Objective:To explore the clinical diagnosis and treatment of invasive gastrointestinal fungal infection plus pulmonary infection after renal transplantation.Methods:Clinical data were analyzed retrospectively for one patient with invasive fungal infection plus pulmonary infection after renal transplantation. The middle-aged female recipient underwent allogeneic kidney transplantation due to end-stage uremia. After successful kidney transplantation, there was postprandial epigastric pain not relieved by proton pump inhibitor. Gastroscopy after admission suggested that the nature of gastric mucosal lesions was to be determined. Pathological examination and special staining confirmed mucor.Results:After clarifying her conditions, the doses of such immunosuppression as tacrolimus, mycophenolate mofetil and prednisone were tapered and discontinued when necessary and using amphotericin B liposome plus posaconazole alleviated the digestive tract symptoms. Chest tightness, fever, shortness of breath after activities hinted at pulmonary infection after renal transplantation. Treatment was guided by the results of sputum culture.Conclusions:Mucor infection is rare in digestive tract complicated with pulmonary infection after renal transplantation. Clinicians should actively search for etiological evidence, seek multidisciplinary consultations for a definite diagnosis and provide empirical anti-infection treatments. Due attention is to be paid for double infection caused by anti-infection treatments and anti-infection treatment strategy should be timely adjusted and the dosage of immunosuppressant based upon immune monitoring.

Animals ; Macaca mulatta ; Optic Disk ; Glaucoma ; Craniocerebral Trauma ; Intraocular Pressure ; Low Tension Glaucoma

Alzheimer's disease (AD) is a leading cause of dementia in the elderly. Mitogen-activated protein kinase phosphatase 1 (MKP-1) plays a neuroprotective role in AD. However, the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, thereby repressing mRNA translation. Here, we reported that the microRNA-429-3p (miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2A^APP AD model cells. We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3'-untranslated region (3' UTR). Inhibition of miR-429-3p by its antagomir (A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation. More importantly, intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase (ERK1/2)-mediated GluA1 hyperphosphorylation at Ser831 site, thereby increasing the surface expression of GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Together, these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice, suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.