Gastrodin relieves cognitive impairment by regulating autophagy via PI3K/AKT signaling pathway in vascular dementia.

Vascular dementia (VaD), the second most common type of dementia, is attributed to lower cerebral blood flow. To date, there is still no available clinical treatment for VaD. The phenolic glucoside gastrodin (GAS) is known for its neuroprotective effects, but the role and mechanisms of action on VD remains unclear. In this study, we aim to investigate the neuroprotective role and underlying mechanisms of GAS on chronic cerebral hypoperfusion (CCH)-mediated VaD rats and hypoxia-induced injury of HT22 cells. The study showed that GAS relieved learning and memory deficits, ameliorated hippocampus histological lesions in VaD rats. Additionally, GAS down-regulated LC3II/I, Beclin-1 levels and up-regulated P62 level in VaD rats and hypoxia-injured HT22 cells. Notably, GAS rescued the phosphorylation of PI3K/AKT pathway-related proteins expression, which regulates autophagy. Mechanistic studies verify that YP-740, a PI3K agonist, significantly resulted in inhibition of excessive autophagy and apoptosis with no significant differences were observed in the YP-740 and GAS co-treatment. Meantime, we found that LY294002, a PI3K inhibitor, substantially abolished GAS-mediated neuroprotection. These results revealed that the effects of GAS on VaD are related to stimulating PI3K/AKT pathway-mediated autophagy, suggesting a potentially beneficial therapeutic strategy for VaD.

[Efficacy of volume-targeted ventilation versus high-frequency oscillatory ventilation in the treatment of neonatal respiratory distress syndrome]. / å®¹é‡ç›®æ ‡é€šæ°”ä¸Žé«˜é¢‘æŒ¯è¡é€šæ°”æ²»ç–—æ–°ç”Ÿå„¿å‘¼å¸çª˜è¿«ç»¼åˆå¾çš„ç–—æ•ˆæ¯”è¾ƒ.

OBJECTIVES: To study the clinical efficacy of volume-targeted ventilation (VTV) versus high-frequency oscillatory ventilation (HFOV) in the treatment of neonatal respiratory distress syndrome (NRDS). METHODS: A retrospective cohort analysis was performed on the medical data of 140 neonates with severe NRDS who were admitted from September 2016 to February 2022, with 55 neonates in the VTV group and 85 in the HFOV group. The neonates in the VTV group received conventional mechanical ventilation and target tidal volume, and those in the HFOV group received HFOV. Arterial blood gas parameters were collected at 48 hours after admission, and related indices during hospitalization were recorded, including mortality rate, duration of invasive mechanical ventilation, duration of oxygen therapy, and the incidence rates of complications. RESULTS: Compared with the VTV group, the HFOV group had significantly lower incidence rates of grade Ⅲ-Ⅳ periventricular-intraventricular hemorrhage and neonatal necrotizing enterocolitis (P<0.05), and there were no significant differences between the two groups in the duration of invasive mechanical ventilation, the duration of oxygen therapy, mortality rate, and the incidence rates of bronchopulmonary dysplasia, hypocapnia, hypercapnia, periventricular leukomalacia, and retinopathy of prematurity (P>0.05). CONCLUSIONS: HFOV has a better clinical efficacy than VTV in the treatment of NRDS.

Successful prolonged cardiopulmonary resuscitation after intraoperative cardiac arrest due to povidone-iodine allergy: A case report.

BACKGROUND: Iodophor (povidone-iodine) is widely used clinically because of its broad-spectrum antibacterial effects. Although extremely rare, it may cause anaphylactic shock, which itself carries the life-threatening risk of cardiac arrest. CASE SUMMARY: We present a case in which a patient with postoperative infection went into anaphylactic shock and cardiac arrest caused by povidone-iodine during secondary surgery. The patient was successfully resuscitated by 2 h of cardiopulmonary resuscitation. CONCLUSION: This is the first known case of cardiac arrest caused by povidone-iodine allergy.

Potential involvement of Fgf10/Fgfr2 and androgen receptor (AR) in renal fibrosis in adult male rat offspring subjected to prenatal exposure to di-n-butyl phthalate (DBP).

BACKGROUND: We previously demonstrated that maternal exposure to di-n-butyl phthalate (DBP) induces dysplasia of the kidney in newborn male offspring and renal fibrosis in adults. But the underlying mechanisms remain elusive. Fgf10/Fgfr2 and androgen receptor (AR) are known to be important for renal development. We therefore investigated whether these genes are involved in DBP-induced renal fibrosis. MATERIALS AND METHODS: Using Sprague-Dawley rats and rat renal proximal tubular cells (NRK52E), we determined the potential involvement of Fgf10, Fgfr2 and AR in DBP-induced renal fibrosis. RESULTS: We found that maternal exposure to DBP induces renal fibrosis in adult male offspring. A lower serum testosterone concentration and reduced expression of Fgf10, Fgfr2 and AR were detected in these animals. These was a trend toward lower expression of Fgf10, Fgfr2 and AR in NRK52E cells subjected to DBP exposure. Furthermore, higher expression levels of TGF-ß and α-SMA were observed in abnormal renal tissue and DBP-treated NRK52E cells. CONCLUSION: Our findings suggest the potential involvement of Fgf10/Fgfr2 and AR in renal fibrosis of adult male rat offspring induced by prenatal exposure to DBP. The anti-androgenic effects of DBP might play an important role in this pathological process.