The intervertebral disc is a complex structure composed of the central nucleus pulposus, the peripheral annulus fibrosus, and the cartilaginous endplates located at the top and bottom. This unique arrangement effectively isolates the nucleus pulposus from the host’s immune system. Additionally, specific substances within the intervertebral disc exhibit inhibitory effects on the infiltration of immune cells and cytokines, which has led to the recognition of the intervertebral disc as an immune-privileged tissue. However, during intervertebral disc degeneration (IDD), the physical barriers that maintain this immune privilege are compromised. As a result, the nucleus pulposus may be perceived as a foreign antigen by the immune system. Simultaneously, inflammatory cytokines released by the degenerating disc attract a significant influx of immune cells, disrupting the delicate immunological balance within the nucleus pulposus and exacerbating the progression of IDD. Recent studies have confirmed the infiltration of immune cells such as macrophages and mast cells into the degenerative intervertebral disc, and the phenotypic characteristics and quantitative changes of these immune cells are closely related to the process of IDD. In terms of treatment strategies, biological agents such as mesenchymal stem cell therapy, gene therapy and growth factors that regulate the immune microenvironment of degenerative intervertebral discs have entered the stage of animal experiments. At the same time, small molecule drugs have shown unique regulatory potential in restoring the immune-privileged status of intervertebral discs.

The intervertebral disc is a complex structure composed of the central nucleus pulposus, the peripheral annulus fibrosus, and the cartilaginous endplates located at the top and bottom. This unique arrangement effectively isolates the nucleus pulposus from the host’s immune system. Additionally, specific substances within the intervertebral disc exhibit inhibitory effects on the infiltration of immune cells and cytokines, which has led to the recognition of the intervertebral disc as an immune-privileged tissue. However, during intervertebral disc degeneration (IDD), the physical barriers that maintain this immune privilege are compromised. As a result, the nucleus pulposus may be perceived as a foreign antigen by the immune system. Simultaneously, inflammatory cytokines released by the degenerating disc attract a significant influx of immune cells, disrupting the delicate immunological balance within the nucleus pulposus and exacerbating the progression of IDD. Recent studies have confirmed the infiltration of immune cells such as macrophages and mast cells into the degenerative intervertebral disc, and the phenotypic characteristics and quantitative changes of these immune cells are closely related to the process of IDD. In terms of treatment strategies, biological agents such as mesenchymal stem cell therapy, gene therapy and growth factors that regulate the immune microenvironment of degenerative intervertebral discs have entered the stage of animal experiments. At the same time, small molecule drugs have shown unique regulatory potential in restoring the immune-privileged status of intervertebral discs.

Discogenic low back pain from intervertebral disc degeneration was one of the major public health problems in the world, leading to global workforce decline. Recent studies showed that microorganisms existed in the intervertebral disc with significant differences between the normal intervertebral disc and the degenerated ones in not only species and numbers but also the changes of their functional activities. In addition, there was an overlap in microbial populations between the gut and the intervertebral disc, suggesting that the gut microbiota may play a key role in the pathological process of intervertebral disc degeneration. To further explore the relationship between gut microbiota and the host immune metabolic system, the concept of gut-organ axis was established. Researchers proposed the theory of gut-intervertebral disc axis to clarify the specific mechanism of intestinal flora in intervertebral disc degeneration. Studies showed that microorganisms could enter the intervertebral disc in a variety of ways, such as hematogenous transmission, lymphatic route, and invasion through annulus fibrosus tears. The arrival of these microorganisms in the intervertebral disc would trigger a series of local immune and inflammatory responses, promoting the degeneration of the intervertebral disc tissue. In the future, precision medical strategies targeting the gut and intervertebral disc microbiome may become promising in the prevention and treatment of intervertebral disc degeneration. With further research in this field, the treatment of intervertebral disc degeneration by targeting the gut and intervertebral disc microbiota showed great clinical value. This article reviewed and discussed the effect of intestinal flora imbalance on intervertebral disc degeneration and the potential therapeutic effect of adjusting intestinal flora on intervertebral disc degeneration. The theory of gut-intervertebral disc axis, which provided a new perspective to understand the pathogenesis of intervertebral disc degeneration, supported innovative treatment methods in the future.

