Sex and age determination of human mandible using anthropological parameters and TCI and Kvaal methods: study of a Serbian medieval sample.

PURPOSE: The aim of the study was to test the efficacy, reliability, and applicability of the Kvaal and Tooth Coronal Index (TCI) age determination techniques, and then to compare them with each other, as well as with the conventional anthropological age and sex determination techniques. METHODS: The analyzed material originates from the medieval necropolis of the Vinca-Belo brdo site. During the research, 60 periapical (PA) and 30 orthopantomographic (OPT) images were analyzed. On each analyzed tooth, age assessment was performed using both TCI and Kvaal techniques. The obtained values of dental estimated age were compared with age estimated by anthropological analysis, and the deviations between the estimated and chronological age were analyzed in relation to the assessment technique, type of dental radiograph, tooth group, sex, and age. RESULTS: The mean error between TCI and the osteological method was 8.44 (SD = 7.56, Min = 0.169, Max = 36.4) and between Kvaal and the osteological method was 7.71 (SD = 5.57, Min = 0.133, Max = 26.7). The average value of age recorded by TCI method was 32.5 years and by Kvaal method was 34.7 years. There was no statistically significant difference based on the two radiographic methods, gender, individual teeth, or tooth group pairs. There was a statistically significant positive correlation between age and the error present. CONCLUSION: Gender determination based only on the mandible has a high correlation with the anthropological gender determination. The Kvaal method and the TCI method have proven their efficiency, reliability, and applicability. Significant correlation has been observed between dental and anthropological age and sex determination methods.

Depression/anxiety symptoms in axial spondyloarthritis and psoriatic arthritis patients in Serbia: a pilot study.

To assess prevalence and change of depression/anxiety symptoms in spondyloarthritis patients and feasibility of depression/anxiety questionnaires. 43 Patients with axial spondyloarthritis (axSpA) and 27 patients with psoriatic arthritis (PsA) were consecutively recruited. There were 34 patients on biologics and 36 patients on nonbiologics. Patients were not previously treated for depression. The demographic variables, pain, patient global assessment, laboratory, clinical findings, diseases activity scores, Beck Depression Inventory (BDI) and Depression Anxiety and Stress Scale-short version (DASS-21) were collected. The study visits were at the beginning, after 1 month, after 3 and after 6 months. In axSpA and PsA patients on biologics, BDI and DASS-21 were significantly lower compared to nonbiologics group during time. The axSpA patients on biologics had significantly lower BDI and depression severity by BDI at each time point and lower DASS-21 after 1, 3 and 6 months. BDI in PsA patients who received biological therapy was significantly lower after 3 and 6 months. In biologics groups, BDI significantly decreased after 3 months in axSpA patients and after 1 month in PsA patients. In axSpA patients, there was a medium correlation between BDI and axial pain, patient global assessment and disease activity scores. The biological therapy significantly affected the depression/anxiety symptoms in axSpA and PsA during time. BDI moderately correlated with pain and disease activity in axSpA. BDI and DASS-21 are easy to use in daily practice.

Construct validity and sensitivity to change of Belgrade Ultrasound Enthesitis Score in patients with spondyloarthritis: a pilot study.

The objective of this study was to determine the construct validity and sensitivity to change of Belgrade Ultrasound Enthesitis Score (BUSES) in spondyloarthritis patients. Seventy-six spondyloarthritis patients with enthesitis were included in this pilot, prospective, double-blinded ultrasound study. Thirty-four patients received biological and forty-two patients received non-biological therapy. BUSES was determined at the beginning, after 1, 3, and 6 months. Spearman's correlation coefficient was calculated between BUSES and baseline characteristics. Brunner-Langer mixed non-parametric ANOVA was used to examine sensitivity to change of BUSES and effect of biological therapy on BUSES. Effect of time on the presence of each of the ultrasound enthesitis signs (increased thickness, hypoehogenicity, Power Doppler, enthesophytes, and erosions) was assessed using Cochran Q test. There was a weak, positive correlation between BUSES and disease duration, clinical enthesitis score, BASFI, BASDAI, and ASDAS-ESR/CRP. BUSES was higher at the beginning than after 1 month (p = 0.004), after 3 months (p < 0.001) and after 6 months (p < 0.001), as well as BUSES was higher after 1 month than after 3 months (p < 0.001) and after 6 months (p = 0.002). There is no difference in efficiency between non-biological and biological therapies on BUSES. Increased thickness, hypoechogenicity, and Power Doppler have decreased on Achilles tendon's and plantar fascia's enthesis over time. BUSES has a certain degree of construct validity because of the weak, positive correlation with parameters referring to severity of spondyloarthritis. BUSES demonstrated sensitivity to change over time due to decreasing of ultrasound acute enthesitis signs in treated spondyloarthritis patients. BUSES could be useful for monitoring the progression of enthesitis and effectiveness of the treatment.

