Functions and mechanisms of cytosolic phospholipase A2 in central nervous system trauma.

Central nervous system (CNS) trauma, including traumatic brain injury and spinal cord injury, has a high rate of disability and mortality, and effective treatment is currently lacking. Previous studies have revealed that neural inflammation plays a vital role in CNS trauma. As the initial enzyme in neuroinflammation, cytosolic phospholipase A2 (cPLA2) can hydrolyze membranous phosphatides at the sn-2 position in a preferential way to release lysophospholipids and ω3-polyunsaturated fatty acid dominated by arachidonic acid, thereby inducing secondary injuries. Although there is substantial fresh knowledge pertaining to cPLA2, in-depth comprehension of how cPLA2 participates in CNS trauma and the potential methods to ameliorate the clinical results after CNS trauma are still insufficient. The present review summarizes the latest understanding of how cPLA2 participates in CNS trauma, highlighting novel findings pertaining to how cPLA2 activation initiates the potential mechanisms specifically, neuroinflammation, lysosome membrane functions, and autophagy activity, that damage the CNS after trauma. Moreover, we focused on testing a variety of drugs capable of inhibiting cPLA2 or the upstream pathway, and we explored how those agents might be utilized as treatments to improve the results following CNS trauma. This review aimed to effectively understand the mechanism of cPLA2 activation and its role in the pathophysiological processes of CNS trauma and provide clarification and a new referential framework for future research.

Mannose-capped lipoarabinomannan-induced B10 cells decrease severity of dextran sodium sulphate-induced inflammatory bowel disease in mice.

Inflammatory bowel disease (IBD) is a chronic, non-specific, inflammatory gastrointestinal disease that mainly consists of Crohn's disease and ulcerative colitis. However, the aetiology and pathogenesis of IBD are still unclear. B10 (IL-10 producing regulatory B) cells, a subset of regulatory B cells, are known to contribute to intestinal homeostasis and the aberrant frequency of B10 cells is associated with IBD. We have recently reported that B10 cells can be induced by ManLAM (mannose-capped lipoarabinomannan), a major cell-wall lipoglycan of M tb (Mycobacterium tuberculosis). In the current study, the ManLAM-induced B10 cells were adoptively transferred into IL(interleukin)-10-/- mice and the roles of ManLAM-induced B10 cells were investigated in DSS (dextran sodium sulphate)-induced IBD model. ManLAM-induced B10 cells decrease colitis severity in the mice. The B10 cells downregulate Th1 polarization in spleen and MLNs (mesenteric lymph nodes) of DSS-treated mice. These results suggest that IL-10 production by ManLAM-treated B cells contributes to keeping the balance between CD4+ T cell subsets and protect mice from DSS-induced IBD.

Minimally invasive surgery for degenerative spondylolisthesis: transforaminal or oblique lumbar interbody fusion.

Aim: To compare the outcomes of minimally invasive surgery (MIS) for degenerative spondylolisthesis transforaminal lumbar interbody fusion (TLIF) and oblique lumbar interbody fusion (OLIF). Materials & methods: The clinical and surgical characteristics and outcomes of 38 patients with MIS-OLIF and 55 with MIS-TLIF were retrospectively evaluated. Results: Procedures and hospital stay were shorter and blood loss was less, with MIS-OLIF than with MIS-OLIF. The clinical and radiographic outcomes were similar. Postoperative changes in disk height and foraminal dimension were greater and patient satisfaction was better with MIS-OLIF than with MIS-TLIF. Conclusion: The clinical findings associated with the two procedures were similar; but patients preferred MIS-OLIF, which is less invasive, to MIS-TLIF. Clinical trial registration number: ChiCTR1800019443.

Mycobacterial mannose-capped lipoarabinomannan: a modulator bridging innate and adaptive immunity.

Mannose-capped lipoarabinomannan (ManLAM) is a high molecular mass amphipathic lipoglycan identified in pathogenic Mycobacterium tuberculosis (M. tb) and M. bovis Bacillus Calmette-Guérin (BCG). ManLAM, serves as both an immunogen and a modulator of the host immune system, and its critical role in mycobacterial survival during infection has been well-characterized. ManLAM can be recognized by various types of receptors on both innate and adaptive immune cells, including macrophages, dendritic cells (DCs), neutrophils, natural killer T (NKT) cells, T cells and B cells. MamLAM has been shown to affect phagocytosis, cytokine production, antigen presentation, T cell activation and polarization, as well as antibody production. Exploring the mechanisms underlying the roles of ManLAM during mycobacterial infection will aid in improving tuberculosis (TB) prevention, diagnosis and treatment interventions. In this review, we highlight the interaction between ManLAM and receptors, intracellular signalling pathways triggered by ManLAM and its roles in both innate and adaptive immune responses.

Effects of diammonium glycyrrhizinate on random skin flap survival in rats: An experimental study.

