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Background: Dexmedetomidine and Midazolam were utilized as adjuvants for extending the duration of analgesia; the most common local anesthetic used globally for Caudal anesthesia (CA) is a single dose of plain bupivacaine. To achieve adequate post-operative analgesia, we aimed to compare bupivacaine-dexmedetomidine and bupivacaine-midazolam in caudal anesthesia in pediatric hypospadias surgeries. Methods: We conducted a prospective randomized double-blind controlled clinical study on 51 patients who were scheduled for hypospadias surgery aged from 3 to 8 years; they were allocated randomly into three equal groups (17 patients in each group): Group C (Control): received bupivacaine 0.25% total volume 1ml/kg only, Group D: who received bupivacaine 0.25% in addition to dexmedetomidine 1µg/kg total volume 1ml/kg, Group M: received bupivacaine 0.25% in addition to midazolam 50µg/kg total volume 1ml/kg. The postoperative vital signs, adverse events and duration of the caudal analgesia were assessed utilizing the pediatrics observational Face, Legs, Activity, Cry, Consolability scale (FLACC) pain scale. Results: Group D had the lowest significant FLACC pain score, followed by Group M, then Group C (P=0.00), Duration of Caudal block was the highest in Group D [14 hours, 95% CI(13.26-14.7)] followed by Group M [10 hours, 95% CI(9.6-10.36)] then Group C [4 hours, 95% CI(3.5-4.49)]. Time to first request analgesics was the highest in Group D [14 hours, 95% CI(12.2-14.7)] followed by Group M [10 hours, 95% CI(9.22-10.7)] then Group C [4 hours, 95% CI(5.23 - 6.77)], with statistically significant differences between the 3 groups (P<0.001). Conclusion: Combining bupivacaine with dexmedetomidine or midazolam dramatically extends the time of postoperative analgesia, which in turn increases the time until the patient requires another analgesic. Compared to a mixture of midazolam and bupivacaine, the analgesic profile of the dexmedetomidine plus bupivacaine combination was superior, and there were no significant side effects or disturbances in hemodynamic parameters. [ABSTRACT FROM AUTHOR]

Airways are exposed to myriad environmental and damaging agents such as reactive oxygen species (ROS), which also have physiological roles as signaling molecules that regulate stem cell function. However, the functional significance of both steady and dynamically changing ROS levels in different stem cell populations, as well as downstream mechanisms that integrate ROS sensing into decisions regarding stem cell homeostasis, are unclear. Here, we show in mouse and human airway basal stem cells (ABSCs) that intracellular flux from low to moderate ROS levels is required for stem cell self-renewal and proliferation. Changing ROS levels activate Nrf2, which activates the Notch pathway to stimulate ABSC self-renewal and an antioxidant program that scavenges intracellular ROS, returning overall ROS levels to a low state to maintain homeostatic balance. This redox-mediated regulation of lung stem cell function has significant implications for stem cell biology, repair of lung injuries, and diseases such as cancer.

Both basal and submucosal gland (SMG) duct stem cells of the airway epithelium are capable of sphere formation in the in vitro sphere assay, although the efficiency at which this occurs is very low. We sought to improve this efficiency of sphere formation by identifying subpopulations of airway basal stem cells (ABSC) and SMG duct cells based on their aldehyde dehydrogenase (ALDH) activity. ALDH(hi) ABSCs and SMG duct cells were highly enriched for the population of cells that could make spheres, while the co-culture of ALDH(hi) differentiated cells with the ALDH(hi) ABSCs increased their sphere-forming efficiency. Specific ALDH agonists and antagonists were used to show that airway specific ALDH isozymes are important for ABSC proliferation. Pathway analysis of gene expression profiling of ALDH(hi) and ALDH(lo) ABSCs revealed a significant upregulation of the arachidonic acid (AA) metabolism pathway in ALDH(hi) ABSCs. We confirmed the importance of this pathway in the metabolism of proliferating ALDH(hi) ABSCs using bioenergetics studies as well as agonists and antagonists of the AA pathway. These studies could lead to the development of novel strategies for altering ABSC proliferation in the airway epithelium.

Background: The present approach for treating type 1 diabetes mellitus (T1DM) in children and adolescents relies heavily on carbohydrate restriction and rigorous insulin treatment. The amount of carbohydrates in each meal or snack is the main factor used to determine the insulin dosages given during meals. Consuming fat and protein along with carbs, however, might postpone stomach emptying and result in late postprandial hyperglycemia. Recent research has emphasised the need of modifying insulin dosages for dietary protein and fat to reduce postprandial glucose excursions. To predict insulin needs for meals' protein and fat compositions, many insulin dosage techniques have been devised. Nevertheless, the contemporary clinical practice still faces difficulties in regulating insulin dosages for dietary fat and protein. Objective: This review presents different studies that assessed the effects of dietary fat and protein on postprandial glycemic responses. Methods: The following search terms were used in PubMed, Google Scholar, and Science Direct searches: Insulin treatment, Dietary fat and protein, and T1DM. The authors carefully analysed all relevant references from the relevant literature, including all respectable research and reviews, and only the most recent or comprehensive study was included. Conclusion: To achieve postprandial euglycemia, insulin dosage adjustments for dietary fat and protein are necessary. The best insulin dosage methods to account for the protein and fat composition of the meals are yet unclear. Combination boluses offer better postprandial glycaemic control for T1DM patients using insulin pumps than conventional and prolonged boluses. It is yet unknown if dividing insulin dosages among patients on the MDI regimen would improve postprandial glycaemic control. [ABSTRACT FROM AUTHOR]