Construct validity and reliability of ultrasound disease activity score in assessing joint inflammation in RA: comparison with DAS-28.

OBJECTIVE: To investigate the construct validity and reliability of US DAS compared with 28-joint DAS (DAS-28) in assessing joint inflammation and in prediction of structural damage in patients with RA. METHODS: Ninety patients with active RA were prospectively recruited and followed up during the 6 months of treatment. The patients underwent clinical, laboratory and X-ray assessment, along with blinded power Doppler US (PDUS) and grey-scale (GS) US (GSUS) examination at baseline and 6 months. A subgroup of 25/90 randomly assigned patients underwent MRI examination of their hands at baseline. A PDUS examination of 22 joints and GSUS examination for effusion/hypertrophy (E/H) of 28 joints were performed by two independent examiners, blinded to clinical findings. E/H was qualitatively assessed as absent or present, and PD signal was semi-quantitatively graded from 0 to 3. PDUS score for synovitis in 22 joints and GS score for E/H in 28 joints were included in US DAS calculation. Clinical scoring, PDUS and GSUS inter-observer reliability were evaluated. RESULTS: Strong correlation was found between US DAS and standard assessment of disease activity such as the DAS-28, ESR and CRP levels. Correlation between US DAS and patients' and physicians' visual analogue scale of activity was moderate, whereas correlations of US DAS with Health Assessment Questionnaire - Disability Index (HAQ-DI) and Short Form 36 Health Survey (SF-36) were weak to moderate. US DAS correlated with X-ray, MRI and US parameters and rates of joint damage. CONCLUSION: US DAS better anticipated future joint damage than standard DAS-28.

Central cholinergic modulation of blood pressure short-term variability.

The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treatment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V(1a) antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.

Central vasopressin V(1a) and V(1b) receptors modulate the cardiovascular response to air-jet stress in conscious rats.

This study investigates the contribution of central vasopressin receptors in the modulation of systolic arterial pressure (SAP) and heart rate (HR) response to air-jet stress in conscious Wistar rats equipped with a femoral arterial catheter and intracerebroventricular cannula using novel non-peptide and selective vasopressin V(1a) (SR49059) and V(1b) (SSR149415) antagonists. The effects of stress on SAP and HR were evaluated by measuring the maximal response to stress, the latency of the maximal response, the duration of the recovery period, and the increase in the low frequency (LF) short-term variability component. Stress induced a parallel and almost immediate increase in both SAP and HR, followed by enhanced LF SAP variability in the recovery period. Pretreatment of rats with V(1a) antagonist did not affect the maximal increase or the latency of SAP and HR response to acute stress, but shortened the recovery period of SAP and HR and prevented the increase in LF SAP. The V(1b) antagonist reduced the maximal increase in SAP without affecting HR and their latencies, shortened the recovery period of SAP and inhibited the increase in LF SAP variability. These results indicate that both central V(1a) and V(1b) receptors mediate cardiovascular changes induced by air-jet stress in conscious rats.

[Ultrasonography of the first metatarsophalangeal joint in gout].

INTRODUCTION: About one half of the first gout attacks occur in the first metatarsophalangeal joint (MTPJ1); in the disease course this joint is practically inevitably affected. Radiographic evidence of bone erosions is the indication for hypouricaemic therapy in order to prevent joint destruction and nephropathy. Advantages of ultrasonography (US) comparing to conventional x-ray findings in depicting early bone erosions in various inflammatory arthropathies have been demonstrated by several studies. OBJECTIVE: The aims of this study were to compare US and x-ray findings in the detection of MTPJ1 erosions in patients with gout, to correlate sonographic and clinical features, and to detect possible characteristic sonographic features of gout. METHODS: Thirty patients (60 MTPJ1) with primary gout (ACR) and 10 age-matched control subjects (20 MTPJ1) with different inflammatory arthropathies were clinically evaluated. Standard dorsiplantar weight bearing and lateral weight bearing x-ray views of both feet were taken. US was performed and interpreted by an independent sonographer on the presence of bone erosions, synovial fluid, synovial hypertrophy, Doppler signal and hyperechoic spots. Statistical analysis was performed (Spearman and Pearson correlation coefficient, Wilcoxon and chi2 test.) RESULTS: Twenty-four studied MTPJ1 had evidence of erosions, 17 only on US and seven both on x-ray and on US (Z = -4.123; p = 0.000). US findings showed that hyperechoic spots were the most prominent feature of gouty MTPJ1 (chi2 = 40.909; p = 0.000), followed by erosions and synovial fluid presentation. CONCLUSION: US of MTPJ1 in gout discovers significantly more erosions than x-ray, which may have therapeutic implications. The evidence of hyperechoic spots (surrogate crystals) of the different size, number and orientation is a major sonographic feature of the MTPJ1 in gout, which may be of importance in the diagnosis of certain cases (low serum urate, unavailable synovial fluid or the urate crystals absence).