Partial necrosis of skin flaps continues to restrict the survival of local skin flaps following plastic and reconstructive surgeries. The aim of the present study was to investigate the effects of diammonium glycyrrhizinate (DG), a salt of glycyrrhetinic acid that has been widely used in the therapy of chronic hepatitis and human immunodeficiency virus infection, on random skin flap survival in rats. McFarlane flaps were established in 60 male Sprague-Dawley rats randomly divided into three groups. Group I served as the control group and was injected with saline (10 mg/kg) once per day. Group II and group III were the experimental groups, and were injected with 10 mg/kg DG once and twice per day, respectively. On day 7, the survival area of the flap was measured. Tissue samples were stained with hematoxylin and eosin and immunohistochemically evaluated. Tissue edema, neutrophil density, superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were evaluated. The mean survival areas of the flaps of group II were significantly larger when compared with those of group I (P<0.05), and the rats of group III exhibited significantly higher survival areas than group II (P<0.05). Histologic and immunohistochemical evaluation showed that microvessel development and the expression level of vascular endothelial growth factor were higher in the two experimental groups than in the control group. Furthermore, SOD activity was significantly increased (P<0.05), while the neutrophil density and MDA level were significantly reduced (P<0.05) in group II when compared with group I. Significant differences between group II and group III with regard to SOD activity and MDA level were also observed (P<0.05). Thus, DG may have a dose-dependent effect on promoting the survival of random skin flaps.

Effects of calcitriol on random skin flap survival in rats.

Calcitriol, a metabolite of vitamin D, is often used in osteoporosis clinics. However, the material has other bioactivities; for example, it accelerates angiogenesis, has anti-inflammatory properties, and inhibits oxidative stress. We investigated the effects of calcitriol in a random skin flap rat model. "McFarlane flap" models were established in 84 male Sprague Dawley rats, divided into two groups. One group received intraperitoneal injections of calcitriol (2 µg/kg/day) whereas control rats received intraperitoneal injections of saline. The percentage flap survival area and tissue water content were measured 7 days later, which showed that calcitriol improved flap survival area and reduced tissue edema. It also increased the mean vessel density and upregulated levels of VEGF mRNA/protein, both of which promote flap angiogenesis. Moreover, it decreased leukocyte and macrophage infiltration, reduced the inflammatory proteins IL1ß and IL6, increased SOD activity, decreased MDA content, and upregulated the level of autophagy. Overall, our results suggest that calcitriol promotes skin flap survival by accelerating angiogenesis, having anti-inflammatory effects, reducing oxidative stress, and promoting autophagy.

Stimulation of autophagy promotes functional recovery in diabetic rats with spinal cord injury.

In this study we examined the relationship between autophagy and apoptosis in diabetic rats after spinal cord injury (SCI), also we determined the role of autophagy in diabetes-aggravated neurological injury in vivo and in vitro. Our results showed that diabetes decreased the survival of neurons, promoted astrocytes proliferation, increased inflammatory cells infiltration and inhibited functional recovery after SCI. Diabetes was shown to confer increased activation of apoptotic pathways, along with an increase in autophagy; similar effects were also observed in vitro in neuronal PC12 cells. Treatment with rapamycin, an autophagy activator, partially abolished the adverse effect of diabetes, suggesting that diabetes may enhance neurological damage and suppress locomotor recovery after SCI, in addition to its effects on apoptosis and autophagy. In contrast, further stimulation of autophagy improved neurological function via inhibition of apoptosis. These results explained how diabetes exacerbates SCI in cellular level and suggested autophagy stimulation to be a new therapeutic strategy for diabetic SCI.

[Progress on the role of autophagy in spinal cord injury].

In recent years, the study of autophagy in spinal cord injury (SCI) gradually becomes the hot spot. However, the function of autophagy in the injured spinal cord is still controversial. In order to further understand the role of autophagy after SCI, we summarized the activation of autophagy, autophagic cell death, the relationship between autophagy and apoptosis, the function of autophagy in promoting the molecular metabolism and the role of autophagy after spinal cord injury. We concluded that the role of autophagy after SCI is a double-edged sword. Upregulating the level of autophagy appropriately can promote damaged proteins metabolism and inhibit apoptosis. However, excessive activation of antophagy may induce autophagic cell dealth. So we consider that the proper regulation of autophagy will be a new target in the treatment of SCI.

A Computed Tomographic Morphometric Study of the Pediatric Occipital Bone Thickness: Implications for Pediatric Occipitocervical Fusion.

STUDY DESIGN: This study is a computed tomographic-based morphometric analysis of the pediatric occipital bones as related to pediatric occipitocervical fusion. OBJECTIVE: To quantify reference data concerning the thicknesses of the immature occipital bones to guide the pediatric occipitocervical fusion. SUMMARY OF BACKGROUND DATA: To the best of our knowledge, no published study has provided insight into the thicknesses of pediatric occiputs with different age groups. METHODS: 80 pediatric patients were divided into 4 age groups, and their occiputs were studied on Philips Brilliance 256 iCT scan. RESULTS: The mean thickness ± standard deviations of the pediatric occipital bones with different age groups is shown. The median and the paramedian regions are always thicker than the more lateral regions at each age group and the thickest point in the occiputs is mostly at the external occipital protuberance. The mean thickness of occiputs showed an obvious significant difference between each 2 age groups and no significant difference between male and female in different age groups except the group 4. CONCLUSION: Our investigation provides insight into the anatomy of occiputs in pediatric population and preoperative CT evaluation must be required to further decrease the risk of occipitocervical fusion.