Notes

Fresh Acridone- as well as (Thio)Xanthone-Derived A single,1-Donor-Acceptor-Substituted Alkenes: pH-Dependent Fluorescence and strange Photooxygenation Components.
to observe the effect of eye acupuncture on cerebral blood flow and autophagy of cerebral tissue in rats with cerebral ischemia-reperfusion injury, so as to explore the mechanism of eye acupuncture underlying improvement of cerebral ischemia-reperfusion injury.

Fifty SD rats were randomly divided into sham operation, model, eye acupuncture, inhibitor and enhancer groups，with 10 rats in each group. The rat model of cerebral ischemia-reperfusion injury was established by occlusion of the middle cerebral artery for 1.5 h. The rats in the eye acupuncture group were treated with eye acupuncture for 30 minutes immediately, 12 h and 24 h after the modeling. Rats in the inhibitor group and enhancer group were given intracerebroventricular injection of autophagy agonist 3-Methyladenine or autophagy inducer Rapamycin 30 min before modeling. Longa's scoring method was used to evaluate the neurological function. The blood flow velocity of the cerebral cortex was mea-sured with a laser doppler blood flow meter, and thre was no significant difference between the enhancer and the model groups in the abovementioned indexes(P>0.05).

Eye acupuncture can improve the neurological function of rats with cerebral ischemia-reperfusion injury, which may be related to accelerating cerebral blood flow and inhibiting autophagy in the ischemic brain.
Eye acupuncture can improve the neurological function of rats with cerebral ischemia-reperfusion injury, which may be related to accelerating cerebral blood flow and inhibiting autophagy in the ischemic brain.
To observe the effect of moxibustion on the growth of tumor and expression of fibroblast growth factor receptor 1 (FGFR1) and vascular endothelial cell growth factor receptor 2 (VEGFR2) in mice with sarcoma, so as to explore its mechanisms underlying inhibiting sarcoma growth.

C57BL/6J mice (half male and half female) were inoculated with S180 sarcoma cells to form transplanted tumors, and divided into model control, medication and moxibustion groups, with 10 mice in each group. Moxibustion was applied to the transplanted tumor directly for 10 min, once a day for 14 days. After the treatment, Luminex liquid suspension chip was used to detect the contents of serum vascular endothelial growth factor (VEGF), FGFR1 and VEGFR2. The weight of the transplanted tumor was measured, and the expression of VEGF in the transplanted tumor was detected by immunohistochemistry, and the expression of FGFR1 and VEGFR2 mRNAs in the transplanted tumor was detected by fluorescence in situ hybridization.

The tumor weight, VEFR1 and VEGFR2 to inhibit angiogenesis.
To observe the effect of electroacupuncture (EA) at "Baihui" (GV20), "Shuigou" (GV26), etc. on the expressions of vascular endothelial growth factor (VEGF), collagen fibrillary acidic protein (GFAP), neuronal nucleus antigen(NeuN), β-catenin and Axin2 protein and mRNA in rats with cerebral ischemia (CI), so as to explore its mechanism underlying improvement of ischemic stroke.

A total of 108 male SD rats were randomly divided into control, model and EA groups, which were further divided into 7 d, 14 d and 21 d subgroups, with 12 rats in each group. The CI model was established by occlusion of the middle cerebral artery. EA (2 Hz/100 Hz, 2-4 V) was applied to GV20, GV26, bilateral "Sanyinjiao" (SP6) and bilateral "Neiguan" (PC6) for 30 min, once daily (except Sundays) for 21 days at most. The neurological deficit score was evaluated according to Longa's methods. The cerebral infarction state was assessed by using a magnetic resonance T2 imaging system. selleck products The expression levels of neurovascular markers as VEGF from injury, reduce the volume of cerebral infarction and improve the symptoms of neurological deficit in cerebral ischemic rats, which may be related to its effects in up-regulating β-catenin expression and in down-regulating Axin2 expression to further activate classical Wnt/ β-catenin signal pathway.
EA can protect the neurovascular units from injury, reduce the volume of cerebral infarction and improve the symptoms of neurological deficit in cerebral ischemic rats, which may be related to its effects in up-regulating β-catenin expression and in down-regulating Axin2 expression to further activate classical Wnt/ β-catenin signal pathway.
The prevalence, morbidity, and mortality associated with Ebstein anomaly (EA) remains poorly characterized in neonates. EA is a rare form of congenital heart disease (CHD) with significant heterogeneity.

To determine the recent, 2000-2018, prevalence, mortality, outcomes, and healthcare utilization of infants admitted at ≤28 days of life with EA in comparison to other critical congenital heart defects (CCHD) in the United States using a national data set.

The National Inpatient Sample (NIS) from the Healthcare Cost and Utilization Project (HCUP) was queried for infants admitted for any reason at ≤28 days of life with a diagnosis of EA between 2000 and 2018 using ICD-9 and 10 codes in the United States. Patient characteristics, morbidity, mortality, and healthcare utilization were evaluated for EA and compared with other CCHD.

From 2000 to 2018 a total of 68,312,952 neonatal admissions were identified, of them 4,398 neonates with isolated EA were identified, representing 7 per 100,000 neonatal admissions and 2.2% of CCHD admissions (4,398/197,881). The number of new EA cases ranged from 138 to 375 per year. In-hospital mortality was 12.3% and surgical repair occurred in 4.2% for infants with EA. There were 470 deaths without surgical repair which is 86.6% of the mortality. Arrhythmias were diagnosed in 10.6% and ECMO was used for 2.6% of neonates with EA.

EA is a rare form of CHD. The prevalence has remained stable over the 19 years whereas other congenital heart defects have had an increase. The mortality in neonates with EA was significantly higher than in pooled CCHD; the burden of mortality occurred in the neonates without surgical intervention.
EA is a rare form of CHD. The prevalence has remained stable over the 19 years whereas other congenital heart defects have had an increase. The mortality in neonates with EA was significantly higher than in pooled CCHD; the burden of mortality occurred in the neonates without surgical intervention.
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