The Pros And Cons Of Liver Conditioning

These stated facts very well implicate an imperative need to investigate promising alternative treatment strategies as well preventive measures. Impairment in cardiac functions, organ (heart) failure or trigger of compensatory mechanisms (hypertrophy, neurohumoral system activation, autokrine, paracrine stimulation, etc) are the result of loss in cardiac myocytes predominantly due to myocardial infarction (Zimmermann and Eschenhagen, 2003). In addition to the traditional treatment of

The MD Anderson Liver Tumor biospecimen resource has been invaluable for a large number of studies or clinical development. The sixth and subsequent editions of the American Joint Committee on Cancer (AJCC) staging of hepatocellular cancer, which was developed by an international consortium led by Jean-Nicolas Vauthey, MD, Professor of Surgery at MD Anderson and co-leader on project 2 of the SPORE, was based upon pathologic review of resected specimens in the Liver Tumor Bank (Vauthey JN J Clin Oncol 2002 20:1527-36). In addition, investigators at MD Anderson examined tissues in the Liver Tumor Bank to elucidate the prognostic significance of the ribonucleoprotein Human Antigen R (HuR) showing that patients with high HuR tumor expression had

I am conducting biomedical research in the laboratory of cardiac physiology under the mentorship of Dr. Elizabeth Murphy. Cardiovascular disease is the major cause of death in the US; therefore, a better understanding of the mechanisms regulating cardiomyocyte death in ischemia and reperfusion injury are important. Mitochondrial calcium plays a crucial role in the normal functioning of many processes, including the regulation of cardiac biochemical pathways and mediating ischemia-reperfusion injury. The uptake of calcium into the mitochondrial matrix is regulated by the mitochondrial calcium uniporter (MCU). An endogenous enzyme, Ca2+ Calmodulin Dependent Kinase II (CaMKII) has shown to regulate cell death and have increased activity during

Prospective randomized double-blind controlled study: Pros & Cons of Norepinephrine infusion versus Terlipressin in patients with hepatorenal syndrome type 1 in intensive care unit (ICU).

Remote ischemic conditioning and local cardiac ischemic conditioning have many fundamental steps in common, including activation of different protein signaling pathways. The extracellular signal-regulated kinase (ERK) and glycogen synthase kinase-3β (GSK-3β) signaling molecules are key components of the pro-survival reperfusion injury salvage kinase (RISK) pathway5. Emerging evidence has indicated that the phosphorylation of GSK-3β at Ser9 results in the inhibition of GSK-3β activity, and that this inhibition of GSK-3β enhances cell survival and limits infarct size post I/R injury6. Also, the activation of ERK1/2 by various stimuli, including ischemic conditioning, may lead to cardioprotection against I/R injury7. These findings prompted us to postulate that liver ischemic conditioning might also protect the heart against I/R injury by the influence of RISK pathways, thereby promoting the myocardial cells towards

Heart disease is prevalent globally, to the extent where almost everyone knows someone, in their family or in their friend circle, who has heart disease or is dealing with the sickness. Myocarditis is a variation thereof and is an inflammatory disease of the heart caused by a variety of agents,

Circulatory shock is a syndrome of widespread cellular hypoxia, triggered by a systemic alteration of perfusion and delivery and/or utilization of tissue oxygen, eventually causing end-organ dysfunction and death [53]. It can be subdivided into 4 distinct categories according to its primary pathophysiological mechanism, namely cardiogenic, hypovolemic, obstructive and distributive

Ischemia-reperfusion injury is seen in strokes, myocardial infarctions, acute kidney injury, mesenteric ischemia, shock liver and systemic shock. Both clinical and experimental data revealed that transplant IRI has deleterious long- and short -term effects, manifesting as augmented incidents of chronic allograft damage and acute rejection[1] Renal ischemia–reperfusion (IRI) is a

KN-92 is an inactive analog of KN-93. KN-93 is the CaM kinase II inhibitor. Hearts were treated with the CaM kinase inhibitor KN-93 or the inactive analog KN-92 (0.5 μM) for 10 min before clofilium exposure. Early afterdepolarizations (EADs) were largely suppressed by KN-93 compared to KN-92. There were little differences in parameters favoring EADs such as monophasic action potential duration or heart rate in KN-93- or KN-92-treated hearts. CaM kinase activity in situ increased 37% in hearts with EADs compared to hearts without EADs. This increase in CaM kinase activity was prevented by pretreatment with KN-93.

