The association between schoolchildren intelligence and refractive error.

PURPOSE: The relationship between refractory errors and intelligence and the importance of genetic, regional and environmental factors in such associations, were investigated in a group of school children. SUBJECTS AND METHODS: One hundred and thirty-seven students (34.3% boys and 65.7% girls) from two primary schools were enrolled in the study. Cycloplegic refraction was performed and a spherical equivalent (SE) > or = 0.5D were determined as hyperopia; <-0.5D myopia and <1 cyl D astigmatism. Demographic factors, parent's education level, teacher based assessment of school performance and average score were also evaluated. RESULTS: Seventy-eight (56.9%) of subjects showed a form of refractory error; 27%, 3% and 2.9% were myope, hyperope or astigmat, respectively, whereas 12.4% of them had both myopia and astigmatism and 10.2% showed hyperopia and astigmatism; 43.1% were normal. CONCLUSIONS: Although our data revealed no distinction of average score between normal group and myopia, hyperopia, astigmatism or hyperopia-astigmatism, there is a statistically significant difference between normal group and those who had both myopia and astigmatism in which the later had a lower mediocre. Our results is somehow in contrast with other parallel studies demonstrating that positive connection between school performance and myopia can be explained by the geographical or racial discrepancies as well as subjects involved in the study and divergent set of cut off limits.

Scintigraphic parameters with emphasis on perfusion appraisal in rest 99mTc-sestamibi SPECT in the recovery of myocardial function after thrombolytic therapy in patients with ST elevation myocardial infarction (STEMI).

INTRODUCTION: This study was performed to determine the clinical application of rest 99mTc-sestamibi in the assessment of viability and functional improvement of the left ventricle (LV) myocardium in the post-thrombolytic therapy of acute myocardial infarction (AMI). MATERIAL AND METHODS: In 37 patients with AMI who received thrombolytic therapy, 2-dimensional (2D) echocardiography, as well as the resting redistribution of 99mTc-sestamibi, was investigated, both within 1 week and 3-5 months after AMI. The predictive capacity of the perfusion percentage for myocardial function recovery was evaluated. Also, the capacities of the possible variables in the prediction of recovery of myocardial function resulting from a change in LV ejection fraction (EF) were evaluated using stepwise multiple regression analysis. RESULTS: Thirty-seven patients (30 men and 7 women; mean age: 58±14 years) with AMI were enrolled in the study. Redistribution was observed in 35 and 50 segments of the initial and follow-up scans, respectively. In addition, 146 segments with reverse redistribution (RR), both in the initial scan (118 segments) and the follow-up scan (86 segments), were also observed. An apparent difference in wall motion scores was seen between the initial and follow-up echocardiographs (p<0.001). Furthermore, using the optimal cut-off point of perfusion percentage in each image set, sensitivity as well as specificity and likelihood ratio (LR) for the improvement of regional wall motion after 3-5 months were defined. CONCLUSION: These data showed that redistribution and reverse redistribution of 99mTc-sestamibi post thrombolytic therapy can be used as a marker of viability to predict the recovery of segmental wall motion abnormality (stunning), as well as the improvement of segmental perfusion uptake. This study also demonstrates that the resting 99mTc-sestamibi SPECT can be used for an approximate assessment of LV function status and can predict the recovery of jeopardized myocardium function after thrombolytic therapy.

Impact of Ramadan fasting on intraocular pressure, visual acuity and refractive errors.

INTRODUCTION: Fasting evidently influences a variety of physiological parameters that can impact the ocular system. Among these modifications are alterations in insulin secretion, sympathetic activity, free fatty acids, lipid profile, melatonin, cortisol, electrolytes and catecholamines. In this study, we investigated the possible alterations in intraocular pressure (IOP), visual acuity and refractive errors during Ramadan fasting. METHODS: IOP, visual acuity and refractive errors of both eyes of volunteers were measured on the first and last days of Ramadan (once in the morning and evening). Body weight was measured so as to estimate the amount of dehydration. Data from the two examinations was analysed using one-way analysis of variance. A p-value of less than 0.05 was considered statistically significant. RESULTS: 58 healthy, fasting male volunteers with a mean age of 40.7 +/- 7.1 years participated in the study. Statistical analysis demonstrated no difference in IOP, visual acuity or refractive errors on the first and last days of Ramadan, or within a single day (from morning to evening). CONCLUSION: Our results reveal that Islamic Ramadan fasting does not profoundly affect physiological IOP, refractive error or visual acuity values in healthy volunteers. However, more detailed investigations using animal models should be designed to evaluate whether fasting has a pivotal influence on pathological conditions.

