Ischemic stroke is a leading cause of morbidity and mortality worldwide, with oxidative stress playing a key role in the injury mechanism of thrombolytic therapy. There is increasing evidence that oxidative stress damages endothelial cells (ECs), degrades tight junction proteins (TJs), and contributes to increased blood-brain barrier (BBB) permeability. It has been demonstrated that the breakdown of BBB could increase the risk of intracerebral hemorrhagic transformation in ischemic stroke. And an episode of cerebral ischemia/reperfusion (I/R) also initiates oxidative stress-mediated inflammatory processes in ECs, which further promotes BBB disruption and the progression of brain injury. Previous studies have revealed that antioxidants could inhibit ROS generation and attenuate BBB disruption after cerebral I/R. Peroxiredoxin 4 (Prx4) is a member of the antioxidant enzymes family (Prx1-6) and has been characterized to be an efficient H2O2 scavenger. It should be noted that Prx4 may be directly involved in the protection of ECs from the effects of ROS and function in ECs as a membrane-associated peroxidase. This paper reviewed the implication of Prx4 on vascular integrity and neuroinflammation following a cerebral I/R injury.
Previous studies in patients with arterial claudication have focused on calf hemodynamic recovery. We hypothesized that the duration of hemodynamic recovery with TcpO2 at calf and non-calf levels would be shorter than 10min. We analyzed the factors that influence the recovery time.
We monitored limb changes minus chest changes from rest (DROP) of transcutaneous oximetry on buttocks, thighs and calves, during and following a treadmill test (3.2km/h; 10% grade). We calculated the time required to reach 50% (50%RT) and 10% (90%RT) of minimal DROP value (DROPm) from walking cessation. Regression analyses were used to determine the factors associated to 50%RT and 90%RT.
Of the 132 patients studied, 18.2% reported isolated non-calf pain by history. Of the 792 recovery time values, only 3 (0.4%) and 23 (2.9%) were in excess of 10min for 50%RT and for 90%RT, respectively. A weak correlation was found between each of the 792 DROPm and 50%RT (r=-0.270, p<0.001) as well as for 90%RT (r=-0.311 p<0.001). Lowest DROPm and BMI (but not age, sex, the use of beta-blockers, the duration of the walking period) were associated to both 50%RT and 90%RT.
Although recovery duration correlates significantly with the severity of ischemia of the same location, a wide discrepancy exists and the longest recovery time does not always correlate to the localization of the most severe ischemia. Non-calf ischemia should be measured when one aims at objectifying the biological effects of exercise or the effects of treatments on recovery from exercise.
Although recovery duration correlates significantly with the severity of ischemia of the same location, a wide discrepancy exists and the longest recovery time does not always correlate to the localization of the most severe ischemia. Non-calf ischemia should be measured when one aims at objectifying the biological effects of exercise or the effects of treatments on recovery from exercise.Human pancreatic lipase (triacylglycerol acyl hydrolase EC3.1.1.3) is the most widely studied member of the human lipase superfamily related to carboxyl esterase. It is secreted from the acinar cell of pancreas and has strong preference for triacylglycerides over cholesterol esters, phospholipids, and galactolipids. Apart from the hydrolysis of triacylglycerides, pancreatic lipase may cause the hydrolysis of retinyl esters in vivo. So, it is very much evidenced that pancreatic lipase with its cofactor colipase has prominent role in efficient digestion of dietary fat. Hence, the modulation of human pancreatic lipase may represent a new insight in the discovery of a number of therapeutics that can inhibit the absorption of fat in body and can be used in obesity and other related metabolic disorders. Even, the only Food and drug administration (FDA) approved antiobesity drug, orlistat, is also an inhibitor of pancreatic lipase. This review summarizes studies about structure, mechanistic approach of pancreatic lipase enzyme while emphasizing on the various synthetic pancreatic lipase inhibitors with their structure activity relationship (SAR).
Ryanodine receptor-1 (RyR1) is essential for skeletal muscle cell functions. However, its roles in vascular smooth muscle cells (SMCs) are well recognized. This study aims to determine the potential physiological importance and difference in systemic and pulmonary artery SMCs (SASMCs and PASMCs).
Local and global Ca
release were measured using a laser scanning confocal microscope and wide-field fluorescence microscope; membrane currents were recorded using a patch clamp recording; muscle contraction was determined using an organ bath system; RyR protein expression was assessed using immunofluorescence staining. Homozygous and heterozygous RyR1 gene knockout (RyR1
and RyR1
) mice were used to determine its specific functions.
Ca
sparks were more prominently decreased in RyR1
ASMCs than in PASMCs. Caffeine induced a smaller increase in [Ca
]
in both RyR1
and RyR1
ASMCs than in PASMCs. High K
produced a reduced [Ca
]
increase in RyR1
PASMCs and ASMCs as well as a reduced contraction in RyR1
pulmonary artery and aortic tissues. ATP elicited a smaller increase in [Ca
]
in RyR1
ASMCs and PASMCs with a greater inhibition in ASMCs. Norepinephrine-elicited muscle contraction was reduced in RyR1
aortic and pulmonary arteries. IP
dialysis-induced Ca
release was much smaller in RyR1
ASMCs and PASMCs. Hypoxia-induced large Ca
and contractile responses were inhibited in RyR1
PASMCs. ABBV-744 cost However, hypoxic exposure did not evoke a notable increase in [Ca
]
in ASMCs.
Our findings for the first time provide clear genetic evidence for the functional importance and difference of RyR1 in systemic and pulmonary artery SMCs.
Our findings for the first time provide clear genetic evidence for the functional importance and difference of RyR1 in systemic and pulmonary artery SMCs.ABBV-744 cost
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