cellular DNA. This induction is maximal between 24 and 36 hours postcytokine exposure that is triggered by 7.6-fold (p < 0.001) up-regulation of PDGF-β receptor mRNA and associated increase in PDGF-β receptor protein after 48 hours. TGF-β1-dependent HSC proliferation is mimicked by H2 O2 that is inhibited by catalase, implying that TGF-β1 action is mediated via reactive oxygen species. HSC proliferation is blunted by PDGF-β receptor-neutralizing antibody as well as by specific inhibitors of PI3 kinase (PI3K), AKT, and p70(S6K) , indicating that the action of TGF-β1 involves the activation of PDGF-β receptor via the PI3K/AKT/p70(S6K) signaling pathway. TGF-β1 also induces a reorganization of actin and myosin filaments and cell morphology leading to the formation of palisades although their myosin and actin contents remained constant. These findings suggest that TGF-β1-mediated oxidative stress causes the transdifferentiation of HSC and primes them for extracellular matrix (ECM) deposition and scar contraction., Conclusions: We conclude that liver injury up-regulates TGF-β1 that inhibits parenchymal cell proliferation, but stimulates HSC proliferation leading to the production of ECM and type I collagen resulting in fibrosis., (Copyright © 2013 by the Research Society on Alcoholism.)