COVID-19 and the urological practice: changes and future perspectives.

INTRODUCTION: The COVID-19 pandemic has brought great challenges to the management of urological patients. Like most surgical specialties, urology has shifted towards an emergency mentality. Currently, the beginning of the de-escalation phase of the pandemic has been observed, which will certainly pose new challenges to the urological community. MATERIAL AND METHODS: A non-systematic search was conducted through the Medline and Web of Science databases. The main keywords used in the search were: 'COVID-19', 'SARS-CoV-2', 'urology'. The search included articles without time and language limitation. RESULTS: During the peak of the COVID-19 pandemic urological services had to focus on maintaining urgent-oncological and emergency-trauma procedures. First adapted recommendations were released at the end of March 2020. Primarily, they included information regarding the prioritization of surgical procedures. Currently, the beginning of the de-escalation phase in many countries has forced the necessity of establishing new degrees of priority for surgical interventions.During the COVID-19 pandemic, cancellations and rescheduling significantly extend the waiting time for outpatient appointments and surgical procedures. A network of expert high-volume centres, at every level of referentiality, should guarantee the continuity of oncological care, supported with telemedicine systems.The COVID-19 pandemic has caused a substantial decrease in clinical activity of urology residents. There also is huge potential for remote technology to address and improve education and training continuation in this field. CONCLUSIONS: Urological care has been severely impaired by the COVID-19 pandemic. Urologists must adapt to the dynamically changing reality, prioritizing the safety and well-being of their patients and their clinic workforce.

The prognostic value of programmed cell death protein ligand 1 in patients with non-muscle-invasive bladder cancer treated with bacille Calmette-Guérin immunotherapy: Current status.

OBJECTIVE: To summarise the current evidence of the significance and prognostic value of programmed cell death protein ligand 1 (PD-L1) expression in patients with non-muscle-invasive bladder cancer (NMIBC) treated with bacille Calmette-Guérin (BCG) immunotherapy. METHODS: A search was conducted in May 2020 of three electronic databases; MEDLINE, Scopus, and EMBASE. In this review we included results from original studies investigating the relationship between the PD-L1 expression and BCG response in patients with NMIBC. RESULTS: Only five relevant articles were identified in the literature to date. Some studies showed an association between increased PD-L1 expression and BCG unresponsiveness; however, other authors provided contradictory results and suggested that PD-L1 evaluation could not be used for reliable prediction of BCG response. CONCLUSIONS: The value of PD-L1 evaluation in predicting BCG response is debatable. Current evidence, based only on retrospective analyses, is inconsistent. Comparability of the results is diminished by the methodological limitations of immunohistochemistry assessment. Further multicentre, randomised trials are needed to make definitive conclusions. ABBREVIATIONS: ICs: immune cells; IHC: immunohistochemical staining; (N)MIBC: (non-) muscle-invasive bladder cancer; PD-L1: programmed cell death protein ligand 1; PD-1: programmed cell death protein 1; RC: radical cystectomy; TCs: tumour cells.

Post-treatment with rapamycin does not prevent epileptogenesis in the amygdala stimulation model of temporal lobe epilepsy.

Approximately 30% of all epilepsy cases are acquired. At present there is no effective strategy to stop epilepsy development after the precipitating insult. Recent data from experimental models pointed to the mTOR pathway, which can be potently inhibited by rapamycin. However, data on the antiepileptic and antiepileptogenic properties of rapamycin are conflicting. Therefore, we tested whether rapamycin post-treatment influences epileptogenesis in the amygdala stimulation model of temporal lobe epilepsy in rats. Animals were treated with rapamycin (6mg/kg) or vehicle daily for 2 wks, beginning 24h after stimulation. Sham-operated animals were treated with rapamycin or vehicle but were not stimulated. Animals were video-EEG monitored to detect spontaneous seizures. Animals were sacrificed 4 wks later and brains were collected for Timm staining. There were no significant differences in the number of stimulated rats developing epilepsy; latency to first spontaneous seizure; number of seizures, or seizure frequency in epileptic animals. The area occupied by mossy fibers was significantly increased in stimulated vs. sham-operated animals but was not different in animals treated with rapamycin vs. vehicle. Collectively, our data suggest that the antiepileptic or antiepileptogenic action of rapamycin is not a universal phenomenon and might be limited to certain experimental models or experimental conditions.

Status epilepticus evokes prolonged increase in the expression of CCL3 and CCL4 mRNA and protein in the rat brain.

CCL3 and CCL4 are proinflammatory chemokines belonging to the CC family. Increase in expression of mRNA coding for various chemokines including CCL3 and CCL4 has been often detected with global transcriptome profiling of brain tissue following epileptogenic stimuli as well as in epilepsy in experimental models and in human patients. Despite this, little is known about the expression of these proteins in epileptogenesis or epilepsy. In the present work CCL3 and CCL4 mRNA and protein expression were studied in the amygdala stimulation model of temporal lobe epilepsy using quantitiative PCR and immunohistochemistry. Expression of CCL3 and CCL4 mRNA in the block of tissue containing enthorinal and piriform cortices, amygdala and piriform nucleus was markedly up-regulated at 1, 4, 14 and 30 days following stimulation and in hippocampal CA1 was significantly increased at 1 and 4 days following stimulation. Expression of CCL3 and CCL4 proteins was elevated in astrocytes in the enthorinal and piriform cortices, amygdala, and hippocampus showing the largest increase at 4D after status epilepticus. Increase in mRNA and protein levels of CCL3 and CCL4 in the animal model of temporal lobe epilepsy suggests their role in disease development or recovery form epileptogenic insult. Existence of multiple targets for these chemokines in the damaged brain allows several possibilities of influencing neuronal and glial functions.