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1.
Phys Med Rehabil Clin N Am ; 31(2): 245-254, 2020 05.
Article in English | MEDLINE | ID: mdl-32279727

ABSTRACT

Utilization of muscle relaxants varies for treatment of acute and chronic pain. This article provides an overview of the different types muscles relaxants and their adverse effects. Appropriate medication selection based on clinical indications is also examined.


Subject(s)
Acute Pain/drug therapy , Chronic Pain/drug therapy , Low Back Pain/drug therapy , Muscle Relaxants, Central/therapeutic use , Humans
7.
J Invest Surg ; 25(4): 271-7, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22853814

ABSTRACT

Liver ischemia-reperfusion (I/R) injuries are significant clinical challenges implicated in various hepatic surgical procedures and transplantations. Associated with varying degrees of insult, the hallmark of I/R is the excessive inflammatory response potentiated by the host immune system. Toll-like receptors (TLRs), known to play an important role in pathogen-derived inflammation, are now thought to participate in I/R injury-derived inflammation signaling pathways. Endogenous particles (proteins, cytokines, nucleic acids) that are released from damaged host cells bind to TLR2, TLR4, and TLR9, resulting in even further injury by subsequent inflammatory reactions and activation of the innate immune system. This review aims to systematically examine the current literature about TLR signaling mechanisms, allowing for a greater understanding of the precise role of TLRs in hepatic I/R injuries.


Subject(s)
Liver/blood supply , Reperfusion Injury/etiology , Signal Transduction/physiology , Toll-Like Receptors/physiology , Animals , Humans
10.
J Invest Surg ; 23(4): 228-38, 2010 Aug.
Article in English | MEDLINE | ID: mdl-20690849

ABSTRACT

Calcium plays a major role in intracellular signaling mechanisms during ischemia reperfusion (I/R) injury of a liver cell. Under ischemic conditions, the absence of oxygen arrests oxidative phosphorylation, thereby eliminating the energy source by which hepatocellular mechanisms maintain homeostasis of calcium. This, in turn, leaves nonselective plasma membrane influx pores unopposed and results in a net increase in intracellular calcium concentrations. Subsequent reperfusion marks the onset and progression of apoptosis and necrosis, as it involves inflammatory responses as well as free-radical formation due to re-oxygenation of cells. These processes destroy the structural integrity of organelles, leading to disruptive redistribution of calcium between cellular and subcellular compartments. This initial elevation and later imbalance of intracellular calcium concentrations associated with I/R induce various molecular responses within each organelle. In the cytoplasm, a series of pro-apoptotic pathways involving various calcium sensitive enzymes are activated. The injury is further exacerbated in the endoplasmic reticulum (ER) due to the malfunction of mechanisms responsible for intracellular calcium sequestration. Both the mitochondria and the nucleus are also adversely affected, as their structural integrity and physiologic functions are disrupted. To date, however, the precise pathophysiology of these calcium-mediated signaling pathways is not fully understood due to its complex nature. This review aims to systematically examine the current literature about individual molecular signaling pathways in the cytoplasm, ER, mitochondria, and the nucleus prior to causing time-sensitive progression of permanent tissue injury.


Subject(s)
Calcium Signaling/physiology , Liver/physiopathology , Reperfusion Injury/physiopathology , Animals , Apoptosis/physiology , Cell Membrane/physiology , Cytoplasm/physiology , Endoplasmic Reticulum/physiology , Humans , Liver/pathology , Mitochondria/physiology
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