ABSTRACT
Research over the past two decades has confirmed that noncoding RNAs (ncRNAs), which are abundant in cells from yeast to vertebrates, are no longer "junk" transcripts but functional regulators that can mediate various cellular and physiological processes. The dysregulation of ncRNAs is closely related to the imbalance of cellular homeostasis and the occurrence and development of various diseases. In mammals, ncRNAs, such as long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), have been shown to serve as biomarkers and intervention targets in growth, development, immunity, and disease progression. The regulatory functions of lncRNAs on gene expression are usually mediated by crosstalk with miRNAs. The most predominant mode of lncRNA-miRNA crosstalk is the lncRNA-miRNA-mRNA axis, in which lncRNAs act as competing endogenous RNAs (ceRNAs). Compared to mammals, little attention has been given to the role and mechanism of the lncRNA-miRNA-mRNA axis in teleost species. In this review, we provide current knowledge about the teleost lncRNA-miRNA-mRNA axis, focusing on its physiological and pathological regulation in growth and development, reproduction, skeletal muscle, immunity to bacterial and viral infections, and other stress-related immune responses. Herein, we also explored the potential application of the lncRNA-miRNA-mRNA axis in the aquaculture industry. These findings contribute to an enhanced understanding of ncRNA and ncRNA-ncRNA crosstalk in fish biology to improve aquaculture productivity, fish health and quality.
Subject(s)
MicroRNAs , RNA, Long Noncoding , Animals , MicroRNAs/genetics , MicroRNAs/metabolism , RNA, Messenger/genetics , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Biomarkers/metabolism , Mammals/metabolismABSTRACT
Raynaud's phenomenon is a symptom complex manifested as intermittent fingertip ischemia caused by cold or other sympathetic drivers. Secondary Raynaud's phenomenon is often more severe and could even lead to finger ulceration, making it particularly complicated to treat. We describe a case of severe Raynaud's phenomenon secondary to subclinical hypothyroidism lasting for more than 6 hours in a 65-year-old woman. The patient was also diagnosed with hypothyroidism, epilepsy, and secondary soft tissue infection of the right middle and ring fingers. After careful multidisciplinary consultation and discussion, the patient received vasodilation, anticoagulation, thyroxine supplementation, stellate ganglion block, hyperbaric oxygen therapy and debridement. The patient responded well to the medication, avoiding amputation or obviously dysfunction. Multidisciplinary team gathering the doctors from different departments proposes appropriate strategies for patients with severe Raynaud's phenomenon and could improve the prognosis and satisfaction of patient effectively.
Subject(s)
Hypothyroidism , Raynaud Disease , Female , Humans , Aged , Hypothyroidism/complications , Raynaud Disease/etiology , Raynaud Disease/therapy , Raynaud Disease/diagnosisABSTRACT
Raynaud's phenomenon is a symptom complex manifested as intermittent fingertip ischemia caused by cold or other sympathetic drivers. Secondary Raynaud's phenomenon is often more severe and could even lead to finger ulceration, making it particularly complicated to treat. We describe a case of severe Raynaud's phenomenon secondary to subclinical hypothyroidism lasting for more than 6 hours in a 65-year-old woman. The patient was also diagnosed with hypothyroidism, epilepsy, and secondary soft tissue infection of the right middle and ring fingers. After careful multidisciplinary consultation and discussion, the patient received vasodilation, anticoagulation, thyroxine supplementation, stellate ganglion block, hyperbaric oxygen therapy and debridement. The patient responded well to the medication, avoiding amputation or obviously dysfunction. Multidisciplinary team gathering the doctors from different departments proposes appropriate strategies for patients with severe Raynaud's phenomenon and could improve the prognosis and satisfaction of patient effectively.
Subject(s)
Female , Humans , Aged , Hypothyroidism/complications , Raynaud Disease/diagnosisABSTRACT
Parkinson's disease (PD) is a progressive and degenerative disorder of the central nervous system, characterized by the loss of dopaminergic neurons and muscular rigidity. Treatment with propofol (2,6diisopropylphenol) has been observed to attenuate oxidative stress injury via inhibition of programmed cell death. Results from the present study indicate that propofol treatment attenuates 1methyl4phenylpyridinium (MPP+)induced oxidative stress, which was demonstrated by increased levels of reactive oxygen species, 4hydroxy2nonenal and protein carbonyls. Furthermore, it was demonstrated that propofol may ameliorate MPP+induced mitochondrial dysfunction by increasing the level of ATP and the mitochondrial membrane potential. MTT and lactate dehydrogenase assays indicated that propofol treatment reduces cell vulnerability to MPP+induced insult. Propofol was also observed to prevent apoptotic signals by reducing the ratio of Bcl2associated X protein to Bcell lymphoma 2, reducing the expression level of cleaved caspase3 and attenuating cytochrome c release. Thus, propofol may present as a novel therapeutic strategy for the treatment of PD.