In acute myocardial infarction animal models, myocardial reperfusion injury accounts for more than half of the final myocardial infarction injury. Therefore, prevention of myocardial ischemia-reperfusion injury is one of the major measures for the prevention of cardiac and vascular adverse events in patients with cardiac surgery and vascular surgery. Currently, many studies focus on the prevention of ischemic-reperfusion injury, including preconditioning and postconditioning (1,2). The postconditioning measures include ischemia postconditioning, volatile anesthetic postconditioning, sufentanil postconditioning, and propofol postconditioning (3-6). In 2003, Zhao et al proposed the concept of ischemic-postconditioning to provide many rounds of

4. Provides cardiovascular protection Curcumin has been shown to be effective in preventing cholesterol oxidation in the body. Cholesterol oxidation can lead to plaque build-up and damage to the blood vessels, thereby causing stroke or heart attack. Turmeric is also a good source of vitamin B6, which helps keep the levels of homocysteine low. High levels of homocysteine are known to damage the walls of the blood vessels. When this happens, the risk of getting heart attack and atherosclerotic plaque build-up increases.

With development of genetically altered mice, there is intense interest in developing murine models to study mechanisms operative in cardiovascular disease. To study the effect of coronary artery occlusion and reperfusion on myocardium and the methods involved to perform such studies both acutely and chronically, Michael et al [64] developed the open chest mouse model using male FVB mice. LAD coronary artery was occluded permanently or for 30-60 min followed by reperfusion. It was suggested that, as compared with permanent occlusion there was a significant decrease in infarct size as a percentage of the area at risk in reperfusion. Infiltration of leukocytes into the ischemic region as well as contraction bands was found in re-perfused myocardium. With the help of this model the complex pathophysiology, area at risk, infarct size and cardiac function in mouse can be assessed. This model allows the induction of myocardial infarctions of varying degrees and long-term survival of mouse. It also allows studying the effect of the absence or over-expression of a gene product in the progression of injury and inflammation in ischemic reperfusion in a transgenic mouse.

Hematoxylin and Eosin staining In order to evaluate the myocardial tissue alterations in the xenograft model, rats were killed at (24) post Qingyi Decoction treating and left ventricular myocardial tissues were collected from each group and fixed in 10% formalin, processed and embedded in paraffin wax. Thin sections of 3-5 microns thickness were cut and placed on microscopic slides. The tissues were deparaffinized in xylene solution, rehydrated in downstream serial dilutions of ethanol and stained with hematoxylin for 10 minutes, bluing for 10 minutes in running tap water, decolorized for 3 seconds by 1% acid alcohol, and the tissues were stained with eosin for 1 minute, washed with water and let to air dry. Fix the cover slips on the tissues. The slides were examined under a light microscope at a magnification of 40x, to detect the histological changes in the left ventricular myocardial tissues of each experimental groups

1). Opposite to STIM1/Ori1SOCE expressions both in genes and proteins level, indicating that STIM1/Ori1SOCE playing a key role in the protective effect of Qingyi Decoction versus ASP-induced myocardial injury (Fig.2A) (P.value <0.001), (Fig.2B) (P.value <0.001) and (Fig.2C) (P.value 0.001) (Fig. 3a+b) with no statistical difference with 2-APB group (p. value 0.7491) (Table1, Fig.2).

The Liver is the body's largest gland, weighing about three to four pounds. It is located beneath the diaphragm in the right upper quadrant (RUQ) of the abdominal cavity. Without the liver, our bodies would be poisoned and unfit for us to do anything at all. It is a metabolically active organ responsible for many vital life functions. The primary functions of the liver are: Bile productions and excretion. Excretion of bilirubin, cholesterol, hormones, and drugs. Metabolism of fats, proteins, and carbohydrates. Enzyme activation. Storage of glycogen, vitamins, and minerals. Synthesis of plasma proteins, such as albumin, and clotting factors. And blood detoxification and purification.