Roles of pyroptosis in intervertebral disc degeneration.

Intervertebral disc degeneration (IDD), the key pathological process in low back pain, is characterized by chronic inflammation and progressive cell death. Pyroptosis is a type of pro-inflammatory programmed necrosis mediated by inflammasomes that is dependent on the gasdermin family of proteins. An in-depth study of the pathological mechanisms of IDD has revealed that pyroptosis plays an important role in its occurrence and development. The molecular characteristics and activation signaling mechanisms of pyroptosis are reviewed in this paper. Moreover, the specific roles of pyroptosis in IDD pathology are outlined and various targeted drugs for its treatment are highlighted.

Mechanisms and functions of long noncoding RNAs in intervertebral disc degeneration.

Intervertebral disc degeneration (IDD) is a key pathological process underlying low back pain. Although, to date, specific molecular mechanisms have not been elucidated, at the cellular level, it is mainly due to pathological changes in the life process of nucleus pulposus (NP) cells in the intervertebral disc (IVD). These changes are closely related to cell proliferation, apoptosis, senescence, autophagy, inflammation, and extracellular matrix (ECM) remodeling. Long noncoding RNAs (lncRNAs) have gradually become a focus of scientific research because of their functional complexity and local tissue specific expression. Moreover, they mediate a series of cellular signaling pathways in NP cells by competing for microRNA (miRNA) or directly targeting gene expression by mRNA adsorption, thereby regulating cell life activities that play a vital role in the mechanism underlying IDD. In-depth studies on lncRNAs can help identify new therapeutic targets or aid in developing IDD treatment strategies at the gene level and those based on regenerative medicine, thus providing new ideas for researchers. This article reviews the classification, biological functions, mechanisms of action, and therapeutic potential of lncRNAs in IDD.

Ski Regulates the Inflammatory Response of Reactive Astrocytes Induced by Oxygen Glucose Deprivation/Reoxygenation (OGD/R) Through the NF-κB Pathway.

Spinal cord injury (SCI) is a common disease of the nervous system, including primary and secondary injuries. Neuronal inflammation after SCI is the most important pathological process of SCI and a chemical barrier to nerve function recovery after injury. Ski, an evolutionarily conserved functional transcriptional regulator protein, is upregulated in reactive astrocytes after SCI and regulates the biological characteristics of astrocytes. However, its role in the glial inflammatory response triggered by reactive astrocytes after spinal cord ischemia and its exact mechanism remains unclear. This study investigated the role and mechanism of Ski in the inflammatory response triggered by reactive astrocytes induced by oxygen and sugar deprivation/reoxygenation (OGD/R) model in vitro. In the ODG/R model, Ski expression was upregulated. In contrast, Ski upregulation was accompanied by increased levels of iNOS, IL-1ß, IL-6, TNF-α, and other inflammation-related factors. These results indicated that the inflammatory response triggered by astrocytes was significantly enhanced in OGD/R-stimulated astrocytes. Astrocytes were transfected with Ski specific siRNA to knock out Ski and subsequently attenuate OGD-induced astrocyte-triggered inflammation. Our results also suggest that Ski downregulation downregulates the expression of iNOS, IL-1ß, IL-6, and TNF-α in OGD/R-induced reactive astrocytes by inhibiting the activity of the NF-κB signaling pathway. In conclusion, downregulation of Ski can effectively inhibit glial inflammation in SCI by inhibiting the activity of the NF-κB pathway. These findings suggest that Ski is a promising therapeutic target for inflammatory responses after SCI.In conclusion, Ski downregulation can effectively inhibit glial inflammation in SCI by inhibiting the activity of the NF-κB pathway. These findings suggest that Ski might serve as a promising target for the treatment of inflammatory responses after SCI.

Ski regulates proliferation and migration of reactive astrocytes induced by lipopolysaccharide (LPS) through PI3K/Akt pathway.

Spinal cord injury (SCI) is a leading cause of disability and death worldwide. Reactive astrogliosis, a typical feature of SCI, undergoes various molecular and morphological changes and contributes to glial scar formation, which impedes axonal regeneration. Ski is a novel molecule that regulates the biological characteristics of astrocytes after spinal cord injury, but its function and the exact mechanism of its overexpression in reactive astrocyte proliferation and migration after SCI remain unclear. The purpose of this study was to elucidate the effect and mechanism of Ski on the proliferation and migration of reactive astrocytes, and to regulate the spatiotemporal formation of glial scars after SCI. In an in vitro lipopolysaccharide (LPS)-induced astrocyte injury model, the expression of Ski was upregulated in a time-dependent manner in LPS-induced astrocytes, and the upregulation of Ski was accompanied by that of PCNA, CDK4, CyclinD1, and other proliferation-related proteins. Our findings suggest that Ski promotes the proliferation and migration of reactive astrocytes. Next, astrocytes were transfected with a specific lentivirus to cause the overexpression of Ski, which significantly enhanced the proliferation and migration of reactive astrocytes and LPS-induced activation of the PI3K/Akt pathway. The PI3K/Akt pathway inhibitor LY294002 significantly inhibited the proliferation and migration of LPS-induced reactive astrocytes after Ski overexpression. In conclusion, Ski regulates LPS-induced astrocyte proliferation and migration through the PI3K/Akt pathway, making Ski a promising target for strategies to combat glial scarring after SCI.