The OMERACT Ultrasound Group: status of current activities and research directions.

Ultrasound (US) is a relatively new imaging modality in rheumatology that offers great potential as a diagnostic and management tool. In 2004, an OMERACT Ultrasound Special Interest Group was formed to address the metric qualities of US as a potential outcome measure. A preliminary systematic review highlighted the deficiencies in the literature, particularly with regard to the reliability of interpreting and acquiring images; as a consequence, a number of exercises were proposed to address these issues. This report describes a series of iterative studies that have resulted in improved intra- and inter-reader reliability for detecting and scoring synovitis from both static and real-time images of the hand joints of patients with rheumatoid arthritis. The reliability of acquiring images was also enhanced using standardized positions. Future studies will assess the value of US in clinical trials.

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study.

Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V(1a), V(1b), and V(2) antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (T(b)) was also investigated. Under basal conditions, V(1a) antagonist increased HF-BP and T(b), and this was prevented by metamizol. V(1b) antagonist enhanced HF-BP without affecting T(b), and V(2) antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V(1a) antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V(1b) antagonist prevented BP but not HR variability changes, whereas V(2) antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V(1a) and V(1b) but not V(2) antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V(1a), V(1b), and cognate V(2) receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V(1a) or V(1b), but not V(2) receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.

Specific enhancement of sarcomeric response to Ca2+ protects murine myocardium against ischemia-reperfusion dysfunction.

Alteration in myofilament response to Ca2+ is a major mechanism for depressed cardiac function after ischemia-reperfusion (I/R) dysfunction. We tested the hypothesis that hearts with increased myofilament response to Ca2+ are less susceptible to I/R. In one approach, we studied transgenic (TG) mice with a constitutive increase in myofilament Ca2+ sensitivity in which the adult form of cardiac troponin I (cTnI) is stoichiometrically replaced with the embryonic/neonatal isoform, slow skeletal TnI (ssTnI). We also studied mouse hearts with EMD-57033, which acts specifically to enhance myofilament response to Ca2+. We subjected isolated, perfused hearts to an I/R protocol consisting of 25 min of no-flow ischemia followed by 30 min of reperfusion. After I/R, developed pressure and rates of pressure change were significantly depressed and end-diastolic pressure was significantly elevated in nontransgenic (NTG) control hearts. These changes were significantly blunted in TG hearts and in NTG hearts perfused with EMD-57033 during reperfusion, with function returning to nearly baseline levels. Ca2+- and cross bridge-dependent activation, protein breakdown, and phosphorylation in detergent-extracted fiber bundles were also investigated. After I/R NTG fiber bundles exhibited a significant depression of cross bridge-dependent activation and Ca2+-activated tension and length dependence of activation that were not evident in TG preparations. Only NTG hearts demonstrated a significant increase in cTnI phosphorylation. Our results support the hypothesis that specific increases in myofilament Ca2+ sensitivity are able to diminish the effect of I/R on cardiac function.

Effects of nonpeptide and selective V1 and V2 antagonists on blood pressure short-term variability in spontaneously hypertensive rats.

Effects of V(1) (OPC-21268) and V(2) (OPC-31260) vasopressin antagonists on blood pressure (BP) short-term variability were investigated in adult spontaneously hypertensive rats (SHR) under basal conditions and after the stimulation of vasopressin release by hemorrhage. BP was recorded intra-arterially and sampled at 20 Hz to be analyzed on a personal computer. BP time spectra were calculated on 30 stationary overlapping 2048 point-time series. Spectral power was estimated in total (0.00976 - 3 Hz), very low frequency (VLF: 0.00976 - 0.195 Hz), low frequency (LF: 0.195 - 0.605 Hz), and high frequency (HF: 0.8 - 3 Hz) regions. Under basal conditions a V(1) antagonist (5 mg/kg, i.v.) decreased BP without affecting BP variability, while combined (V(1) + V(2)) blockade or V(2) blockade (1 mg/kg, i.v.) alone did not affect cardiovascular parameters. Mild hemorrhage (5 ml/kg per min) increased HF-BP variability, while moderate (10 ml/kg per min) and massive (15 ml/kg per min) hemorrhage did not affect it. In V(1), but not V(2), antagonist pre-treated SHR HF-BP increased significantly after moderate and massive hemorrhage. V(1) or V(2) antagonist pre-treatment also enhanced VLF-BP variability during massive hemorrhage. Moreover V(1) blockade prevented hemorrhage-induced bradycardia, while V(2) blockade potentiated it. It follows that in adult SHR, vasopressin buffers BP oscillations in HF and VLF frequency domains only in hypovolaemic conditions and that the modulation of the autonomic adjustment of the HR to hemorrhage by vasopressin is preserved.