Backgrounds: Cognitive functions (CF) decline has been reported in end-stage renal disease (ESRD) patients. However, the influence of dialysis modalities on CF has not been investigated systematically. Methods: A systematic literature search was conducted in MEDLINE, Embase, Cochrane library and unpublished database Clinicaltrials.gov to identify the studies comparing the cognitive functions or risk of dementia between hemodialysis (HD) and peritoneal dialysis (PD). After data extraction, quality of studies was assessed using the Newcastle-Ottawa scale. Both qualitative and quantitative analyses were performed. Results: After study inclusion, totally 15 cohort or cross-sectional studies were included, comparing the cognitive functions using neuropsychological tests and covering the executive function, memory, orientation, attention, etc. By qualitative analysis, it showed that more studies are inclined to PD compared with HD with better cognitive functions. By quantitative analysis, it showed that PD showed better performance in the tests of Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), stroop interference test and exhibited lower risk of dementia compared with HD. Conclusions: In this meta-analysis, we draw preliminary conclusion that patients treated with PD had better cognitive functions and lower dementia risk compared with patients with HD. Still more large-scale and well-conducted prospective cohort studies are needed to draw more convincing conclusions.

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Autologous platelet-rich plasma (au-PRP) has been widely used for the management of refractory chronic wounds. However, patients with diabetic lower extremity ulcers (DLEUs) usually have complicated clinical conditions, and the utility of au-PRP is limited. In this study, the feasibility, effectiveness, and safety of allogeneic platelet-rich plasma (al-PRP) and au-PRP were investigated and compared in the treatment of DLEUs. A total of 75 in-patients with type 2 diabetes were assigned to the al-PRP group ( n = 20), au-PRP group ( n = 25), and conventional wound therapeutic (CWT) group ( n = 30) matched by the ankle brachial index and ulcer size from December 2015 to August 2018. Based on metabolic and nutritional regulation, infective control, and topical wound management, al-PRP, au-PRP, and CWT were administered to each group, respectively. Evaluation of treatment outcomes was determined by the parameters of wound healing and adverse reactions. The therapeutic times and average concentration of platelets were not significantly different between the au-PRP and al-PRP groups. The wound healing times of the al-PRP group (56.9 ± 29.22 d) and au-PRP group (55.6 ± 33.8 d) were significantly shorter than those of the CWT group (88.0 ± 43.4 d) ( P < 0.01), but there was no significant difference between the groups with PRP treatment. Although there was no significant difference in the daily healing area among all groups ( P > 0.05), the trend of the healing rate in the al-PRP group (16.77 ± 12.85 mm2), au-PRP group (14.31 ± 18.28 mm2), and CWT group (9.90 ± 8.51 mm2) gradually decreased. No obvious adverse reactions (fever, edema, pain, skin itching, rash, or other sensory abnormalities) were observed in either the au-PRP or the al-PRP groups. Both al-PRP and au-PRP could effectively and safely promote wound healing in patients with DLEUs. Alternatively, al-PRP could be used for DLEUs as an off-the-shelf solution when au-PRP is limited. Registration number of clinical trials: ChiCTR1900021317

Background: Alzheimer's disease (AD), which results in cognitive deficits, usually occurs in older people and is mainly caused by amyloid beta (Ab) deposits and neurofibrillary tangles. The bile acid receptor, farnesoid X receptor (FXR), has been extensively studied in cardiovascular diseases and digestive diseases. However, the role of FXR in AD is not yet understood. The purpose of the present study was to investigate the mechanism of FXR function in AD. Material/Methods: Lentivirus infection, flow cytometry, real-time PCR, and western blotting were used to detect the gain or loss of FXR in cell apoptosis induced by Ab. Co-immunoprecipitation was used to analyze the molecular partners involved in Ab-induced apoptosis. Results: We found that the mRNA and protein expression of FXR was enhanced in Ab-triggered neuronal apoptosis in differentiated SH-SY5Y cells and in mouse hippocampal neurons. Overexpression of FXR aggravated Ab-triggered neuronal apoptosis in differentiated SH-SY5Y cells, and this effect was further increased by treatment with the FXR agonist 6ECDCA. Molecular mechanism analysis by co-immunoprecipitation and immunoblotting revealed that FXR interacted with the cAMP-response element-binding protein (CREB), leading to decreased CREB and brain-derived neurotrophic factor (BDNF) protein levels. Low expression of FXR mostly reversed the Ab-triggered neuronal apoptosis effect and prevented the reduction in CREB and BDNF. Conclusions: These data suggest that FXR regulates Ab-induced neuronal apoptosis, which may be dependent on the CREB/BDNF signaling pathway in vitro.