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Introduction. Endometriosis has been described as the presence of endometrial tissue outside uterine cavity. Scar endometriosis (SE) is a rare disease reported in 0.03-1.08% of women following gynaecologic surgery. In our retrospective observational cohort study we studied anamnesis, symptoms, surgical procedures and outcomes linked to scar endometriosis in our medical experience from 2004 to 2018. Methods. We reviewed the medical records of 46 patients with a histopathological diagnosis of SE. All patients had a history of at least one previous caesarean section (n=46, 100%). Forty-two patients (91,3%) complained gradually growing nodular abdominal mass near or adjacent to caesarean incision scar, while only 4 patients (8,6%) complained aspecific abdominal pain. Ultrasound scan was performed in all patients (n=46, 100%) and mean size of the nodules at US was 26,8 ± 13,8 mm. Results. All patients underwent surgery. Seven patients (15,2%) needed mesh implantation, while 39 patients (84,8%) underwent local resection with reconstruction of muscle fascia. Mean follow-up was 31,6 ± 14 months and no patients reported local recurrence of disease. Conclusion. high suspicion of scar endometriosis are painful nodule in the abdominal scar. Wide surgical excision is the treatment of choice. [ABSTRACT FROM AUTHOR]

Objectives: Aberrant movement-related cortical activity has been linked to impaired motor function in Parkinson's disease (PD). Dopaminergic drug treatment can restore these, but dosages and long-term treatment are limited by adverse side-effects. Effective non-pharmacological treatments could help reduce reliance on drugs. This experiment reports the first study of home-based electroencephalographic (EEG) neurofeedback training as a non-pharmacological candidate treatment for PD. Our primary aim was to test the feasibility of our EEG neurofeedback intervention in a home setting., Methods: Sixteen people with PD received six home visits comprising symptomology self-reports, a standardised motor assessment, and a precision handgrip force production task while EEG was recorded (visits 1, 2 and 6); and 3 × 1-hr EEG neurofeedback training sessions to supress the EEG mu rhythm before initiating handgrip movements (visits 3 to 5)., Results: Participants successfully learned to self-regulate mu activity, and this appeared to expedite the initiation of precision movements (i.e., time to reach target handgrip force off-medication pre-intervention = 628 ms, off-medication post-intervention = 564 ms). There was no evidence of wider symptomology reduction (e.g., Movement Disorder Society Unified Parkinson's Disease Rating Scale Part III Motor Examination, off-medication pre-intervention = 29.00, off-medication post intervention = 30.07). Interviews indicated that the intervention was well-received., Conclusion: Based on the significant effect of neurofeedback on movement-related cortical activity, positive qualitative reports from participants, and a suggestive benefit to movement initiation, we conclude that home-based neurofeedback for people with PD is a feasible and promising non-pharmacological treatment that warrants further research., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Conclusion: High suspicion of scar endometriosis are painful no-dule in the abdominal scar. Wide surgical excision is the treatment of choice., Introduction: Endometriosis has been described as the presence of endometrial tissue outside uterine cavity. Scar endometriosis (SE) is a rare disease reported in 0.03-1.08% of women following gynaecologic surgery. In our retrospective observational cohort study we studied anamnesis, symptoms, surgical procedures and outcomes linked to scar endometriosis in our medical experience from 2004 to 2018., Methods: We reviewed the medical records of 46 patients with a histopathological diagnosis of SE. All patients had a history of at least one previous caesarean section (n=46, 100%). Forty-two patients (91,3%) complained gradually growing nodular abdominal mass near or adjacent to caesarean incision scar, while only 4 patients (8,6%) complained aspecific abdominal pain. Ultrasound scan was performed in all patients (n=46, 100%) and mean size of the nodules at US was 26,8 ± 13,8 mm., Results: All patients underwent surgery. Seven patients (15,2%) needed mesh implantation, while 39 patients (84,8%) underwent local resection with reconstruction of muscle fascia. Mean follow-up was 31,6 ± 14 months and no patients reported local recurrence of disease.

The objectives of this paper were to directly examine the roles of central and peripheral vision in hazard perception and to test whether perceptual training can enhance hazard perception. We also examined putative cortical mechanisms underpinning any effect of perceptual training on performance. To address these objectives, we used the gaze-contingent display paradigm to selectively present information to central and peripheral parts of the visual field. In Experiment 1, we compared hazard perception abilities of experienced and inexperienced drivers while watching video clips in three different viewing conditions (full vision; clear central and blurred peripheral vision; blurred central and clear peripheral vision). Participants' visual search behaviour and cortical activity were simultaneously recorded. In Experiment 2, we determined whether training with clear central and blurred peripheral vision could improve hazard perception among non-licensed drivers. Results demonstrated that (i) information from central vision is more important than information from peripheral vision in identifying hazard situations, for screen-based hazard perception tests, (ii) clear central and blurred peripheral vision viewing helps the alignment of line-of-gaze and attention, (iii) training with clear central and blurred peripheral vision can improve screen-based hazard perception. The findings have important implications for road safety and provide a new training paradigm to improve hazard perception., (Crown Copyright © 2020. Published by Elsevier Ltd. All rights reserved.)

