Ischemic stroke,a major public health challenge,is marked by high incidence,disability,and mortality rates.The pathophysiology of stroke is complex,and inflammation reaction plays a crucial role throughout the process.In recent years,anti-inflammatory treatment has become a major focus in researches of ischemic stroke.Current preclinical and clinical investigations have revealed the potential of various anti-inflammatory strategies for ischemic stroke.However,which patient populations benefit from existing drugs are not yet elucidated.Additionally,drugs targeting innate immune cascades have become a new research hot spot.This article reviewed the latest clinical advances in anti-inflammatory therapy for ischemic stroke and discusses its promising prospects,aiming to provide novel clinical application strategies and future research directions.

Ischemic stroke,a major public health challenge,is marked by high incidence,disability,and mortality rates.The pathophysiology of stroke is complex,and inflammation reaction plays a crucial role throughout the process.In recent years,anti-inflammatory treatment has become a major focus in researches of ischemic stroke.Current preclinical and clinical investigations have revealed the potential of various anti-inflammatory strategies for ischemic stroke.However,which patient populations benefit from existing drugs are not yet elucidated.Additionally,drugs targeting innate immune cascades have become a new research hot spot.This article reviewed the latest clinical advances in anti-inflammatory therapy for ischemic stroke and discusses its promising prospects,aiming to provide novel clinical application strategies and future research directions.

The development, progression, and curative efficacy of head and neck squamous cell carcinoma (HNSCC) are influenced by complex interactions between epithelial and immune cells. Nevertheless, the specific changes in the nature of these interactions and their underlying molecular mechanisms in HNSCC are not yet fully understood. Cuproptosis, a form of programmed cell death that is dependent on copper, has been implicated in cancer pathogenesis. However, the understanding of cuproptosis in the context of HNSCC remains limited. In this study, we have discovered that cuproptosis-related long non-coding RNAs (CRLs) known as JPX play a role in promoting the expression of the oncogene urokinase-type plasminogen activator (PLAU) by competitively binding to miR-193b-3p in HNSCC. The increased activity of the JPX/miR-193b-3p/PLAU axis in malignant epithelial cells leads to enhanced cell proliferation, migration, and invasion in HNSCC. Moreover, the overexpression of PLAU in tumor epithelial cells facilitates its interaction with the receptor PLAUR, predominantly expressed on macrophages, thereby influencing the abnormal epithelial-immune interactome in HNSCC. Notably, the JPX inhibitor Axitinib and the PLAU inhibitor Palbociclib may not only exert their effects on the JPX/miR-193b-3p/PLAU axis that impacts the malignant tumor behaviors and the epithelial-immune cell interactions but also exhibit synergistic effects in terms of suppressing tumor cell growth and arresting cell cycle by targeting epidermal growth factor receptor (EGFR) and cyclin-dependent kinase (CDK4/6) for the treatment of HNSCC.
Humans ; MicroRNAs/metabolism* ; RNA, Long Noncoding/metabolism* ; Head and Neck Neoplasms/metabolism* ; Cell Proliferation ; Squamous Cell Carcinoma of Head and Neck/genetics* ; Urokinase-Type Plasminogen Activator/genetics* ; Cell Movement ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Carcinoma, Squamous Cell/genetics* ; Neoplasm Invasiveness

The development,progression,and curative efficacy of head and neck squamous cell carcinoma(HNSCC)are influenced by complex interactions between epithelial and immune cells.Nevertheless,the specific changes in the nature of these interactions and their underlying molecular mechanisms in HNSCC are not yet fully understood.Cuproptosis,a form of programmed cell death that is dependent on copper,has been implicated in cancer pathogenesis.However,the understanding of cuproptosis in the context of HNSCC remains limited.In this study,we have discovered that cuproptosis-related long non-coding RNAs(CRLs)known as JPX play a role in promoting the expression of the oncogene urokinase-type plasminogen activator(PLAU)by competitively binding to miR-193b-3p in HNSCC.The increased activity of the JPX/miR-193b-3p/PLAU axis in malignant epithelial cells leads to enhanced cell proliferation,migration,and invasion in HNSCC.Moreover,the overexpression of PLAU in tumor epithelial cells facilitates its interaction with the receptor PLAUR,predominantly expressed on macrophages,thereby influencing the abnormal epithelial-immune interactome in HNSCC.Notably,the JPX inhibitor Axitinib and the PLAU inhibitor Palbociclib may not only exert their effects on the JPX/miR-193b-3p/PLAU axis that impacts the malignant tumor behaviors and the epithelial-immune cell interactions but also exhibit synergistic effects in terms of suppressing tumor cell growth and arresting cell cycle by targeting epidermal growth factor receptor(EGFR)and cyclin-dependent kinase(CDK4/6)for the treatment of HNSCC.

