ABSTRACT
A systematic review and meta-analysis were conducted to evaluate the association between periodontitis (PD) and chronic kidney disease (CKD) and to explore the potential influence of periodontal treatment in patients with CKD. Databases (PubMed, Web of Science, Science direct, Cochrane Database) were screened for relevant articles, focusing on the periodontal status of patients with CKD, published until December 2017. Five hundred and fifty-three articles were identified, and 37 fulfilled the inclusion criteria and were considered in this systematic review. Seventeen articles were included in the meta-analysis and 7 in the review focusing on the impact of periodontal treatment. Most of the identified studies indicated an increased incidence of PD in patients with CKD. Meta-analysis showed an association between CKD and PD, and strength of this association was increased when severe PD was considered (OR = 2.39 (1.70-3.36)). The association could be observed even after adjustment for major CKD risk factors or use of precise diagnosis criteria (OR = 2.26 for severe PD (1.69-3.01)). Analysis of cohort studies indicated an incident rate ratio (IRR) of 1.73. Periodontitis is associated with CKD after multivariable adjustment. Further studies are necessary to determine whether prevention or treatment of PD can reduce the incidence and/or severity of CKD.
Subject(s)
Periodontitis/epidemiology , Periodontitis/therapy , Renal Insufficiency, Chronic/epidemiology , Humans , Incidence , Renal Insufficiency, Chronic/physiopathology , Risk FactorsABSTRACT
This study compared the tibialis anterior (TA) surface electromyographic (sEMG) to force relationship for males and females. One-hundred participants (50 males and 50 females) performed three isometric contractions at 20, 40, 60, 80, and 100% of maximal voluntary contraction (MVC) in an apparatus designed to isolate the action of the dorsiflexors. The sEMG signal was amplified (1000x), band-pass filtered (10-500 Hz), and sampled at 2048 Hz. The load cell signal was low-pass filtered at 100 Hz and sampled at the same rate. Males were stronger than females (p < 0.05). However, there was no significant difference in the root-mean-square (RMS) amplitude of the sEMG signal between males and females (p < 0.05). Both groups exhibited a quadratic increase in the RMS across force levels (p < 0.05). The mean power frequency (MNF) of the sEMG signal for males was greater than for females (p < 0.05). Males and females exhibited a linear increase in MNF means up to 80% of MVC (p < 0.05). Between 80 and 100% MVC, the frequency values for the females plateaued while males showed a decrease (p < 0.05). The magnitude of the difference in MNF between males and females was consistent with the observation that males have greater type II muscle fiber diameters. In general, the pattern of means for RMS and MNF between males and females revealed no differences between groups in the sEMG-force relationship. We therefore conclude that there are no differences between males and females in the gradation of muscle force.
Subject(s)
Electromyography , Isometric Contraction/physiology , Muscle Strength/physiology , Muscle, Skeletal/physiology , Adolescent , Adult , Body Size , Female , Humans , Leg , Male , Muscle Fatigue/physiology , Reference Values , Sex Factors , Young AdultABSTRACT
S-[(2-Chloroethyl)carbamoyl]glutathione (SCCG), a compound formed during the decomposition of BCNU in the presence of GSH, induces DNA damage in a human lymphoblastoid cell line. This GSH conjugate was shown by direct fast atom bombardment mass spectrometric analysis to transfer an aminoethyl group to the N-7 position of guanosine. The resulting N7-(aminoethyl)guanosine adduct readily undergoes depurination. From these model studies, DNA aminoethylation appears to represent a plausible explanation as the major cause for the DNA-damaging effects exerted by SCCG.
Subject(s)
Carmustine/toxicity , DNA Damage , Glutathione/physiology , Chromatography, High Pressure Liquid , Glutathione/analogs & derivatives , Glutathione/chemistry , Glutathione/toxicity , Guanosine/chemistry , Humans , Mutagens/toxicity , Spectrometry, Mass, Fast Atom Bombardment , Spectrophotometry, Ultraviolet , Tumor Cells, Cultured/drug effects , Tumor Cells, Cultured/metabolismABSTRACT
A coumarin mercapturic acid, N-acetyl-S-(3-coumarinyl)cysteine, has been identified in the urine of coumarin-treated rats. [14C]Coumarin was applied by gavage as a single dose to male Wistar rats (10-150 mg/kg body weight). Twenty-four-hour urine was collected, and the deproteinized concentrate was analyzed for radiolabeled metabolites by HPLC. The new mercapturic acid metabolite is supposed to result from oxidative biotransformation of coumarin to its 3,4-epoxide and subsequent coupling with glutathione.