Chronic sleep loss/fragmentation prevalent in the current 24/7 society is associated with irreversible consequences on health and overall wellbeing. Various studies have well documented the ill effects of acute sleep loss on cognitive functions of individuals; however, the underlying mechanism behind the chronic sleep loss is yet to be explored. The present study was aimed to investigate whether chronic sleep deprivation (CSD) triggers anxiety-like behaviour and memory decline in male Wistar rats. Rats were sleep deprived by placing them over slowly rotating drum (2 rpm) for 18 h (between 4 pm and 10 am) followed by 6 h of recovery sleep for 21 consecutive days. Post CSD regimen, rats were subjected to behavioural tests such as elevated plus maze (EPM), Novel Object Recognition (NOR) and Rotarod performance test and then sacrificed to remove brain for further molecular studies. The study demonstrated that CSD rats showed anxiogenic behaviour along with recognition memory decline compared to control rats. CSD rats further showed elevated levels of inflammatory cytokines (TNFα, IL-1β) along with activation of NFκB and AP1 transcription factors in hippocampus and piriform cortex (PC) regions of brain. These observations were also accompanied by enhanced expression of GFAP and Iba1 in the two brain regions. The data suggest that CSD triggered low-grade neuroinflammation which caused anxiogenic response and recognition memory impairment. The study provides preliminary leads to further explore the role of astrocytes/microglial cells and inflammatory cytokines in mediating these neurobehavioural consequences of chronic sleep loss and to develop effective interventions to combat them.

No abstract

MIE is a safe alternative to open esophagectomy for the treatment of locally advanced esophageal cancer. The presence of comorbidities increased operative time, length of hospital stay, and postoperative complications while worsening overall survival.

Sleep deprivation (SD) leads to the spectrum of mood disorders like anxiety, cognitive dysfunctions and motor coordination impairment in many individuals. However, there is no effective pharmacological remedy to negate the effects of SD. The current study examined whether 50% ethanolic extract of Tinospora cordifolia (TCE) can attenuate these negative effects of SD. Three groups of adult Wistar female rats - (1) vehicle treated-sleep undisturbed (VUD), (2) vehicle treated-sleep deprived (VSD) and (3) TCE treated-sleep deprived (TSD) animals were tested behaviorally for cognitive functions, anxiety and motor coordination. TSD animals showed improved behavioral response in EPM and NOR tests for anxiety and cognitive functions, respectively as compared to VSD animals. TCE pretreatment modulated the stress induced-expression of plasticity markers PSA-NCAM, NCAM and GAP-43 along with proteins involved in the maintenance of LTP i.e., CamKII-α and calcineurin (CaN) in hippocampus and PC regions of the brain. Interestingly, contrary to VSD animals, TSD animals showed downregulated expression of inflammatory markers such as CD11b/c, MHC-1 and cytokines along with inhibition of apoptotic markers. This data suggests that TCE alone or in combination with other memory enhancing agents may help in managing sleep deprivation associated stress and improving cognitive functions.

No abstract