Brain-computer interface (BCI) can collect and analyze the brain signals and provide direct communication between the brain and various external devices. Based on the maturity of neurointerventional technology, endovascular BCI has emerged and gained widespread attention due to its minimally invasive and efficient advantages. This article reviews the concept, feasibility, safety and application of endovascular BCI in nervous system related diseases, in order to strengthen the understanding of scientific research or clinical medical staff and provide reference for follow-up research.

Brain-computer interface (BCI) can collect and analyze the brain signals and provide direct communication between the brain and various external devices. Based on the maturity of neurointerventional technology, endovascular BCI has emerged and gained widespread attention due to its minimally invasive and efficient advantages. This article reviews the concept, feasibility, safety and application of endovascular BCI in nervous system related diseases, in order to strengthen the understanding of scientific research or clinical medical staff and provide reference for follow-up research.

Objective:To explore the effects of direct antiviral agent (DAAs) on the frequency of peripheral blood mononuclear cells and their activating factors sCD14s and CD163 in patients with chronic hepatitis C.Methods:Data of 15 treatment-naive chronic hepatitis C patients and 10 healthy controls were collected. Patients with chronic hepatitis C were treated with DAAs for 12 weeks. Blood samples were collected at 0, 4 and 12 weeks respectively, and blood samples of healthy controls were used as controls. Flow cytometry was used to detect the frequency of classical CD14 ++CD16 - mononuclear cells and pro-inflammatory CD14 +CD16 + mononuclear cells in peripheral blood. Serum sCD14s and sCD163 were detected by enzyme-linked immunosorbent assay. The comparison between the two groups was performed by t-test. The comparison between multiple groups was performed by analysis of variance, and further pairwise comparison was performed by LSD-t test. Results:Prior DAAs treatment, peripheral blood CD14 +CD16 + mononuclear cell frequency (18.49% ± 1.54% vs. 10.65% ± 0.83%), serum sCD14s [(64 407.38 ± 5778.49) pg/ml vs. (28 370.76 ± 2 357.68 ) pg/ml] and sCD163 [(22 853.80 ± 4 137.61) pg/ml vs. (2 934.41 ± 223.31) pg/ml] were all higher than healthy controls ( P < 0.05), while the frequency of CD14 ++CD16 - mononuclear cells in peripheral blood was lower than healthy controls (59.14%±0.54% vs. 72.75%±1.31%, P < 0.01). During DAAs treatment, CD14 +CD16 + mononuclear cells frequency, serum sCD14 and sCD163 were all decreased significantly. After 12 weeks of treatment, CD14 +CD16 + mononuclear cells had decreased to nearly normal level (12.42% ± 1.60% vs. 10.65% ± 0.83%, P > 0.05), and serum sCD14 and scd163 were still higher than those of healthy controls [sCD14: (44 390.06 ± 3 330.17) pg / ml vs. (28 370.76 ± 2 357.68) pg/ml, Scd163: (11 494.79 ± 1 836.97) pg / ml vs. (2 934.41 ± 223.31) pg / ml, P < 0.01], while the frequency of CD14 ++CD16 -mononuclear cells had gradually increased during the course of treatment and neared healthy control level after 12 weeks of treatment. There was no statistically significant difference between the two groups (71.54) % ± 2.99% vs. 72.75% ± 1.31%, P > 0.05). Conclusion:DAAs therapy can reduce the activation of peripheral blood mononuclear cells in patients with chronic hepatitis C.