BACKGROUND:Serum-specific biomarkers between normal healthy individuals and populations with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome)have not been fully defined. OBJECTIVE:To screen and identify the potential biomarkers of developmental cervical canal stenosis with Qi deficiency and blood stasis. METHODS:Serum samples were collected from nine patients with developmental cervical canal stenosis with Qi deficiency and blood stasis and eight healthy people.Differentially expressed proteins in serum were screened and identified using isotope relative labeling and absolute quantification combined with liquid chromatography tandem mass spectrometry.Western blot was used to verify some significant differentially expressed proteins. RESULTS AND CONCLUSION:A total of 61 differentially expressed proteins(P<0.05)were identified using tandem mass spectrometry techniques.Compared with the healthy normal population group,14 differentially expressed proteins such as complement component C1q receptor,apolipoprotein A4,and C-C motif chemokine ligand 18 were significantly upregulated,while 47 differentially expressed proteins such as myosin light chain 3,mitochondrial translation elongation factor,and nucleolar phosphoprotein 1 were significantly downregulated.The results of gene ontology enrichment analysis indicated that these differentially expressed proteins might participate in molecular functions such as regulation of chromosomal tissue,mitochondrial membrane tissue,and muscle system processes.Protein-protein interaction network analysis showed that 38 common differential proteins,including complement component C1q receptor,apolipoprotein A4,C-C motif chemokine ligand 18,myosin light chain 3,mitochondrial translation elongation factor,and nucleolar phosphoprotein 1,were located at functional network nodes between healthy normal individuals and those with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome),and were closely related to the local energy metabolism of the cervical spine,the production of cervical vertebral osteocytes,and the formation of osteoclasts.The main differentially expressed protein myosin light chain 3 was validated using western blot assay,and the validation results were consistent with the proteomic results.To conclude,the preliminary discovery of differentially expressed proteins in serum between healthy normal individuals and those with developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome)through absolute quantitative technology combined with liquid chromatography tandem mass spectrometry technology suggests that myosin light chain 3 may be a specific serum marker for developmental cervical canal stenosis(Qi deficiency and blood stasis syndrome).

Discogenic low back pain from intervertebral disc degeneration was one of the major public health problems in the world, leading to global workforce decline. Recent studies showed that microorganisms existed in the intervertebral disc with significant differences between the normal intervertebral disc and the degenerated ones in not only species and numbers but also the changes of their functional activities. In addition, there was an overlap in microbial populations between the gut and the intervertebral disc, suggesting that the gut microbiota may play a key role in the pathological process of intervertebral disc degeneration. To further explore the relationship between gut microbiota and the host immune metabolic system, the concept of gut-organ axis was established. Researchers proposed the theory of gut-intervertebral disc axis to clarify the specific mechanism of intestinal flora in intervertebral disc degeneration. Studies showed that microorganisms could enter the intervertebral disc in a variety of ways, such as hematogenous transmission, lymphatic route, and invasion through annulus fibrosus tears. The arrival of these microorganisms in the intervertebral disc would trigger a series of local immune and inflammatory responses, promoting the degeneration of the intervertebral disc tissue. In the future, precision medical strategies targeting the gut and intervertebral disc microbiome may become promising in the prevention and treatment of intervertebral disc degeneration. With further research in this field, the treatment of intervertebral disc degeneration by targeting the gut and intervertebral disc microbiota showed great clinical value. This article reviewed and discussed the effect of intestinal flora imbalance on intervertebral disc degeneration and the potential therapeutic effect of adjusting intestinal flora on intervertebral disc degeneration. The theory of gut-intervertebral disc axis, which provided a new perspective to understand the pathogenesis of intervertebral disc degeneration, supported innovative treatment methods in the future.

Objective    To assess the feasibility and safety of ultra-micro 5 mm single-port endoscopic thoracic sympathicotomy in selected patients with primary palmar hyperhidrosis. Methods    From March 1, 2018 to February 1, 2021, 90 patients with primary palmar hyperhidrosis who underwent ultra-micro 5 mm single-port endoscopic thoracic sympathicotomy at the Thoracic Surgery Department of the University of Hong Kong-Shenzhen Hospital. There were 47 males and 43 females, with a median age of 26.0 (22.0, 31.0) years. During the operation, T3 and/or T4 thoracic sympathetic nerve chain was transected using an ultra-micro 5 mm single-port incision near the areola or under the axilla. The surgical data of the patients were retrospectively reviewed and analyzed. Results     All patients successfully completed the operation without major bleeding during the operation and no conversion to thoracotomy. There was no death or serious complication during the perioperative period. The operation time was 43.0 (23.0, 60.0) min, and the intraoperative blood loss was 2.0 (1.0, 2.0) mL. In the perioperative period, only one patient needed a tiny chest tube indwelling. The symptoms of hyperhidrosis on the hands all disappeared after the operation. The pain score on the postoperative day was 2.0 (2.0, 2.0) points. The hospital stay after surgery was 1.0 (1.0, 1.0) d. In the first month after the operation, the symptoms of hyperhidrosis on the hands were significantly relieved compared with those before the operation. The surgical incisions healed well, the wounds were concealed, and there was no wound infection or poor healing. The patients' satisfaction with the surgical incisions was 100.0%. After the operation, 14 (15.6%) patients had mild compensatory hyperhidrosis, 5 (5.6%) patients had moderate compensatory hyperhidrosis, and no patient had severe compensatory hyperhidrosis. Overall satisfaction rate was 94.0%. Conclusion     The clinical application of ultra-micro 5 mm single-port endoscopic thoracic sympathicotomy in selected patients with primary palmar hyperhidrosis is safe and feasible. The surgical wound is extremely small and hidden, the operation time is short, the pain is very slight, and the clinical outcome is good. It can fully meet the patients' pursuit of beauty.

