Correlation Analysis of Patients with Adverse Reactions Caused by Postoperative Morphine Analgesia

In the current medical field of clinical surgery, we often have to contact a large number of patients with severe fractures caused by serious accidental injuries. Generally, these trauma patients often need to be treated by repair surgery. Postoperative patients usually have a certain degree of local pain. In order to alleviate the physiological pain of postoperative patients, And can prevent the braking caused by the aggravation of local pain of the injured patients. The use of analgesic pump for postoperative analgesia has become a common method after surgery and has been widely used in clinic. Good postoperative analgesia can inhibit the body's stress response and is conducive to restoring the coordination and stability of local breathing and circulation of the patients after operation, Reduce the local pain symptoms of some patients and effectively reduce their postoperative related complications, and indirectly promote the recovery of patients with pain. For the application of analgesic pump for pain relief, there are often a variety of auxiliary ways and preparation methods of analgesic drugs such as arteriovenous and epidural circulation, which should be selected and configured according to the physical conditions and medication conditions of patients with pain, such as ns100ml Morphine 5mg, bupivacaine 75mg, etc., of which morphine is often used as a common drug component for pain relief, but some special patients often have a series of dependent reactions after using morphine for pain relief. In view of this situation, combined with the physical conditions and adverse reactions of some special patients, this paper analyzes the possible adverse effects on patients with special constitution when using morphine for pain relief after clinical operation and relevant research

The Anti-Warburg Effect Elicited by the cAMP-PGC1α Pathway Drives Differentiation of Glioblastoma Cells into Astrocytes

Summary: Glioblastoma multiforme (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed as a potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established an induced differentiation model of GBM using cAMP activators that specifically directed GBM differentiation into astroglia. Transcriptomic and proteomic analyses revealed that oxidative phosphorylation and mitochondrial biogenesis are involved in induced differentiation of GBM. Dibutyryl cyclic AMP (dbcAMP) reverses the Warburg effect, as evidenced by increased oxygen consumption and reduced lactate production. Mitochondrial biogenesis induced by activation of the CREB-PGC1α pathway triggers metabolic shift and differentiation. Blocking mitochondrial biogenesis using mdivi1 or by silencing PGC1α abrogates differentiation; conversely, overexpression of PGC1α elicits differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induce tumor growth inhibition and differentiation. Our data show that mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation of tumor cells. : Xing et al. show that the metabolic shift from glycolysis to oxidative phosphorylation drives differentiation of GBM cells into astrocytes by cAMP activation. Mechanistically, the cAMP-CREB-PGC1α signal mediates mitochondrial biogenesis, which leads to metabolic reprogramming, induced differentiation, and tumor growth inhibition. Keywords: glioblastoma, induced differentiation, Warburg effect, metabolic reprogramming, oxidative phosphorylation, glycolysis, mitochondrial biogenesis, cyclic adenosine monophosphate, cAMP, PPARγ coactivator-1α, PGC1