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Objective@#To classify the expression of RyR2 in the brain of prion infected hamsters.@*Methods@#Immunohistochemical assays was used to verify that the location of RyR2 in the brain slices of hamster. Assays of the brain samples of intracranial inoculation of scrapie infected hamster (agent 263 K) and normal hamster were tested to evaluate the RyR2 expression by Western Blotting. Immunofluorescent assays were used to verify the co-location between RyR2 and PrP protein.@*Results@#RyR2 mainly located in cortex and Purkinje cells with parts of which are distributed in thalamus, hippocampus and olfactory bulb. The expression of RyR2 significantly decreased in the 263 K infected hamster at terminal stage. The Immunofluorescence tests showed that RyR2 was colocalized with PrP protein.@*Conclusions@#The experimental data showed that RyR2 may play a crucial role in prion disease, which might be closely linked to the cognition impairment and neuron loss. The relation between RyR2 and prion disease still needs further research.
ABSTRACT
Diabetic cystopathy is one of the most common complications caused by diabetes in urinary system.There were no obvious clinical manifestations in the early stage of the disease.With the progress of the disease, various complicated lower urinary tract symptoms appeared gradually.All these clinical manifestations cause grate trouble in the health and the quality of life of patients.However, its pathogenesis is not clear, myogenic and neurogenic is the main theory of its pathogenesis.Some studies indicate that long-term consumption of caffeine can reduce the incidence of it, and this article will discuss the cause of this disease and the treatment of caffeine in order to guide clinical practice.
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BACKGROUND: Calcium calmodulin-dependent kinase Ⅱ (CaMKⅡ) can be more active in patients with left ventricular hypertrophy (LVH), which in turn causes phosphorylation of ryanodine receptors, resulting in inactivation and the instability of intracellular calcium homeostasis. The present study aimed to determine the effect of CaMKⅡ–ryanodine receptor pathway signaling in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia. METHODS: Forty New Zealand rabbits were randomized into four groups (10 per group): sham group, LVH group, KN-93 group (LVH+KN-93), and ryanodine group (LVH+ryanodine). Rabbits in the LVH, KN-93, and ryanodine groups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta, while those in the sham group did not undergo the coarctation. After eight weeks, action potentials (APs) were recorded simultaneously in the endocardium and epicardium, and a transmural electrocardiogram (ECG) was also recorded in the rabbit left ventricular wedge model. Drugs were administered to the animals in the KN-93 and ryanodine groups, and the frequency of triggered APs and ventricular tachycardia was recorded after the rabbits were given isoprenaline (1 mol/L) and high-frequency stimulation. RESULTS: The frequency (animals/group) of triggered APs was 0/10 in the sham group, 10/10 in the LVH group, 4/10 in the KN-93 group, and 1/10 in the ryanodine group. The frequencies of ventricular tachycardia were 0/10, 9/10, 3/10, and 1/10, respectively. The frequencies of polymorphic ventricular tachycardia or ventricular fibrillation were 0/10, 7/10, 2/10, and 1/10, respectively. The frequencies of triggered ventricular arrhythmias in the KN-93 and ryanodine groups were much lower than those in the LVH group (P<0.05). CONCLUSIONS: KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH. The CaMKⅡ–ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia.
ABSTRACT
Objective To inquire into T-type calcium channel effects on RyR and IP 3R of sarcoplasmic reticulum in atrial myocytes during atrial fibrillation.Methods Ten dogs underwent continuous rapid atrial pacing (500 beats/min) to create persistent atrial fibrillation.In five rapidly-paced dogs,mibefradil dihydrochloride was given beginning 2 days after pacemaker implantation,continuing until the twenty-fourth week.A group of size-matched dogs (n=5) without given mibefradil was used as a pure atrial fibrillation group.Another group of size-matched dogs (n=5) without pacemaker implantation was used as a control group.Canine atrial myocytes isolated by enzymatic dissociation were used to study T-type Ca 2+ channel blocker effects on expression and function changes of RyR and IP 3R in atrial myocytes by confocal microscopy.Results RyR/IP 3R ratio (0.2965?0.01812) was markedly lower than that of control group (2.7043?0.2293),but there was no difference compared with that of atrial fibrillation group (0.2472?0.1355).Ca 2+transient of atrial myocytes was nremarkably changed (1.3031?0.1056)(P