Recent progresses in the field of Induced Pluripotent Stem Cells (iPSCs) have opened up many gateways for the research in therapeutics. iPSCs are the cells which are reprogrammed from somatic cells using different transcription factors. iPSCs possess unique properties of self renewal and differentiation to many types of cell lineage. Hence could replace the use of embryonic stem cells (ESC), and may overcome the various ethical issues regarding the use of embryos in research and clinics. Overwhelming responses prompted worldwide by a large number of researchers about the use of iPSCs evoked a large number of peple to establish more authentic methods for iPSC generation. This would require understanding the underlying mechanism in a detailed manner. There have been a large number of reports showing potential role of different molecules as putative regulators of iPSC generating methods. The molecular mechanisms that play role in reprogramming to generate iPSCs from different types of somatic cell sources involves a plethora of molecules including miRNAs, DNA modifying agents (viz. DNA methyl transferases), NANOG, etc. While promising a number of important roles in various clinical/research studies, iPSCs could also be of great use in studying molecular mechanism of many diseases. There are various diseases that have been modeled by uing iPSCs for better understanding of their etiology which maybe further utilized for developing putative treatments for these diseases. In addition, iPSCs are used for the production of patient-specific cells which can be transplanted to the site of injury or the site of tissue degeneration due to various disease conditions. The use of iPSCs may eliminate the chances of immune rejection as patient specific cells may be used for transplantation in various engraftment processes. Moreover, iPSC technology has been employed in various diseases for disease modeling and gene therapy. The technique offers benefits over other similar techniques such as animal models. Many toxic compounds (different chemical compounds, pharmaceutical drugs, other hazardous chemicals, or environmental conditions) which are encountered by humans and newly designed drugs may be evaluated for toxicity and effects by using iPSCs. Thus, the applications of iPSCs in regenerative medicine, disease modeling, and drug discovery are enormous and should be explored in a more comprehensive manner.

The coronavirus disease 2019 pandemic is an issue of global significance that has taken the lives of many across the world. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus responsible for its pathogenesis. The pulmonary manifestations of COVID-19 have been well described in the literature. Initially, it was thought to be limited to the respiratory system; however, we now recognize that COVID-19 also affects several other organs, including the nervous system. Two similar human coronaviruses (CoV) that cause severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) are also known to cause disease in the nervous system. The neurological manifestations of SARS-CoV-2 infection are growing rapidly, as evidenced by several reports. There are several mechanisms responsible for such manifestations in the nervous system. For instance, post-infectious immune-mediated processes, direct virus infection of the central nervous system (CNS), and virus-induced hyperinflammatory and hypercoagulable states are commonly involved. Guillain-Barré syndrome (GBS) and its variants, dysfunction of taste and smell, and muscle injury are numerous examples of COVID-19 PNS (peripheral nervous system) disease. Likewise, hemorrhagic and ischemic stroke, encephalitis, meningitis, encephalopathy acute disseminated encephalomyelitis, endothelialitis, and venous sinus thrombosis are some instances of COVID-19 CNS disease. Due to multifactorial and complicated pathogenic mechanisms, COVID-19 poses a large-scale threat to the whole nervous system. A complete understanding of SARS-CoV-2 neurological impairments is still lacking, but our knowledge base is rapidly expanding. Therefore, we anticipate that this comprehensive review will provide valuable insights and facilitate the work of neuroscientists in unfolding different neurological dimensions of COVID-19 and other CoV associated abnormalities.

To compare different doses of tranexamic acid, 150 consecutive children with congenital cyanotic heart disease were randomly assigned to one of 5 groups of 30 each. Group A served as a control. Group B received 50 mg.kg(-1) of tranexamic acid at induction of anesthesia. Group C received 10 mg.kg(-1) at induction followed by an infusion of 1 mg.kg(-1).h(-1). Group D had 10 mg.kg(-1) at induction, 10 mg.kg(-1) on bypass, and 10 mg.kg(-1) after protamine. Group E had 20 mg.kg(-1) at induction and again after protamine. The control group had the longest sternal closure time, the greatest blood loss in the first 24 hours, and the highest requirements for blood and blood products. Among the 4 groups given tranexamic acid, group D (triple dose) had the best results, followed by group E (double dose). Group B (single dose) had the worst results among the groups receiving tranexamic acid.

