Glioma is the most common primary malignant tumor of the central nervous system in adults. Despite the standard treatment of surgery combined with radiotherapy and chemotherapy, the prognosis for high-grade glioma patients remains poor, highlighting the urgent need to further explore its pathogenesis and develop new therapeutic strategies. This article reviews the research progress in the field of glioma in China in 2024, covering tumorigenesis mechanisms, tumor immune microenvironment composition, advances in imaging techniques and novel imaging agents, improvements in surgical approaches, mechanisms of radio- and chemoresistance, and explorations of new therapeutic modalities. These studies provide a solid theoretical foundation for advancing clinical diagnosis and treatment of gliomas and may offer new opportunities to improve patient outcomes.

Microglial cells are the resident immune cells of brain. The activated microglia produces a range of deleterious substances, which plays an important role in the inflammation of post-stroke, such as superoxide, nitric oxide, matrix metalloproteinases, etc. The activa-tion of microglia may involve triggering receptor expressed on myeloid cells-1, Toll-like receptors 4, peroxisome proliferator-activated re-ceptors, purinergic receptors, etc. Intervention targeted to microglial receptor is becoming a new strategy for ischemic stroke.

Autophagy plays an important role in the regulation of activation and inflammation of microglia after ischemic stroke. The interaction between autophagy of microglia and the inflammation mediated by microglia after ischemic stroke was complex and a large num-ber of molecules were involved. The receptors of microglia activation and related substances may be possible mechanism in the regulation of microglia autophagy. Autophagy inhibitors and microglia receptor targeting therapy may provide new strategies for the clinical treatment of ischemic stroke. This paper summarized the progress of microglia autophagy after ischemic stroke.

AIM: To study the mechanism of protective effect of exogenous carbon monoxide (CO) in the lung injury induced by ischemia-reperfusion (IR) of hind limbs in rats. METHODS: Thirty-two SD rats were randomly divided into 4 groups: control, control+CO, IR and IR+CO. A rat model of ischemia in hind limbs and the reperfusion lung injury was made. The rats in IR+CO and control+CO groups were exposed to air containing 2.5?10~ -8 CO for 1 h before reperfusion or the corresponding control time point, while the other two groups were exposed to the routine air. The lung tissue structure, polymorphonuclear leukocyte (PMN) count, wet-to-dry weight ratio (W/D), malondialdehyde (MDA) content and the animal survival rate were observed. The carboxyhemoglobin (COHb) levels in artery blood were detected with CO-oximeter and the expression of intercellular adhesion molecule-1 (ICAM-1) in the lung was detected by Western blotting. RESULTS: Compared to control, the animal mortality, lung PMNs number, W/D , MDA content and ICAM-1 expression were all significantly increased in IR group. Compared with the IR group, the blood COHb level was significantly increased and the animal mortality, lung PMNs number, W/D, MDA content and ICAM-1 expression were all significantly decreased in IR+CO group. CONCLUSION: These data suggest that exogenous CO attenuate limb IR- induced lung injury by down-regulatiny ICAM-1 expression and suppressing PMN sequestration in the lung following limb IR in rats.