The protective effort of GPCR kinase 2-interacting protein-1 in neurons via promoting Beclin1-Parkin induced mitophagy at the early stage of spinal cord ischemia-reperfusion injury.

In spinal cord ischemia-reperfusion (I/R) injury, large amounts of reactive oxygen species can cause mitochondrial damage. Therefore, mitophagy acts as the main mechanism for removing damaged mitochondria and protects nerve cells. This study aimed to illustrate the important role of GPCR kinase 2-interacting protein-1 (GIT1) in mitophagy in vivo and in vitro. The level of mitophagy in the neurons of Git1 knockout mice was significantly reduced after ischemia-reperfusion. However, the overexpression of adeno-associated virus with Git1 promoted mitophagy and inhibited the apoptosis of neurons. GIT1 regulated the phosphorylation of Beclin-1 in Thr119, which could promote the translocation of Parkin to the mitochondrial outer membrane. This process was independent of PTEN-induced kinase 1 (PINK1), but it could not rescue the role in the absence of PINK1. Overall, GIT1 enhanced mitophagy and protected neurons against ischemia-reperfusion injury and, hence, might serve as a new research site for the protection of ischemia-reperfusion injury.

Ultrasonographic characteristics of Killian-Jamieson diverticula.

PURPOSE: A Killian-Jamieson diverticulum (KJD) may be mistaken for a thyroid nodule on ultrasound (US). The purpose of this retrospective study was to search for specific US features that would help differentiate between KJD and thyroid nodules. METHODS: A total of 12 patients with KJD who had undergone an US examination of the neck were identified. The size, shape, boundary, echopattern, location, color flow signals on color Doppler US of KJD and the relationship between the lesion and esophageal wall were analyzed. The change of size, shape and internal echotexture were also observed when the lesion was compressed with the probe and when the patient was asked to drink water. RESULTS: All KJD were confirmed by barium esophagography. All KJD were posterior to the left thyroid lobe on US, and were associated with a semicircular hypoechoic anterior wall. The internal echotexture was heterogeneous. In eight cases, the connection to the esophageal wall was seen. When compressing with the US probe or when the patients swallowed water, the size, shape or internal echotexture of the lesion changed. CONCLUSION: The specific criteria for US diagnosis of KJD included the connection to the esophageal wall and the fact that the internal echotexture, shape and size of KJD changed in real-time when the patient swallowed water or when the lesion was compressed with the transducer.

Macrophage MSR1 promotes the formation of foamy macrophage and neuronal apoptosis after spinal cord injury.

BACKGROUND: A sustained inflammatory response following spinal cord injury (SCI) contributes to neuronal damage, inhibiting functional recovery. Macrophages, the major participants in the inflammatory response, transform into foamy macrophages after phagocytosing myelin debris, subsequently releasing inflammatory factors and amplifying the secondary injury. Here, we assessed the effect of macrophage scavenger receptor 1 (MSR1) in phagocytosis of myelin debris after SCI and explained its possible mechanism. METHODS: The SCI model was employed to determine the critical role of MSR1 in phagocytosis of myelin debris in vivo. The potential functions and mechanisms of MSR1 were explored using qPCR, western blotting, and immunofluorescence after treating macrophages and RAW264.7 with myelin debris in vitro. RESULTS: In this study, we found improved recovery from traumatic SCI in MSR1-knockout mice over that in MSR1 wild-type mice. Furthermore, MSR1 promoted the phagocytosis of myelin debris and the formation of foamy macrophage, leading to pro-inflammatory polarization in vitro and in vivo. Mechanistically, in the presence of myelin debris, MSR1-mediated NF-κB signaling pathway contributed to the release of inflammatory mediators and subsequently the apoptosis of neurons. CONCLUSIONS: Our study elucidates a previously unrecognized role of MSR1 in the pathophysiology of SCI and suggests that its inhibition may be a new treatment strategy for this traumatic condition.

[Expression and prognostic value of galectin-9 in hepatocellular carcinoma patients].

OBJECTIVE: To explore the prognostic value of galectin-9 in patients with hepatocellular carcinoma (HCC). METHODS: Galectin-9 was validated by immunohistochemisty in tissue microarrays from HCC patients (n = 147) and statistically assessed for the prognosis. The serum levels of galectin-9 from another independent cohort including HCC patients (n = 31) were assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Patients with a lower expression of galectin-9 had significantly worse prognosis than those with a higher expression. The serum level of galectin-9 of HCC patients (8.36 ± 2.12) µg/L was significantly lower than that in healthy (4.62 ± 1.59 )µg/L and liver cirrhosis controls (5.11 ± 1.92 )µg/L (P < 0.05). Multivariate Cox proportional hazard analysis showed that galectin-9 was an independent marker for predicting a poor prognosis of HCC patients. CONCLUSION: Involved in the poor prognosis of HCC patients, galectin-9 may be a new predictor of recurrence for HCC patients and serve as a high-priority therapeutic target.