Hepatocellular carcinoma （HCC）， an insidious malignant tumor with high incidence and lethality， poses a major threat to physical and mental health of human beings. The pathological mechanism needs to be further studied. Surgery， radiotherapy， chemotherapy， and targeted drugs are effective but induce many adverse reactions. Traditional Chinese medicine （TCM） has unique advantages and abundant clinical experience in the treatment of HCC. There has been an explosion of research on the pathways， targets， and mechanism of TCM against HCC from the perspective of molecular biology. According to previous research， Chinese medicinals or compound Chinese medicine prescriptions， directly or indirectly prevent the occurrence and progression of HCC through multiple pathways and targets， which is closely related to the pathophysiological processes such as cell proliferation， metastasis， apoptosis， autophagy， inflammatory response， and immune response. This paper summarizes and analyzes research on the action pathways and mechanisms of Chinese medicine against HCC. Specifically， isoliquiritigenin， dendrobium candidum and Yexiazhu compound Ⅱ regulate phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway to inhibit the growth， proliferation and metastasis of tumor cells. Toad venom and dioscorea zingiberensis induce and enhance HCC autophagy by modulating mammalian target of rapamycin （mTOR） signaling pathway. Myricetin， asparagus， and Biejiajian Wan regulate mitogen-activated protein kinase （MAPK） signaling pathway to promote HCC cell cycle arrest， inhibit angiogenesis， and induce apoptosis. Polygonum odoratum， tetragonum， and plantainoside modulate nuclear factor-kappa B （NF-κB） to inhibit inflammatory response and HCC metastasis and reduce drug resistance. Quercetin and erigeron breviscapus control the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway to suppress epithelial-mesenchymal transition （EMT） and remodel cytoskeleton. This paper is expected to lay a theoretical basis for the in-depth research on and clinical application of Chinese medicine in the treatment of HCC.

Objective:To study the diagnostic efficacy and prognostic evaluation value of QT interval dispersion (QTd) in children and adolescents with cardioinhibitory vasovagal syncope (VVS-CI).Methods:From July 2010 to January 2020, 80 children and adolescents who received their first visit or admission to the Pediatric Syncope Clinic of The Second Xiangya Hospital of Central South University and definite diagnosed of VVS-CI due to syncope or presyncope were selected as the VVS-CI group, meanwhile, 80 children and adolescents who had physical examination in the hospital were selected as the control group.QT interval were measured by 12-lead electrocardiogram at the baseline.Results:(1) Comparison between the two groups: Compared with the control group, the VVS-CI group had a significantly lower heart rate ( P<0.05) and significantly longer QT interval, such as the maximum QT interval (QTmax), minimum QT interval (QTmin), QTd, corrected maximum QT interval (QTcmax) and corrected QT interval dispersion (QTcd) ( P<0.05). After follow-up 84 (45, 127) days, compared with the responsive group, the non-responsive group had a significantly longer QT interval, such as QTmax, QTd, QTcmax, corrected minimum QT interval (QTcmin)and QTcd ( P<0.05). (2) Diagnostic efficiency: QTmax, QTmin, QTd, QTcmax and QTcd had a certain diagnostic value in children and adolescents with VVS-CI ( P<0.001). QTd had the largest area under the curve (AUC) (0.914), and had a sensitivity of 86.30% and a specificity of 84.95% at the optimal cut-off value of 28.50 ms for VVS-CI diagnosis.(3) Prognostic evaluation value: QTmax, QTd, QTcmax, QTcmin, QTcd had an estimated value for the prognosis of VVS-CI in children and adolescents ( P<0.05 or 0.01). QTd had the largest AUC (0.906) and the best cut-off value was 34.50 ms, the sensitivity to predict response to VVS-CI intervention was 90.00%, and the specificity was 82.35%. Conclusion:QTd of electrocardiogram has a good estimation value in the diagnosis and prognosis of VVS-CI in children and adolescents.