Self-talk is a psychological skill that benefits motor performance by controlling and organizing performers' thoughts. While the behavioral effects of self-talk are clear, research on the mechanisms underpinning the effects of different modes of self-talk is sparse. To address this issue, we propose and test a psychophysiological model of the effects of self-talk on motor performance. Forty golf novices practiced a golf putting task while using either instructional or motivational self-talk preceding each putt. We measured performance (radial error), technique (club kinematics and muscle activity), cardiac activity (heart-rate and event-related heart-rate change), as well as electroencephalographic alpha power and connectivity in a randomized (group: instructional self-talk, motivational self-talk) experimental design. Instructional self-talk promoted superior technique and was associated with greater parietal alpha power and weaker connectivity between frontal and parietal electrodes and all other scalp sites, possibly indicative of increased top-down control of action. These findings provide initial evidence for an information-processing mechanism underlying the benefits of instructional self-talk. They also cast doubt on the validity of left-frontotemporal connectivity as a measure of verbal-analytic processing during motor tasks. Motivational self-talk led to increased heart-rate and reduced event-related heart rate variability, suggesting an effort-based mechanism to explain the benefits of motivational self-talk. Our study represents the most complete multi-measure investigation of self-talk to date. We hope that our psychophysiological model of self-talk will encourage researchers to move beyond the exclusive reliance on behavioral and self-report measures to discover the mechanisms underlying the benefits of self-talk for performance., (© 2020 The Authors. Psychophysiology published by Wiley Periodicals LLC on behalf of Society for Psychophysiological Research.)

This study was designed to test the theorized link between reinvestment, motor chunks, and conscious processing, to provide a thorough examination of reinvestment theory. The authors measured electroencephalographic power and connectivity alongside self-reported conscious processing and behavioral indices of chunking in a 2 (group) × 5 (block) mixed-model design. A total of 55 individuals acquired a motor sequence (blocks A1, A2, A3, and A4) by relatively explicit (errorful) or implicit (errorless) paradigms. Then they performed in a pressure condition (block T). Results confirmed that chunking characterizes both modes of acquisition. However, explicit acquisition resulted in quicker chunking, reduced conscious processing, and increased cortical efficiency (left-temporal high-alpha power). In support of reinvestment theory, self-reported conscious processing tended to increase under pressure among explicit trainees only. In contrast to reinvestment theory, this had no adverse effect on performance. The results endorse explicit acquisition as an effective mode of training and provide a new neurophysiological explanation of this phenomenon.

While the majority of phosphatases are metalloenzymes, the prevailing model for the reactions catalyzed by protein tyrosine phosphatases does not involve any metal ion, yet both metal cations and oxoanions affect their enzymatic activity. Mg 2+ and Zn 2+ activate and inhibit, respectively, protein tyrosine phosphatase 1B (PTP1B). Molecular dynamics simulations, metadynamics, and quantum chemical calculations in combination with experimental investigations demonstrate that Mg 2+ and Zn 2+ compete for the same binding site in the active site only in the closed conformation of the enzyme in its phosphorylated state. The two cations have different effects on the arrangements and activities of water molecules that are necessary for the hydrolysis of the phosphocysteine intermediate in the second catalytic step of the reaction. Remarkable differences between the established structural enzymology of PTP1B investigated ex vivo and the function of PTP1B in vivo become evident. Different reaction pathways are viable when the presence of metal ions and their cellular concentrations are considered. The findings suggest that the substrate delivers the inhibitory Zn 2+ ion to the active site. The inhibition and activation can be ascribed to the different coordination chemistries of Zn 2+ and Mg 2+ ions and the orientation of the metal-coordinated water molecules. Metallochemistry adds an additional dimension to the regulation of PTP1B and presumably other members of this enzyme family.

