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Purpose Several studies have shown benefits of peer mentoring on wellness among medical students and health care professionals. Peer mentorship has also been pointed as having interesting potential for International Medical Graduates. However, the literature on peer mentoring at the residency level is very limited. The purpose of this paper is to assess the benefits of a resident-led pilot peer-mentoring initiative at McGill University. Design/methodology/approach Over 2 years, 17 residents from various residency programs were put in contact with a volunteer peer mentor by e-mail. The structure of the mentorship was flexible. A survey using Likert scale and free text responses was sent to all the participants. Findings There were response rates of 65 percent for mentees and 59 percent for mentors. The majority of mentees thought the service was either moderately helpful (18 percent) or helpful (36 percent). Several residents noted that communication by e-mails and lack of in-person contacts were a limitation in the mentorship experience. The most frequent challenge that led to consult the service was immigration or arrival from another province. Originality/value The results show that the program can be helpful to medical residents, is cost-effective, flexible and could be adapted and replicated elsewhere. In the future, the program will adjust to tend toward a more structured frame, highlighting the importance of in-person contacts. The small sample size of participants and the recall bias are some limitations of our study.

We present the case of likely COVID-19 associated encephalopathy in a male in his early 50s with a history of non-psychotic depression and personality disorder who presented with delirium, new psychotic symptoms and who developed paratonia and obtundation. After initial questions of neuroleptic malignant syndrome, serotonin syndrome, and stiff person syndrome were decided to not be supported by the clinical picture, conservative management and the repeated treatment of a co-ocurring mastoiditis led to improvement of mental status, regained ability to walk and speak, though a dysexecutive syndrome was left when patient was discharged to rehabilitation services. We explore the role the patient's psychiatric comorbidity had in terms of both his clinical course and the decisions and diagnostic considerations of the various treating teams involved.

Objective Depression and poor functional status (FS) frequently co-occur. Though both predict adverse surgical outcomes, research examining preoperative functional performance (FP; self-reported) and functional capacity (FC; performance-based) measures in depressed cancer patients is lacking. Prehabilitation, a preoperative intervention including exercise, nutrition, and stress-reduction, may improve FC; however, whether depressed patients benefit from this intervention remains unknown. The primary objectives were to (a) assess differences in FP and FC and (b) explore the impact of prehabilitation on FC in individuals with depressive symptoms versus those without. Method A secondary analysis was conducted on 172 colorectal cancer patients enrolled in three studies comparing prehabilitation with a control group (rehabilitation). Measures were collected at 4 weeks pre- and 8 weeks postoperatively. FP, FC, and psychological symptoms were assessed using the 36-Item Short Form Health Survey, Six-Minute Walk Distance (6MWD), and Hospital Anxiety and Depression Scale (HADS), respectively. Subjects were divided into three groups according to baseline psychological symptoms: no psychological-symptoms (HADS-N), anxiety-symptoms (HADS-A), or depressive-symptoms (HADS-D). Main objectives were tested using analyses of variance, chi-square tests, and multivariate logistic regression. Results At baseline, HADS-D reported lower FP, had shorter 6MWD, and a greater proportion walked ≤ 400 m. Prehabilitation was associated with significant improvements in 6MWD in HADS-D group but not in HADS-N or HADS-A groups. Conclusion Poorer FS was observed in subjects with depressive symptoms, and these subjects benefited most from prehabilitation intervention. Future research could examine whether severity of depression and co-occurrence of anxiety differentially impact FS and whether prehabilitation can improve psychological symptoms and quality of life. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Despite the increased morbidity and mortality associated with psychiatric illnesses, there remains a substantial level of inaccuracy of the initial psychiatric diagnoses given by nonpsychiatric physicians. This study examines the accuracy of initial psychiatric diagnoses by non-psychiatric physicians at the McGill University Health Center (MUHC).We conducted a retrospective chart review for all consultations requested from the consultation-liaison psychiatry service at MUHC. We included all the consultations from January 1, 2018, to December 30, 2018, and excluded patient data with established psychiatric diagnoses. In all requested consults, each diagnosis of a referring physician was compared with the final diagnosis given by the C-L psychiatry team. Conformity between the 2 was validated as accurate.Of the 980 referred inpatients, 875 were enrolled. Patients ranged in age and those older than 70 years constituted the largest group: 54.4% were male. For 467 patients (55.20%), the initial diagnostic impression given by the referring physicians agreed with the final diagnosis made by the C-L psychiatry team, while in 379 patients (44.80%), the initial diagnostic impression was not consistent with the final diagnosis made by the C-L team.Diagnostic impressions of neurocognitive and substance use disorders were highly accurate, but this was not the case when the referring physicians suspected depression or bipolar, personality, or psychotic disorders. This study shows that around half of the referrals were accurately diagnosed, which evinces that nonpsychiatric physicians' knowledge regarding psychiatric conditions is not optimal and that might negatively impact screening and treating these conditions.

Aripiprazole is a third-generation antipsychotic. It is prepared in many different formulations including oral, intravenous and intramuscular. The intramuscular option is currently available in fast-acting form while the long-acting (extended-release, depot) formulation was just approved by the US FDA. The purpose of this article is to review the current literature regarding the long-acting formulation of aripiprazole. Medical literature published in English on ‘aripiprazole’ or ‘Abilify®’ (Otsuka America Pharmaceutical Inc., MD, USA) was found using Pubmed, Medline and EMBASE. Publications containing the words ‘depot’, ‘long-acting’ or ‘intramuscular’ in their title or abstract were utilized. In total, two publications were reviewed for the purposes of this article. There is a scarcity of publications on the effectiveness of long-acting aripiprazole in the treatment of schizophrenia and schizoaffective disorder. However, the available literature suggests that aripiprazole depot is a well tolerated, maintenance treatment option for schizophrenia.

Pharmacological inhibitors of JNK (SP600125) and p38 (PD169316) sensitize tumor cells to Fas-mediated apoptosis. PD169316 is less potent than SP600125 and diminishes its effect when present together. Because the p38 isoforms that promote (p38alpha) or inhibit (p38beta) apoptosis are both suppressed by PD169316, we investigated their regulatory involvement in Fas-signaling. We report here, that p38alpha, but not p38beta, exerts its proapoptotic effect by inhibiting the phosphorylation and presence of c-FLIPS, but not c-FLIPL, in the DISC to promote caspase-8 activation and type I signaling in Fas-activated Jurkat cells. Its effect was enhanced by enforced expression of Flag-tagged p38alpha and was attenuated by its inactive mutant (p38alpha-AGF) or by translational silencing. By contrast, type II signaling was facilitated by p38alpha-dependent mitochondrial presence of tBid and inhibition of Bcl-2 (Ser70) phosphorylation as well as by p38alpha/beta-dependent mitochondrial localization of Bax and inhibition of phosphorylation of Bad (Ser112/Ser155). Potentiation of Fas-mediated apoptosis by the inhibition of JNK1/2 correlated with the loss of Bad (Ser136) phosphorylation and was dependent on the stimulatory effect of p38alpha on DISC and the downstream effects of both p38alpha and p38beta. These data underscore the need to reassess the findings obtained with pan-p38 inhibitors and suggest that activation of p38alpha coupled with targeted inhibition of p38beta and JNK1/2 should optimally sensitize tumor cells to Fas-mediated apoptosis.