Background:Achieving a good apical seal for root canals is known to be associated with good mineral trioxide aggregate (MTA) adaptation to dentin.Aims:This study aims to compare the marginal adaptation of MTA with root dentin between orthograde and retrograde application techniques using microcomputed tomography (micro-CT) analysis.Settings and Design:Fifty-two single-rooted human teeth were divided into four equal groups: (Group 1) Retrograde MTA (RMTA), (Group 2) Orthograde MTA (OMTA), (Group 3) Etched RMTA (ERMTA), and (Group 4) Etched OMTA (EOMTA).Materials and Methods:For Group 1, 3-mm retrograde cavities were prepared and filled with MTA. For Group 2, the apical 6 mm of the canals were filled with MTA and sealed with sealer cement and warm gutta-percha. In Groups 3 and 4, canals were treated the same as Groups 1 and 2, respectively, except that before placing the MTA, canals were irrigated with 17% ethylenediaminetetraacetic acid (EDTA). After 48 hours, all the teeth were analyzed using a micro-CT scanner.Statistical Analysis:Mean dentin-MTA contact and the mean length and width of each gap was analysed using one-way analysis of variance (ANOVA). Statistical significance was set at an α level of 5%.Results:No significant difference in gap volumes was observed in the dentin-MTA adaptation in both orthograde and retrograde application techniques. However, significant difference in the gap volumes was observed between RMTA and ERMTA (P = 0.045). Etching significantly improved the MTA-Dentin adaptation (P < 0.05). The type of application technique did not significantly improve the dentin-MTA adaptation, instead with the use of 17% EDTA, a significant improvement could be achieved.Conclusion:Within the limitations of the present study, it concludes that MTA adaptation to dentin tooth structure is not significantly different between an orthograde and retrograde approach. However, the use of EDTA significantly improved the MTA-Dentin adaptation.
Aims/hypothesis The aim of this work was to investigate whether different clinical pain phenotypes of diabetic polyneuropathy (DPN) are distinguished by functional connectivity at rest. Methods This was an observational, cohort study of 43 individuals with painful DPN, divided into irritable (IR, n = 10) and non-irritable (NIR, n = 33) nociceptor phenotypes using the German Research Network of Neuropathic Pain quantitative sensory testing protocol. In-situ brain MRI included 3D T1-weighted anatomical and 6 min resting-state functional MRI scans. Subgroup differences in resting-state functional connectivity in brain regions involved with somatic (thalamus, primary somatosensory cortex, motor cortex) and non-somatic (insular and anterior cingulate cortices) pain processing were examined. Multidimensional reduction of MRI datasets was performed using a machine-learning approach to classify individuals into each clinical pain phenotype. Results Individuals with the IR nociceptor phenotype had significantly greater thalamic–insular cortex (p false discovery rate [FDR] = 0.03) and reduced thalamus–somatosensory cortex functional connectivity (p-FDR = 0.03). We observed a double dissociation such that self-reported neuropathic pain score was more associated with greater thalamus–insular cortex functional connectivity (r = 0.41; p = 0.01) whereas more severe nerve function deficits were more related to lower thalamus–somatosensory cortex functional connectivity (r = −0.35; p = 0.03). Machine-learning group classification performance to identify individuals with the NIR nociceptor phenotype achieved an accuracy of 0.92 (95% CI 0.08) and sensitivity of 90%. Conclusions/interpretation This study demonstrates differences in functional connectivity in nociceptive processing brain regions between IR and NIR phenotypes in painful DPN. We also establish proof of concept for the utility of multimodal MRI as a biomarker for painful DPN by using a machine-learning approach to classify individuals into sensory phenotypes. Graphical abstract
Loss-of-function mutations/inactivating mutations of the human chorionic gonadotropin/luteinizing hormone receptor (hCG/LHR), a G-protein coupled receptor, lead to impaired Leydig cell differentiation. Leydig cell hypoplasia/agenesis/dysplasia (LCH) is one of the causes of male pseudohermaphroditism (MPH). We studied a 19-year-old MPH patient with female phenotype and 46,XY karyotype. Testicular histology and hormonal profile of the patient is typical of LCH. Nucleotide sequencing of exon 11 of hLHR identified a novel T1505C transversion mutation. The mutation is homozygous in the patient and is heterozygous in both parents. The single base mutation caused the substitution of a conserved leucine at 502 position to proline in transmembrane helix (TM) IV of the hLHR. This is the first LCH causing mutation identified in TM IV of the hLHR. Expression study of the mutated hLHR in human embryonic kidney (HEK)293 cells showed reduced cAMP production and ligand binding. Receptor trafficking was not affected by the mutation when the green fluorescence protein conjugated mutated receptor was expressed in HEK293 cells. The mutation caused inactivation of the hLHR and resulted in LCH in the patient.
Aims: Painful diabetic neuropathy (Painful-DN) is a common disabling condition, with no objective biomarkers and less than optimal treatments. RS-fMRI is a quick (5 minute) functional imaging method that evaluates regional cortical interactions that occur when a subject is at rest. The aim of this study was to explore resting functional connectivity of the somotomotor network in painful DN as a possible objective biomarker for neuropathic pain. Methods: 46 patients with diabetes (No DN, n=16; Painful DN, n=15; Painless DN, n=15) and 16 healthy volunteers underwent detailed clinical and neurophysiological assessments. RS-fMRI data were acquired at 3T (Philips Healthcare) and functional connectivity analysis was performed using FSL (www.fmrib.ox.ac.uk/fsl). Results: There was reduced functional connectivity in the sensorimotor network (postcentral gyrus -42,-22,56; all TFCE, corrected p<0.05) and default mode network (precuneus -6,-46,40; p<0.05), superior frontal gyrus (34,62,60; p<0.05), Heschl’s gyrus (-42,-22,12; p<0.05), insular cortex (34,62,60; p<0.05) and superior parietal lobule (-22,-42,68; p<0.05). Somatomotor network functional connectivity significantly correlated with quantitative pain assessments (Short Form 36, r=-0.52; p=0.03 and Chronic Pain Acceptance Questionnaire r=-0.55, p=0.045). Conclusion: These findings demonstrate that chronic pain has a widespread impact on overall brain function in diabetes, and suggests that disruptions of the resting state networks may underlie the cognitive and behavioural impairments accompanying chronic pain. Specifically within the somatomotor network, we have demonstrated abnormal functional connectivity in painful DPN which correlates with clinical measures of pain and behaviour. RS-fMRI has the potential to serve as an objective biomarker for the chronic pain condition in DPN. Disclosure D. Selvarajah: None. M. Awadh: None. R. Gandhi: None. I.D. Wilkinson: None. S. Tesfaye: Speaker's Bureau; Self; Pfizer Inc.. Other Relationship; Self; Janssen Pharmaceuticals, Inc., Takeda Development Centre Europe Ltd.. Advisory Panel; Self; Wörwag Pharma GmbH & Co. KG.
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