[Effects of reductive soil disinfestation during low-temperature stubble free period on the control of watermelon Fusarium wilt]. / ä½Žæ¸©èŒ¬å£ç©ºé—²æœŸåœŸå£¤å¼ºè¿˜åŽŸæ¶ˆæ¯’å¯¹è¥¿ç“œæž¯èŽç— çš„å½±å“.

In order to clarify the controlling effect of reductive soil disinfestation (RSD) during low-temperature stubble idle period on watermelon Fusarium wilt, we conducted a pot experiment, containing control (CK), flooded control (FCK), and RSD treatments incorporated with 2% (w/w) alfalfa meal (AL), 0.25% acetic acid (AC), and AL+AC. Real time PCR and Illumian Miseq sequencing were used to determine the abundances of fungi and Fusarium oxysporum as well as fungal community composition. The disease incidence and yield of watermelon were measured. Results showed that the abundance of Fusarium oxysporum and the ratio of Fusarium oxysporum to fungi significantly decreased in the FCK and three RSD treatments, and the disinfestation effects of these treatments ranged from 86.1% to 94.6%. The yield and disease incidence of watermelon significantly increased and decreased in all of the RSD treatments, respectively. There was no significant diffe-rence between FCK and CK treatments. The control efficiencies of Fusarium wilt in AL, AC, and AL+AC were 63.2%, 73.7%, and 94.7%, respectively. The compositions of fungal community in the AL and AC treatments were significantly changed, whereas FCK did not affect fungal community. The relative abundances of dominant fungal genera, such as Zopfiella, Pseudeurotium, Geotrichum, Ascobolus, Westerdykella, and Guehomyces, increased in the RSD treatments. Most of those genera were significantly and negatively correlated with the abundance of Fusarium oxysporum, the ratio of Fusarium oxysporum to fungi, and the disease incidence. In conclusion, RSD treated in the low-temperature stubble free period could effectively control watermelon Fusarium wilt by reshaping fungal community composition.

Biological Functions and Therapeutic Potential of Autophagy in Spinal Cord Injury.

Autophagy is an evolutionarily conserved lysosomal degradation pathway that maintains metabolism and homeostasis by eliminating protein aggregates and damaged organelles. Many studies have reported that autophagy plays an important role in spinal cord injury (SCI). However, the spatiotemporal patterns of autophagy activation after traumatic SCI are contradictory. Most studies show that the activation of autophagy and inhibition of apoptosis have neuroprotective effects on traumatic SCI. However, reports demonstrate that autophagy is strongly associated with distal neuronal death and the impaired functional recovery following traumatic SCI. This article introduces SCI pathophysiology, the physiology and mechanism of autophagy, and our current review on its role in traumatic SCI. We also discuss the interaction between autophagy and apoptosis and the therapeutic effect of activating or inhibiting autophagy in promoting functional recovery. Thus, we aim to provide a theoretical basis for the biological therapy of SCI.

Role of HAND2-AS1 in human tumors.

Long noncoding RNAs (lncRNAs) are molecules more than 200 nucleotides in length. They play roles in various cells, mainly regulating cell growth, differentiation, and apoptosis. They also participate in the pathogenesis of many diseases. In fact, several studies have shown that lncRNAs function as cancer or tumor suppressor genes and play important roles in the occurrence and development of cancer in humans. New evidence has shown that lncRNA heart and neural crest derivatives expressed 2-antisense RNA 1 (lncRNA HAND2-AS1) hinders the occurrence and development of various tumors. Overexpression of HAND2-AS1 was found to be significantly related to the clinical and pathological characteristics of cancer patients, as well as the regulation of cell proliferation, apoptosis, invasion, metastasis, and energy metabolism through several possible mechanisms. Therefore, HAND2-AS1 may be a promising tumor biomarker and therapeutic target. Here, we review the biological functions, mechanisms, and potential clinical significance of HAND2-AS1 in numerous human tumors.

The role of long non-coding RNA MIAT in cancers.