Objective: To investigate the effects of direct-acting antiviral agents (DAA) therapy on the frequency of myeloid-derived suppressor cells (MDSC) and their subset of monocytic myeloid-derived suppressor cells (M-MDSC) in chronic hepatitis C (CHC) patients. Methods: A total of 32 treatment-naive CHC patients and 16 healthy controls were recruited at Third Affiliated Hospital of Sun Yat-Sen University from June 2016 to June 2017. The peripheral blood mononuclear cells (PBMC) were separated from the peripheral blood of patients with CHC before DAA therapy, at four weeks after DAA therapy, at 12 weeks after DAA therapy and 12 weeks after the end of DAA therapy. The frequencies of MDSC and M-MDSC were detected by the flow cytometer. The t test, U test and chi-square test was employed to analyze the data. Results: All the 32 treatment-naive patients achieved the rapid virological response and no virological breakthrough was observed. Before DAA therapy, the frequency of MDSC in CHC patients was 2.18%, which was higher than healthy individuals (0.60%; Z=-4.593, P<0.01), and positively correlated with the plasma levels of hepatitis C virus (HCV) RNA (r=0.688, P<0.01) and aspartate aminotransferase (r=0.735, P<0.01). After four weeks of DAA therapy, the frequency of MDSC decreased significantly to 1.07%, with no statistical significance compared to the controls (Z=-1.221, P>0.05). However, at 12 weeks after DAA therapy, the MDSC frequency increased, with statically significance compared to the controls (1.64% vs 0.60%, Z=-3.117, P=0.002). At 12 weeks after the end of DAA therapy, the MDSC frequency had decreased to 1.29% again, with no statistical significance compared to the controls (Z=-1.387, P=0.664). The changes of M-MDSC frequency were slightly different. Before DAA therapy, the frequency of M-MDSC in CHC patients was higher compared to healthy controls (1.66% vs 0.81%, Z=-2.745, P<0.01). The frequencies of M-MDSC were 0.91%, 1.09% and 1.10% at four, 12 weeks after DAA and 12 weeks after the end of DAA therapy, respectively. The differences were not statistically significant compared to the controls (Z=-0.589, -1.028 and -0.486, respectively, all P>0.05). Conclusion Immune status of the peripheral MDSC and M-MDSC can return to normal after DAA therapy in CHC patients.

Objective To investigate the effect of dexmedetomidine on perioperative cell immune function in patients undergoing hepatoma surgery. Methods Sixty patients (40-65 y/o, 50-80 kg body weight, ASA grad-ing I-II) with hepatoma were allocated into two groups each containing 30 patients:control group (group C) and dex-medetomidine group (group D). 15 minutes before anesthesia induction, a loading dose of dexmedetomidine 0.5μg/kg was injected intravenously, followed by infusion at 0.4μg/(kg · h)until the end of operation in group D. The equal volume of normal saline was administered in group C.Blood samples were obtained from jugular vein before induc-tion of anesthesia (T0), the end of operation(T1) and 24 h after the end of surgery (T2) for detections of the levels of T lymphocyte subsets (CD3+, CD4+, CD8+) and NK cells by flow cytometry. CIM+/CD8+ratio was calculated. Serum IL-2 and IL-10 were detected by ELISA methods. Results When compared with the baseline value (T0), the levels of CD3+, CD4+, CD4+/CD8+ratio and NK cells significantly decreased at T1 and T2 in group C, and the levels of CD3+and CD4+also significantly decreased at T1 and T2 in group D (P<0.05). Compared with group C, the levels of CD3+, CD4+, NK cells and IL-2 at T1 and T2 were significantly higher in group D, and level of IL-10 at T1 and T2 were significantly lower in group D (P < 0.05). Conclusion Dexmedetomidine could improve the postoperative suppression of immune function in patients undergoing hepatoma surgery.

Objective To investigate the levels of the mRNA expression of TIM-3 and Galectin-9 in peripheral blood mono-cytes (PBMCs)of acute exacerbation asthma patients and their clinical significances.Methods 60 patients with acute exac-erbation asthma (eliminating 15 cases of non-conform to the regulations)and 30 cases of healthy subjects were collected from January to October of 2014.Used fluorescence quantitative real-time reverse transcription-polymerase chain reaction to measure the mRNA expression of TIM-3 and Galectin-9 in PBMCs of patients with asthma and healthy controls.Results The expression of TIM-3,Galectin-9 and IFN-γmRNA in the PBMCs from acute exacerbation asthma patients were all ab-normally higher than healthy controls (U =458.5,P =0.019;U =437.5,P =0.010;U =260,P <0.001).There were statis-tically significant differences between them.Conclusion TIM-3/Galectin-9 pathway may participate in the occurrence,devel-opment of asthma.TIM-3 or (and)Galectin-9 may prove to be an important target for treatments to asthma.