As platelets are rich in growth factors for tissue regeneration, autologous platelet-rich plasma (PRP) has been used to treat some refractory corneal defects. Although PRP is effective, the cost of its preparation is very high. This article presents three cases of refractory corneal ulcer under the prescription of autologous PRP. The autologous PRP used in these cases was easily prepared in the blood bank laboratory. In this paper, we collected three patients with refractory corneal ulcer who were unresponsive to conventional treatment. The patients presented with neurotrophic ulcer, exposure corneal ulcer, and limbal deciency with corneal ulcer after hepatitic keratitis. Although we easily prepared autologous PRP eye drops using simple laboratory centrifugation, this preparation still had a clinical effect on corneal defect. The mean intervention time was 24 ± 6.9 days. The case with exposure corneal ulcer had significant wound healing and the other two cases felt subjective symptom relief. There were some clinical improvements of refractory corneal ulcers in our three cases. We present the clinical results of three cases and report an easy procedure for the preparation of autologous PRP. Autologous PRP prepared simply in the laboratory, it may be an alternative option for treating refractory corneal ulcer.
Obesity and its associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are a particular worldwide health problem at present. Momordica cochinchinensis (MC) is consumed widely in Southeast Asia. However, whether it has functional effects on fat-induced metabolic syndrome remains unclear. This study was conducted to examine the prevention effect of Momordica cochinchinensis aril (MCA) on obesity, non-alcoholic fatty liver and insulin resistance in mice. MCA protected the mice against high-fat diet (HFD)-induced body weight gain, hyperlipidemia and hyperglycemia, compared with mice that were not treated. MCA inhibited the expansion of adipose tissue and adipocyte hypertrophy. In addition, the insulin sensitivity-associated index that evaluates insulin function was also significantly restored. MCA also regulated the secretion of adipokines in HFD-induced obese mice. Moreover, hepatic fat accumulation and liver damage were reduced, which suggested that fatty liver was prevented by MCA. Furthermore, MCA supplementation suppressed hepatic lipid accumulation by activation of the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) signaling pathway in the human fatty liver HuS-E/2 cell model. Our data indicate that MCA altered the microbial contents of the gut and modulated microbial dysbiosis in the host, and consequently is involved in the prevention of HFD-induced adiposity, insulin resistance and non-alcoholic fatty liver disease.
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