We undertook a randomised, double-blind, placebo-controlled study to compare the analgesic efficacy of pre-operative stellate ganglion block on postoperative pain relief after upper limb orthopaedic surgery. Patients were administered a 3-ml injection during ultrasound-guided stellate ganglion block; 15 patients received lidocaine 2% and 15 patients received 0.9% saline. Following the block, all patients received standardised general anaesthesia. Postoperative analgesia included regular intravenous diclofenac, paracetamol and patient-controlled analgesia with tramadol for 24 h. Patients were observed at 0, 2, 4, 6, 8, 12 and 24 h after surgery for tramadol consumption, cardiovascular variables and visual analogue scale pain scores at rest and on movement. The mean (SD) hourly tramadol consumption was significantly reduced in the lidocaine group compared with the saline group at 4 h (8.0 (10.1) mg vs 28.0 (12.6) mg, respectively; p = 0.001), 6 h (5.3 (10.8) mg vs 17.3 (12.7) mg, respectively; p = 0.013) and 8 h (5.3 (11.8) mg vs 21.3 (9.1) mg, respectively; p = 0.001). The cumulative 24-h tramadol consumption was 97.3 (16.6) mg in the lidocaine group and 150.6 (26.0) mg in the saline group (p = 0.001). There were significant differences in the pain visual analogue scale at rest at two time points; at 4 h the median (IQR [range]) visual analogue scale scores were 4 (4-6 [2-8]) in the lidocaine group and 5 (4-6 [2-7]) in the saline group (p = 0.03), and at 6 h visual analogue scale scores were 3 (3-4 [3-6]) and 4 (4-6 [2-7]), respectively (p = 0.04). Pain visual analogue scale on movement was lower in the lidocaine group at all time intervals compared with the saline group, but this did not reach statistical significance. The present study has demonstrated a postoperative tramadol-sparing and analgesic effect of pre-operative stellate ganglion block in patients undergoing upper limb orthopaedic surgery under general anaesthesia.

Recent studies have demonstrated that selenium (Se) and selenium nanoparticles (Se-NPs) exhibited toxicity at a higher concentration. The lethal concentration of Se and Se-NPs was estimated as 5.29 and 3.97 mg/L at 96 h in Pangasius hypophthalmus. However, the effect of different definite concentration of Se (4.5, 5.0, 5.5, and 6.0 mg/L) and Se-NPs (2.5, 3.0, 3.5, and 4.0 mg/L) was decided for acute experiment. Selenium and Se-NPs alter the biochemical attributes such as anti-oxidative status [catalase (CAT), superoxide dismutase (SOD), and glutathione-S-transferase (GST) activities], neurotransmitter enzyme, cellular metabolic enzymes, stress marker, and histopathology of P. hypophthalmus in a dose- and time-dependent manner. CAT, SOD, and GST were significantly elevated (p < 0.01) when exposed to Se and Se-NPs, and similarly, a neurotransmitter enzyme (acetylcholine esterase (AChE)) was significantly inhibited in a time- and dose-dependent manner. Further, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and malate hydrogenase were noticeably (p < 0.01) affected by Se and Se-NPs from higher concentration to lower concentration. Stress markers such as cortisol and HSP 70 were drastically enhanced by exposure to Se and Se-NPs. All the cellular metabolic and stress marker parameters were elevated which might be due to hyperaccumulation of Se and Se-NPs in the vital organ and target tissues. The histopathology of liver and gill was also altered such as large vacuole, cloudy swelling, focal necrosis, interstitial edema, necrosis in liver, and thickening of primary lamellae epithelium and curling of secondary lamellae due to Se and Se-NP exposure. The study suggested that essential trace element in both forms (inorganic and nano) at higher concentration in acute exposure of Se and Se-NPs led to pronounced deleterious alteration on histopathology and cellular and metabolic activities of P. hypophthalmus.