Cyclooxygenase 2 plays a role in Emdogain-induced proliferation.

BACKGROUND AND OBJECTIVE: Enamel matrix proteins are involved in the development and regeneration of root cementum and in its attachment to dentin; however, the mechanisms through which this occurs have yet to be elucidated. The present study was therefore carried out to evaluate the mitogenic and proliferative responses of human periodontal fibroblast (HPLF) cells to Emdogain (EMD), and the potential role of cyclooxygenase 2 (COX-2) in this process. MATERIAL AND METHODS: We investigated the effects of EMD on 5-bromo-2'-deoxyuridine (BrdU) incorporation, colchicine freezing of mitosis, XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction and Trypan Blue dye exclusion, with or without celecoxibe, a selective cyclooxygenase-2 (COX-2) inhibitor; we also evaluated the expression of COX-2 mRNA and COX-2 protein in response to EMD. RESULTS: EMD significantly enhanced mitosis in, and proliferation of, human periodontal ligament fibroblasts in a dose-dependent manner; however, there was a small increase of DNA synthesis only in response to a high dose of EMD (200 µg/mL). EMD (100 and 200 µg/mL) elicited an increase in COX-2 expression (p ≤ 0.05). Celecoxibe (20 µm) diminished the EMD-induced mitosis and proliferation of HPLF cells (p ≤ 0.05). CONCLUSION: Celecoxibe hampered EMD-induced mitosis and proliferation, which, in association with EMD-increased COX-2 expression, indicates that COX-2 may be involved in the proliferative response of HPLF cells to EMD.

The effect of full length and mature NAG-1 protein overexpression on cytotoxicity of celecoxib, tamoxifen and doxorubicin in HT1080.

BACKGROUND AND THE PURPOSE OF THE STUDY: Non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) is involved in inflammation, apoptosis/survival and tumorigenesis as well as resistance to chemotherapy. NAG-1 protein is synthesized as pro-peptide, cleaved and secreted as mature protein. Regulation of NAG-1 is not completely discovered and increased level of NAG-1 has been reported in many cancers. The expression of NAG-1 in cancer cells could affect the progression of tumor growth. In addition the secretion of full length and mature forms of NAG-1 can influence cell proliferation in other cells. In this study the role of full length and mature forms of NAG-1 on viability of HT-1080 and MCF-7 cells were evaluated, and the cytotoxicity of celecoxib, indomethacin, tamoxifen and doxorubicin in HT1080 cells stably expressing NAG-1 were also tested. METHODS: Full length and mature NAG-1 was cloned from cDNA library of HCT116 cells and stably transfected in HT1080 cells. Cells were treated with different concentrations of indomethacin, celecoxib, tamoxifen and doxorubicin and viability was assessed by MTT assay. The effect of conditioned medium of NAG-1 expressing cells on proliferation of MCF-7 and HT1080 cells were also tested. RESULTS: The growth curves of HT1080 cells expressing full length and mature NAG-1 were not different. The viability of HT1080 cells expressing NAG-1 in the presence of indomethacin, doxorubicin and tamoxifen compared to untransfected cells was higher. The proliferation of HT1080 and MCF-7 cells were inhibited by conditioned medium of NAG-1 expressing cells in 24 and 48 hrs. MAJOR CONCLUSION: NAG-1 expression enhances drug resistance to tamoxifen, indomethacin and doxorubicin in HT1080. In addition, condition medium of NAG-1 expression cells inhibits proliferation in MCF-7 and HT1080 cells. Thus, NAG-1 expression can induce drug resistance in NAG-1 expressing cells and inhibition of viability in non expressing cells. Thus, NAG-1 is suggested as a marker for effective cancer chemotherapy and tumor progression.

ATP depletion as a consequence of hypoxia enhances tamoxifen antiproliferative effects in T47D breast carcinoma cells.

