OBJECTIVETo innovatively establish a new platform of myocardial ischemia-reperfusion injury (MIRI) animal model by observing abnormal savda carrier MIRI indicators, and to observe changes of myocardial ultrastructure.

METHODSAccording to Uyghur medical theories, an abnormal savda carrier animal model was established and confirmed using multifactor, and then MIRI models set up. Totally 36 male white SD rats were randomly divided into the normal sham-operation group, the normal operation group, the model sham-operation group, and the model operation group, 9 in each group. ECG changes, myocardial enzymes (CK-MB), and cardiac troponin (cTnT), and ultramicrostructures were observed.

RESULTSCompared with the normal sham-operation group, some damage of ultramicrostructures occurred in heart muscles of rats in the normal operation group and the model operation group, such as lowered myoplasm density, loosely arranged myofilament, dilated myofibris, reduced mitochondria number, vacuole and swelling mitochondrion. Ultramicrostructural damage of cardiac muscle cells was more severe in rats of the model operation group. Compared with the normal sham-operation group, CK-MB and cTnT increased in the normal operation group with statistical difference (P < 0.01). Compared with the normal sham-operation group, there was no statistical difference in CK-MB or cTnT in the model sham-operation group (P > 0.05). Compared with the model operation group, CK-MB and cTnT obviously decreased in the model sham-operation group and the normal operation group with statistical difference (all P < 0.01).

CONCLUSIONAbnormal savda carrier MIRI model established in this experiment could provide favorable conditions for further MIRI intervention treatment.

Animals ; Disease Models, Animal ; Male ; Medicine, Traditional ; Myocardial Reperfusion Injury ; Myocardium ; ultrastructure ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley

Objective    To investigate whether the individualized anticoagulation therapy based on CYP2C9 and VKORC1 gene is superior to empirical anticoagulation therapy after artificial heart valve replacement surgery in Uygur patients. Methods    From December 2012 to December 2015, 210 Uygur patients who underwent artificial heart valve replacement surgery at the First Affiliated Hospital of Xinjiang Medical University were randomly assigned to a genetic anticoagulation therapy group (group A, n=106, 41 females and 65 males, aged 44.7±10.02 years) or an empirical anticoagulation therapy group (group B, n=104, 47 females and 57 males, aged 45.62±10.01 years) according to the random number table. CYP2C9 and VKORC1 genotypes were tested in the group A and then wafarin of administration in anticoagulation therapy was recommended. Patients in the group B were treated with conventional anticoagulation. Patients in both groups were followed up for 1 month and coagulation function was regularly tested. Results    The percentage of patients with INR values of 1.8-2.5 after 4 weeks warfarin anticoagulation treatment in the group A was higher than that in the group B (47.1% vs. 32.7%, P=0.038). The rate of INR≥3.0 in the warfarin anticoagulation therapy period in the group A was lower than that in the group B (21.6% vs. 26.5%, P=0.411). The time to reach the standard INR value and the time to get maintenance dose were shorter in the group A compared with the group B (8.80±3.07 d vs.   9.26±2.09 d, P=0.031; 14.25±4.55 d vs. 15.33±1.85 d, P=0.032). Bleeding occured in one patient in the group A and three patients in the group B (P=0.293). Embolic events occured in three patients in the group A and five patients in the group B (P=0.436). Conclusion    Compared with the empirical anticoagulation, the genetic anticoagulation based on wafarin dosing model can spend less time and make more patients to reach the standard INR value. However there is no significant difference between the two groups in the ratio of INR≥3.0, bleeding and embolic events in the warfarin anticoagulation therapy.

T cell immunoglobulin and immune receptor tyrosine-based inhibitory motif domain (TIGIT) is a co-inhibitory receptor, which is highly expressed in a variety of malignant tumors.It can inhibit T cells and NK cells, and plays a key role in regulating immune response and tumor immune escape.TIGIT is closely related to the growth, metastasis and prognosis of urologic tumors, and its overexpression is associated with tumor progression and poor prognosis.Currently, TIGIT-based urologic tumors treatment strategies include monoclonal antibody therapy and combined immunotherapy, such as combination therapy with PD-1/PD-L1 and other drugs.Experimental and clinical studies on TIGIT are also being carried out and significant progress has been made.Therefore, TIGIT is expected to become a new target for immunotherapy and a biomarker for predicting the prognosis of patients with urologic tumors.This article reviews the research progress of TIGIT in urologic tumors.