Long non-coding RNAs (lncRNAs), a kind of non-coding single-strand RNAs, play an important role as carcinogenic genes or tumor suppressors in the development of human cancer. Myocardial infarction-associated transcript (MIAT) was first identified as a lncRNA in 2006 and originally isolated as a candidate gene for myocardial infarction. Later, it was reported that MIAT exhibits regulatory effects on the human cell cycle. Since its discovery, MIAT has also been identified as a carcinogenic regulator in many malignant tumors. High expression of MIAT is related to the clinicopathological characteristics of cancer patients. It can also regulate cell proliferation, invasion, metastasis, and anti-apoptosis through a variety of mechanisms. Therefore, MIAT is considered a potential biomarker and therapeutic target in cancer. In this review, we summarize the biological function, mechanism, and potential clinical significance of MIAT during tumorigenesis.

Role of SNHG16 in human cancer.

A growing body of evidence suggests that long non-coding RNAs (lncRNAs), a novel class of non-coding endogenous single-stranded RNA, play a key role in multiple physiological and pathological processes through transcriptional interference, post-transcriptional regulation, and epigenetic modification. Furthermore, many studies have shown that lncRNAs-as oncogenes or tumour suppressors-play an important role in the occurrence and development of human cancers. Small nucleolar RNA host gene 16 (SNHG16) was initially identified as an oncogenic lncRNA in neuroblastoma, and has since been identified as a carcinogenic regulator of various malignant tumours. Overexpression of SNHG16 is associated with clinical and pathological characteristics of cancer patients, and regulates cell proliferation, apoptosis, invasion and metastasis through a variety of potential mechanisms. Therefore, SNHG16 may be a promising biomarker and therapeutic target for cancers. In this review, we summarize the biological function, related mechanisms and potential clinical significance of SNHG16 in multiple human cancers.

Measurement of scoliosis Cobb angle by end vertebra tilt angle method.

BACKGROUND: Scoliosis is a common deformity, and its severity is usually assessed by measuring the Cobb angle on the spinal X-ray film. The measurement of the Cobb angle is an important basis for selecting therapeutic methods and evaluating therapeutic effects. To measure and calculate the scoliosis Cobb angle by end vertebra tilt angle method (tilt angle method) and assess its accuracy and usability. METHODS: It is deduced that the Cobb angle is the sum of upper and lower end vertebra tilt angles through the law of plane geometry. The project included 32 patients with scoliosis who have received treatment in our hospital from June 2011 to July 2016, whose Cobb angles were measured at various segments (total 50). The measuring results of the tilt angle method and the classical method were compared, and the time spent for the measurement of the two groups was respectively recorded with an electronic stopwatch for comparison. The interference of line marking in imaging data pixel in the two groups was compared using Beyond Compare software. RESULTS: The measuring results through PACS (picture archiving and communication systems) were regarded as the reference standard. There was no statistical difference for measuring the Cobb angle between the PACS method, end vertebra tilt angle method, and classical method. The end vertebra tilt angle method takes less measuring time than the classical method. The measuring error between the classical method and the tilt angle method showed no statistical significance for the difference. CONCLUSION: The scoliosis Cobb angle can be measured accurately and rapidly using the principle of the Cobb angle being equal to the sum of tilt angles of the upper and lower end vertebra, where in the film data of imaging will not be easily contaminated. Under special conditions, the average measuring error is ± 3°.

Knockdown of Ski decreased the reactive astrocytes proliferation in vitro induced by oxygen-glucose deprivation/reoxygenation.

Glia scar is a pathological marker in late phase of brain ischemia disease, which constitutes a major physical biochemical barrier to impede axonal regrowth. Astrocytes are known to be critically involved in the formation of glial scar. However, their response to ischemia and their role in neuroprotection after central nervous system (CNS) injury are not completely clear. Recently, we have demonstrated for the first time that Ski was up-regulated in reactive astrocytes after spinal cord injury in vivo and in vitro, which indicates Ski may be a new molecule that control astrocytes biologic properties after CNS injury. However, its role in the process of reactive astrogliosis after cerebral ischemia and its definite mechanism still remains unknown. This study is to elucidate the role of Ski in reactive astrocytes induced by oxygen-glucose deprivation/reoxygenation (OGD/R) model in vitro. The expression of Ski was proved to be up-regulated in OGD/R model. Meanwhile, Up-regulation of Ski was accompanied with high ratio of EdU (+) cells and up-expression of related proteins including GFAP, PCNA, CDK4, and CyclinD1, which demonstrated the distinct activation and proliferation of astrocytes after stimulation by OGD/R. Astrocytes were transfected with Ski-specific siRNA to knockdown Ski expression and subsequently attenuated OGD-induced astrocyte proliferation. Our results also showed that Ski down-regulation could suppress the activity of the Ras-Raf-ERK1/2 signaling pathway. Together, knockdown of Ski can effectively inhibit the proliferation of reactive astrogliosis via suppressing the Ras-Raf-ERK1/2 pathway. These findings indicated that maybe Ski is a promising therapeutic target for cerebral ischemic injury.