Tamoxifen causes a mitochondrial transmembrane potential dysfunction and ATP depletion, which may play a role in tamoxifen cytotoxicity. Administration of oligomycin-2 deoxy glucose (2DG) enhanced tamoxifen antiproliferative effects, which may be due to exacerbated ATP depletion following tamoxifen and oligomycin-2DG coadministration. Sodium nitroprusside (SNP) did not significantly change tamoxifen responsiveness at 0.1, 0.5, and 1 mM; however, 2 mM SNP hampered tamoxifen effects on cell proliferation and cell cycle. Oligomycin-2DG neither changed iNOS expression nor altered its attenuated expression due to tamoxifen exposure, suggesting that ATP depletion-mediated sensitivity to tamoxifen seems to be apart from iNOS.

Pre-protachykinin A mRNA is colocalized with tyrosine hydroxylase-immunoreactivity in bulbospinal neurons.

Previous studies have generated controversy about the extent of co-localization between substance P- and catecholamine-containing neurons that project to the spinal cord. In earlier studies, estimates using immunofluorescence after colchicine have ranged from almost all, to almost none. We sought to resolve this issue by combining in situ hybridization and immunofluorescence. Catecholamine (A1 to A7, C1 to C3; tyrosine hydroxylase immunoreactive) neurons in the rat brainstem were examined to determine their content of mRNA for the preprotachykinin-A gene. In the A1 to A7 and the C1 to C3 cell groups, preprotachykinin-A mRNA was found only in substantial amounts in the C1-C3 cell groups. On average 20.9+/-0.9% (234/1120, n=3) of rostral C1 neurons contained preprotachykinin-A mRNA. Co-localization was also observed in C2 and C3 neurons to a similar extent. Retrograde tract-tracing with cholera toxin B subunit was used to identify bulbospinal neurons and 17.9+/-2.7% (96/529 cells) of the bulbospinal tyrosine hydroxylase-containing neurons of the rostral C1 cell group were found to contain preprotachykinin-A mRNA. In addition a new population of non-catecholaminergic bulbospinal preprotachykinin-A neurons is described in an area corresponding to the recently described caudal pressor area. To confirm that the preprotachykinin-A mRNA observed in cells in the medulla was converted to protein, dual immunofluorescence for fiber labeling at the confocal level was carried out. This confirmed colocalization of substance P and tyrosine hydroxylase in the intermediolateral cell column, but nowhere else, in a small number of cases. The results provide evidence for a much larger population of substance P/neurokinin A containing neurons in the brainstem than was previously suspected. Furthermore, many of these neurons are catecholaminergic and spinally projecting. The specific sympathetic outflow that these neurons influence remains to be determined.

Differential role of kinases in brain stem of hypertensive and normotensive rats.

Spontaneously hypertensive rats (SHR) are characterized by extreme elevations of blood pressure. The genetic factors underlying this are yet to be identified. Here we demonstrate, in vivo, that in SHR and normotensive Wistar-Kyoto rats (WKY), injection of the mitogen-activated protein kinase inhibitor PD 098,059 bilaterally into the rostral ventrolateral medulla (RVLM) dramatically lowers arterial pressure. PD 098,059 does not alter the responses evoked by microinjection of glutamate into the RVLM or brief apnea. Wortmannin (phosphatidylinositol-3 kinase inhibitor) bilaterally into the RVLM causes a 35+/-4% fall in arterial pressure in SHR but has no effect in WKY. Furthermore, wortmannin reduces the pressor response evoked by microinjection of angiotensin (Ang) II in the RVLM of SHR compared with WKY. The response to Ang II microinjection into the RVLM of WKY was unaffected by wortmannin. Simultaneous bilateral injections of PD 098,059 and wortmannin into the RVLM abolished the response to exogenous Ang II in the RVLM but did not affect the response evoked by glutamate in either SHR or WKY. Thus, it appears that PD 098,059- and/or wortmannin-sensitive mechanisms are not involved in the responses evoked by glutamate in the RVLM and that these kinase inhibitors are not neurotoxic. We conclude that a PD 098,059-sensitive pathway in the RVLM of SHR and WKY tonically regulates arterial pressure and that a wortmannin-sensitive pathway in the RVLM is important in the maintenance of hypertension in SHR. This may be related to a phosphatidylinositol-3 kinase-dependent mechanism involved in the action of Ang II on the Ang II type 1 receptor.