A new paradigm in metallobiochemistry describes the activation of inactive metalloenzymes by metal ion removal. Protein tyrosine phosphatases (PTPs) do not seem to require a metal ion for enzymatic activity. However, both metal cations and metal anions modulate their enzymatic activity. One binding site is the phosphate binding site at the catalytic cysteine residue. Oxyanions with structural similarity to phosphate, such as vanadate, inhibit the enzyme with nanomolar to micromolar affinities. In addition, zinc ions (Zn 2+ ) inhibit with picomolar to nanomolar affinities. We mapped the cation binding site close to the anion binding site and established a specific mechanism of inhibition occurring only in the closed conformation of the enzyme when the catalytic cysteine is phosphorylated and the catalytic aspartate moves into the active site. We discuss this dual inhibition by anions and cations here for PTP1B, the most thoroughly investigated protein tyrosine phosphatase. The significance of the inhibition in phosphorylation signaling is becoming apparent only from the functions of PTP1B in the biological context of metal cations as cellular signaling ions. Zinc ion signals complement redox signals but provide a different type of control and longer lasting inhibition on a biological time scale owing to the specificity and affinity of zinc ions for coordination environments. Inhibitor design for PTP1B and other PTPs is a major area of research activity and interest owing to their prominent roles in metabolic regulation in health and disease, in particular cancer and diabetes. Our results explain the apparent dichotomy of both cations (Zn 2+ ) and oxyanions such as vanadate inhibiting PTP1B and having insulin-enhancing ("anti-diabetic") effects and suggest different approaches, namely targeting PTPs in the cell by affecting their physiological modulators and considering a metallodrug approach that builds on the knowledge of the insulin-enhancing effects of both zinc and vanadium compounds.

SLC30A8 encodes a zinc transporter ZnT8 largely restricted to pancreatic islet β- and α-cells, and responsible for zinc accumulation into secretory granules. Although common SLC30A8 variants, believed to reduce ZnT8 activity, increase type 2 diabetes risk in humans, rare inactivating mutations are protective. To investigate the role of Slc30a8 in the control of glucagon secretion, Slc30a8 was inactivated selectively in α-cells by crossing mice with alleles floxed at exon 1 to animals expressing Cre recombinase under the pre-proglucagon promoter. Further crossing to Rosa26:tdRFP mice, and sorting of RFP(+): glucagon(+) cells from KO mice, revealed recombination in ∼ 30% of α-cells, of which ∼ 50% were ZnT8-negative (14 ± 1.8% of all α-cells). Although glucose and insulin tolerance were normal, female αZnT8KO mice required lower glucose infusion rates during hypoglycemic clamps and displayed enhanced glucagon release (p < 0.001) versus WT mice. Correspondingly, islets isolated from αZnT8KO mice secreted more glucagon at 1 mm glucose, but not 17 mm glucose, than WT controls (n = 5; p = 0.008). Although the expression of other ZnT family members was unchanged, cytoplasmic (n = 4 mice per genotype; p < 0.0001) and granular (n = 3, p < 0.01) free Zn(2+) levels were significantly lower in KO α-cells versus control cells. In response to low glucose, the amplitude and frequency of intracellular Ca(2+) increases were unchanged in α-cells of αZnT8KO KO mice. ZnT8 is thus important in a subset of α-cells for normal responses to hypoglycemia and acts via Ca(2+)-independent mechanisms., (© 2015 by The American Society for Biochemistry and Molecular Biology, Inc.)

Zinc ions, though redox-inert, have either pro-antioxidant or pro-oxidant functions at critical junctures in redox metabolism and redox signalling. They are released from cells and in cells, e.g. from metallothionein, a protein that transduces redox signals into zinc signals (1). The released zinc ions inhibit enzymes such as protein tyrosine phosphatases (PTPs), key regulatory enzymes of cellular phosphorylation signalling. The Ki(Zn) value for inhibition of receptor PTPB is 21pM (2). The binding is about as tight as the binding of zinc to zinc metalloenzymes and suggests tonic zinc inhibition. PTP1-B (PTPN1), an enzyme regulating the insulin and leptin receptors and involved in cancer and diabetes pathobiochemistry, has a Ki(Zn) value of about 5nM (3). Zinc ions bind to the enzyme in the closed conformation when additional metal-binding ligands are brought into the vicinity of the active site. In contrast, redox reactions target cysteines in the active sites of PTPs in the open conformation. This work provides a molecular basis how hydrogen peroxide and free zinc ions generated by growth factor signalling stimulate phosphorylation signalling differentially. (Supported by the Biotechnology and Biological Sciences Research Council UK, grant BB/K001442/1.)., (Copyright © 2014. Published by Elsevier Inc.)

