Background:Spinal anaesthesia is the most common approach which is used for lower limb surgery. Dexmedetomidine is the recent drug which acts on α2-adrenergic receptors in the dorsal horn of the spinal cord to produce analgesic effects.Aim:Efficacy and safety of intrathecal dexmedetomidine added to ropivacaine.Setting and Design:Randomised double blind trial.Methods:Sixty patients were randomly allocated to receive intrathecally either 3 ml of 0.75% isobaric ropivacaine + 0.5 ml normal saline (Group R) or 3 ml of 0.75% isobaric ropivacaine + 5 μg dexmedetomidine in 0.5 ml of normal saline (Group D).Results:The mean time of sensory regression to S2 was 468.3±36.78 minutes in group D and 239.33±16.8 minutes in group R. Duration of analgesia (time to requirement of first rescue analgesic) was significantly prolonged in group D (478.4±20.9 minutes) as compared to group R (241.67±21.67 minutes). The maximum visual analogue scale score for pain was less in group D (4.4±1.4) as compared to group R (6.8±2.2).Conclusion:The addition of dexmedetomidine to ropivacaine intrathecally produces a prolongation in the duration of the motor and sensory block.

Background:Various adjuvants have been used with local anesthetics in spinal anesthesia to avoid intraoperative visceral and somatic pain and to provide prolonged postoperative analgesia. Dexmedetomidine, the new highly selective α2-agonist drug, is now being used as a neuraxial adjuvant. The aim of this study was to evaluate the onset and duration of sensory and motor block, hemodynamic effect, postoperative analgesia, and adverse effects of dexmedetomidine or fentanyl given intrathecally with hyperbaric 0.5% bupivacaine.Materials and Methods:Sixty patients classified in American Society of Anesthesiologists classes I and II scheduled for lower abdominal surgeries were studied. Patients were randomly allocated to receive either 12.5 mg hyperbaric bupivacaine plus 5 μg dexmedetomidine (group D, n = 30) or 12.5 mg hyperbaric bupivacaine plus 25 μg fentanyl (group F, n = 30) intrathecal.Results:Patients in dexmedetomidine group (D) had a significantly longer sensory and motor block time than patients in fentanyl group (F). The mean time of sensory regression to S1 was 476±23 min in group D and 187±12 min in group F (P<0.001). The regression time of motor block to reach modified Bromage 0 was 421±21 min in group D and 149±18 min in group F (P<0.001).Conclusions:Intrathecal dexmedetomidine is associated with prolonged motor and sensory block, hemodynamic stability, and reduced demand for rescue analgesics in 24 h as compared to fentanyl.

Aim of the studyVitamin D receptor (VDR) expression and serum vitamin D scores in oral premalignant lesions and oral cancer have not been widely analyzed. The role of vitamin D supplementation in advanced oral cancer for improving quality of life (QOL) is also a matter of research.Material and methodsVitamin D receptor expression and vitamin D scores were analyzed in normal oral mucosa (n = 95), leukoplakia (n = 23) and oral cancer (n = 87). 45 patients with advanced oral cancer subjected to chemoradiation were evaluated for the effect of vitamin D supplementation on most observable QOL parameters such as oral mucositis, swallowing performance and overall QOL.ResultsVitamin D receptor expression was increased in oral neoplastic lesions. Vitamin D scores were significantly lower in cases compared to healthy controls (p = 0.002). Vitamin D supplementation significantly reduced the therapy-related toxicities in advanced cancer, thus reducing morbidity and improving QOL.ConclusionsVitamin D receptor expression is increased in premalignant lesions and oral cancer. Vitamin D insufficiency and deficiency are prevalent in patients with oral neoplastic lesions. Vitamin D supplementation has a role in reducing treatment-related toxicities, especially in advanced cancer.

Innate immunity is mediated by a variety of cell types, including microglia, macrophages, and neutrophils, and serves as the immune system's first line of defense. There are numerous pathways involved in innate immunity, including the interferon (IFN) pathway, TRK pathway, mitogen-activated protein kinase (MAPK) pathway, Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, interleukin (IL) pathways, chemokine pathways (CCR5), GSK signaling, and Fas signaling. JAK/STAT is one of these important signaling pathways and this review focused on JAK/STAT signaling pathway only. The overactivation of microglia and astrocytes influences JAK/STAT's role in neuroinflammatory disease by initiating innate immunity, orchestrating adaptive immune mechanisms, and ultimately constraining inflammatory and immunological responses. The JAK/STAT signaling pathway is one of the critical factors that promotes neuroinflammation in neurodegenerative diseases. Given the importance of the JAK/STAT pathway in neurodegenerative disease, this review discussed the feasibility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegenerative diseases in near future.