Objective: To screen the risk factors of patients with frequent acute exacerbation of chronic obstructive pulmonary disease (COPD) by detecting the clinical indicators of periodontitis and the level of bacterial and inflammatory markers in saliva. Methods: Thirty-eight COPD patients in their stable period were recruited and detected from Beijing Chao-Yang Hospital,Capital Medical University during December 2016 to May 2017. The periodontal index were recorded. The levels of inflammatory factors in saliva samples were examined by using enzyme linked immunosorbent assay (ELISA). The bacteria composition in the saliva samples were identified by using 16SrRNA gene pyrosequencing. All patients were followed up and monitored for acute exacerbation of COPD for 12 months. The patients were divided into frequent acute exacerbation group (≥2 times/year, n=10) and non frequent acute exacerbation group (<2 times/year, n=28). Results: In univariate analysis, the patients′ average age of frequent acute exacerbation group (69.0±7.3) was significantly older than that of non-frequent acute exacerbation group (61.8±8.3) (P=0.02). The numbers of remaining teeth ≤26 [100% (10/10)] was significantly higher and plaque index ≤2.5 (2/10) in frequent acute exacerbation group was significantly lower compared with the remaining teeth ≤26 [43% (12/28)] and the plaque index ≤2.5 [71% (21/28)] in non-frequent acute exacerbation group (P=0.02, P=0.01). The proportions of salivary inflammatory factors interleukin-6 (IL-6) level ≤60 ng/L (10%),C-reactive protein (CRP) level ≤1 550 μg/L (30%), matrix metalloproteinase-8 (MMP-8) level ≤140 μg/L (30%) and fibrinogen level ≤90 mg/L (30%) in frequent acute exacerbation group were significantly lower compared with salivary inflammatory factors IL-6 level ≤60 ng/L (71%),CRP level ≤1 550 μg/L (71%), MMP-8 level ≤140 μg/L (86%) and fibrinogen level ≤90 mg/L (71%) in non-frequent acute exacerbation group (P<0.05). The differences of relative abundances of salivary bacteria,such as species of Chloroflexi, Anaerolineae, Anaeroales, Corynebacteriales, Anaerolineaceae, Tissierellaceae, Leptotrichiaceae, Corynebacteriaceae, Leptotrichia, Moryella, Lachnoanaerobaculum and Corynebacterium between frequent acute exacerbation group and non-frequent acute exacerbation group were significantly different (P<0.05). In multivariate logistics regression analysis,the level of IL-6 >60 ng/L and the relative abundance of Corynebacteriales >0.2 had significant difference (P<0.05). Conclusions The level of IL-6 and the relative abundance of Corynebacteriales might be the markers of frequent acute exacerbation in COPD patients.

Objective To evaluate the role of C-X-C chemokine receptor type 4 ( CXCR4) in the dorsal root ganglia ( DRG) in incisional pain in rats. Methods Thirty-two male Sprague-Dawley rats, aged 7-10 weeks, weighing 250-300 g, in which intrathecal catheters were successfully implanted, were divided into 4 groups (n＝8 each) using a random number table method: sham operation group (group S), CXCR4 antagonist AMD3100 plus sham operation group (group A+S), incisional pain group (group I) and CXCR4 antagonist AMD3100 plus incisional pain group (group A+I). Rats were anesthetized with sevoflu-rane. AMD3100 20 μg (in 10 μl of normal saline) was intrathecally injected, and no incision was made 30 min later in group A+S. A 1-cm longitudinal incision was made through skin, fascia and muscle of the plantar aspect of the left hindpaw in group I. AMD3100 20 μg (in 10 μl of normal saline) was intrathecally injected, and 30 min later the model of incisional pain was established in group A+I. The mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency ( TWL) were measured at 24 h before surgery and 2, 4, 8, 16 and 24 h after surgery. The rats were sacrificed after the last measurement of pain threshold and the DRGs of the lumbar segment (L4-6) were removed for detecting the expression of CXCR4, phosphorylated extracellular regulated protein kinase ( p-ERK) and total ERK ( t-ERK) by Western blot. Results Compared with group S, MWT was significantly decreased and TWL was shortened at T1-5in group I and group A+I, and the expression of CXCR4 and p-ERK in DRGs was significantly up-regulated (P＜0. 05), and no significant change was found in the expression of t-ERK in group I, no significant change was found in the expression of CXCR4, p-ERK and t-ERK in group A+I, and no significant change was found in the parameters mentioned above in group A+S (P＞0. 05). Compared with group I, MWT was significantly increased and TWL was prolonged at T1-5, the expression of CXCR4 and p-ERK in DRGs was down-regulated (P＜0. 05), and no significant change was found in the expression of t-ERK in group A+I (P＞0. 05). Conclusion CXCR4 in DRGs is involved in incisional pain, and the mechanism may be re-lated to activating ERK1∕2 signaling pathway in rats.