Recent research shows that major levels of psychological distress correlate with higher pain and reduced function in patients with shoulder and rotator cuff pathology. A systematic review updating a review published in 2016 was conducted to determine the degree of consistency and the strength of association between psychosocial factors and patient-reported outcomes (PROMs) in patients with rotator cuff repair (RCR) with new high-quality literature.

The bibliographic searches were conducted from May to June 2020 within the following databases MEDLINE/PubMed, EMBASE, Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycINFO, and Web of Science. The articles included should discuss the association between psychosocial factors and outcomes in patients with documented or diagnosed rotator cuff tears through clinical and/or radiological examination. The Methodological Index for Non-Randomized Studies (MINORS) tool was used to assess the methodological quality.

Fifteen articles were included. Negative psychosocial factors were found consistently associated with worse function and disability in the pre- and post-operative period. In particular, psychosocial factors regarding emotional or mental health were associated with a weak to a substantial degree with preoperative and postoperative function/disability and pain intensity in patients undergoing RCR.

In patients undergoing repair of the rotator cuff tear, there was a correlation between poor psychological function before surgery and worsening post-surgical outcomes, such as persistence of postoperative pain intensity and worse levels of function/disability.

In patients undergoing repair of the rotator cuff tear, there was a correlation between poor psychological function before surgery and worsening post-surgical outcomes, such as persistence of postoperative pain intensity and worse levels of function/disability.Although phenylalanine (Phe) is known to be neurotoxic in phenylketonuria (PKU), its exact pathogenetic mechanisms of brain damage are still poorly known. Furthermore, much less is known about the role of the Phe derivatives phenylacetic (PAA), phenyllactic (PLA) and phenylpyruvic (PPA) acids that also accumulate in this this disorder on PKU neuropathology. Previous in vitro and in vivo studies have shown that Phe elicits oxidative stress in brain of rodents and that this deleterious process also occurs in peripheral tissues of phenylketonuric patients. In the present study, we investigated whether Phe and its derivatives PAA, PLA and PPA separately or in combination could induce reactive oxygen species (ROS) formation and provoke DNA damage in C6 glial cells. We also tested the role of L-carnitine (L-car), which has been recently considered an antioxidant agent and easily cross the blood brain barrier on the alterations of C6 redox status provoked by Phe and its metabolites. We first observed that cell viability was not changed by Phe and its metabolites. Furthermore, Phe, PAA, PLA and PPA, at concentrations found in plasma of PKU patients, provoked marked DNA damage in the glial cells separately and when combined. Of note, these effects were totally prevented (Phe, PAA and PPA) or attenuated (PLA) by L-car pre-treatment. In addition, a potent ROS formation also induced by Phe and PAA, whereas only moderate increases of ROS were caused by PPA and PLA. Pre-treatment with L-car also prevented Phe- and PAA-induced ROS generation, but not that provoked by PLA and PPA. Thus, our data show that Phe and its major metabolites accumulated in PKU provoke extensive DNA damage in glial cells probably by ROS formation and that L-car may potentially represent an adjuvant therapeutic agent in PKU treatment.Stress adversely affects the cellular and electrophysiological mechanisms of memory; however, crocin has beneficial effects on brain functions. Nonetheless, the electrophysiological effects of using this active saffron component at different doses are not yet studied in rats under chronic restraint stress. Therefore, this study compared the impact of crocin at different doses on the excitability and long-term potentiation (LTP) in the CA1 area of rats, as well as their electroencephalogram (EEG) responses, hippocampal and frontal cortical glucose levels under chronic restraint stress (an emotional stress model). Forty rats were allocated into five groups of control, sham, restraint stress (6 h/day/21 days), and two stress groups receiving intraperitoneal injections of crocin (30, 60 mg/kg/day). Besides measuring the slope and amplitude of field excitatory postsynaptic potentials (fEPSPs) in the input-output and LTP curves, the EEG waves and hippocampal and frontal cortical glucose levels were assessed in all groups. learn more Chronic restraint stress significantly decreased the fEPSP slope and amplitude in the input-output curves and after LTP induction. Both doses of crocin (60 and particularly 30 mg/kg) significantly improved fEPSP slope and amplitude in the stressed groups. Also, stress and crocin only at a dose of 30 mg/kg altered the EEG waves. Hippocampal and frontal cortical glucose levels displayed no significant differences in the experimental groups. Crocin at doses of 60 mg/kg/day and particularly 30 mg/kg/day reversed the harmful effects of chronic restraint stress on LTP as a cellular memory-related mechanism. However, only the lower dose of crocin affected the electrical brain activity in EEG.In the past decade, monoamine oxidase (MAO) with 2 isoforms, MAO-A and B, has emerged as an important source of mitochondrial reactive oxygen species (ROS) in cardio-metabolic pathologies. We have previously reported that MAO-related oxidative stress mediates endothelial dysfunction in rodent models of diabetes and diabetic patients; however, the role of MAO in the vascular impairment associated to obesity has not been investigated so far. Metformin (METF), the first-line drug in the therapy of type 2 diabetes mellitus, has been reported to elicit vasculoprotective effects via partially elucidated mechanisms. The present study was purported to assess the effects of METF on MAO expression, ROS production and vasomotor function of aortas isolated from rats with diet-induced obesity. After 24 weeks of high calorie junk food (HCJF) diet, isolated aortic rings were prepared and treated with METF (10 μM, 12 h incubation). Measurements of MAO expression (quantitative PCR and immune histochemistry), ROS production (spectrometry and immune-fluorescence) and vascular reactivity (myograph studies) were performed in rat aortic rings.