Protein tyrosine phosphatases (PTPs) are key enzymes in cellular regulation. The 107 human PTPs are regulated by redox signalling, phosphorylation, dimerisation, and proteolysis. Recent findings of very strong inhibition of some PTPs by zinc ions at concentrations relevant in a cellular environment suggest yet another mechanism of regulation. One of the most extensively investigated PTPs is PTP1B (PTPN1). It regulates the insulin and leptin signalling pathway and is implicated in cancer and obesity/diabetes. The development of novel assay conditions to investigate zinc inhibition of PTP1B provides estimates of about 5.6 nM affinity for inhibitory zinc(II) ions. Analysis of three PTP1B 3D structures (PDB id: 2CM2, 3I80 and 1A5Y) identified putative zinc binding sites and supports the kinetic studies in suggesting an inhibitory zinc only in the closed and cysteinyl-phosphate intermediate forms of the enzyme. These observations gain significance with regard to recent findings of regulatory roles of zinc ions released from the endoplasmic reticulum.

Free fatty acids (FFA) cause apoptosis of pancreatic beta-cells and might contribute to beta-cell loss in type 2 diabetes via the induction of endoplasmic reticulum (ER) stress. We studied here the molecular mechanisms implicated in FFA-induced ER stress initiation and apoptosis in INS-1E cells, FACS-purified primary beta-cells and human islets exposed to oleate and/or palmitate. Treatment with saturated and/or unsaturated FFA led to differential ER stress signaling. Palmitate induced more apoptosis and markedly activated the IRE1, PERK and ATF6 pathways, owing to a sustained depletion of ER Ca(2+) stores, whereas the unsaturated FFA oleate led to milder PERK and IRE1 activation and comparable ATF6 signaling. Non-metabolizable methyl-FFA analogs induced neither ER stress nor beta-cell apoptosis. The FFA-induced ER stress response was not modified by high glucose concentrations, suggesting that ER stress in primary beta-cells is primarily lipotoxic, and not glucolipotoxic. Palmitate, but not oleate, activated JNK. JNK inhibitors reduced palmitate-mediated AP-1 activation and apoptosis. Blocking the transcription factor CHOP delayed palmitate-induced beta-cell apoptosis. In conclusion, saturated FFA induce ER stress via ER Ca(2+) depletion. The IRE1 and resulting JNK activation contribute to beta-cell apoptosis. PERK activation by palmitate also contributes to beta-cell apoptosis via CHOP.

Several AA, utilizing the biochemical method (DCC) showed the presence or absence of hormonal receptor in either synchronous or metachronous metastatic nodes (N) can reproduce the receptor assessment (AR) of the primary breast tumor (T). We evaluated the AR in T and in synchronous N, by using two morphological methods, immunocytochemical and histofluorescent, to detect the nuclear Estrogen Receptor (ER1) and cytoplasmic sites of the II type (ER2 and PgR2). We studied 50 patients who underwent radical mastectomy for breast cancer N+. In this series we founded a high correlation between AR in T and in N: 82% for ER1, 94% for ER2, and 92% for PgR2. Also we observed 4 cases (2 ER1 and 2 PgR2) which presented the receptor in N only. These data are comparable to results obtained with the DCC method and confirm the opportunity to perform also morphological techniques to evaluate AR in breast cancer to take into consideration also cellularity and tumor heterogeneity informations.

A study is presented of the characteristics of redox-linked proton translocation in the b-c1 complex isolated from beef-heart mitochondria and reconstituted into phospholipid vesicles. Measurements of the H+/e- stoichiometry, with three different methods, show that four protons are released from the vesicles per 2e- flowing from quinols to cytochrome c, two of these protons formally deriving from scalar oxidation of quinols by cytochrome c. This H+/e- stoicheiometry is independent of the initial redox state of the b-c1 complex (fully reduced or oxidized) and the rate of electron flow through the complex. It does not change in the pH range 6.0 - 7.2, but declines to 1.5 going with pH from 7.2 - 8.3. This decrease is accompanied by enhancement of the rate of electron flow in the coupled state. Collapse of delta psi effected by valinomycin addition to turning-over b-c1 vesicles resulted in substantial oxidation of cytochrome b-566 and comparable reduction of cytochrome c1, with little oxidation of cytochrome b-562. Nigericin alone had no effect on the steady-state redox levels of b and c cytochromes. Its addition in the presence of valinomycin caused oxidation of b cytochromes but no change in the redox state of cytochrome c1. Valinomycin alone caused a marked enhancement of the rate of electron flow through the complex. Nigericin alone was ineffective, but caused further stimulation of electron flow when added in the presence of valinomycin. The data presented are discussed in terms of two mechanisms: the Q cycle and a model based on combination of protonmotive catalysis by special bound quinone and proton conduction along pathways in the apoproteins.