Neurological impairment in the form of stroke, cognitive dysfunction and delirium is a common complication after cardiac surgery and a major cause of postoperative death and long-term disability in patients undergoing cardiac surgery. There have been many studies attempting to identify intervention and treatment strategies, but no standardized protocols for neurological protection have been developed. The purpose of this article is to discuss the risk factors, mechanisms and neuroprotective measures to improve patient prognosis of neurological injury after cardiac surgery, and to review the recent research progress from three aspects: preoperative assessment and intervention, intraoperative management and monitoring, and postoperative diagnosis and treatment, emphasizing that the focus of perioperative prevention and treatment should be on the prevention of ischemic-hypoxic injury. Future research directions should focus on translational research of preclinical experiments and the development of novel imaging techniques to reduce the incidence of neurological complications and improve clinical outcome.

Chronic obstructive pulmonary disease (COPD) is a frequent and common disease of the respiratory system. The problem of low early diagnosis rate, low treatment compliance, and low treatment standardization has persisted in the diagnosis and treatment of COPD. Heterogeneity found in clinical practice is one of the reasons why COPD is difficult to treat. In recent years, it has been gradually recognized that the occurrence and development of COPD are closely related to the immune state of the body. At present, it become one of the hot spots in clinical and basic research that searching for specific and sensitive cell and molecular biomarkers to early diagnose acute exacerbation and subtype differentiation of COPD, which ultimately provide individual diagnosis and treatment strategies for COPD patients. This review focuses on the research progress of immunocytes and immunologic factors as biomarkers to different phenotypes and progression of COPD in recent years, providing a reference for the research on diagnosis and treatment of COPD.

Dexmedetomidine is a highly selective α₂ adrenergic receptor agonist, exerting anti-sympathetic, sedative, analgesic and anti-anxiety effects, with minimal impact on respiration. In recent years, dexmedetomidine has been widely used in clinical anesthesia, perioperative treatment, and intensive care. Organ-protection is an important focus of anesthesia and perioperative medicine, with clinical significance in reducing complications and improving short- and long-term outcomes. Increasing clinical evidence and basic research have shown that the application of dexmedetomidine could protect the heart, brain, lung, kidney, liver, gastrointestinal tract and other important organs. The mechanism may be related to dexmedetomidine's effects of anti-inflammation, anti-oxidation, anti-apoptosis, and autophagy regulation. From our perspectives, clinical use should follow the principle of individualization, and the dose should be adjusted in time according to patients' responses, so as to avoid adverse reactions such as hypotension and bradycardia while protecting the organs. Moreover, more strictly designed clinical studies and in-depth mechanistic investigations are needed for the optimal dexmedetomidine therapy and better organ protection during the perioperative course. In order to facilitate better understanding of clinicians, this paper reviews the organ-protective effects and underlying mechanisms of dexmedetomidine.

Objective To investigate the effects and mechnism of abnormal stress promoting macrophage mobility inhibitory factor (MIF), cyclooxygenase 2 (COX2) and prostaglandin E2 (PGE2) in the progression of temporomandibular joint osteoarthritis (TMJOA). Methods From January 2020 to December 2021, TMJOA and temporomandibular joint internal derangement (TMJID) patients (30 cases in each group, we divided the TMJOA into group TMJ Ⅰ, Ⅱ, Ⅲ according to the stage) who were admitted to TMJOA special clinic of the First Affiliated Hospital of Xinjiang Medical University and accompanied by abnormal occlusion were collected. The pain score of the occlusal state of the patients was evaluated by visual analogue scale. The expression levels of MIF, COX2 and PGE2 in synovial fluid were detected by ELISA. We used the unilateral anterior crossbite for TMJOA (UAC) rats model (the grouped into: UAC-4 weeks, UAC-8 weeks and UAC-12 weeks group), and control group at the same time (grouped into: Ctrl-4 weeks, Ctrl-8 weeks and Ctrl-12 weeks group), each group had 6 rats. The expression levels of MIF, COX2 and PGE2 in serum and synovial fluid of rats were detected by ELISA. The expression levels of IL-1β, IL-18, MIF, COX2 and PTGER2 in temporomandibular joint of rats were detected by Western blotting. The fluid flow shear stress (FFSS) model of fibroblast-like synovial cells (FLSs) was established, and the mRNA and protein expression levels of above indexes were detected by RT-PCR and Western blotting. Results Visual analogue scale evaluation showed that the pain score of TMJOA Ⅰ and Ⅱ group was significantly higher than that of TMJID (P<0.001). ELISA results showed that the expression levels of MIF, COX2 and PGE2 in synovial fluid in TMJOA group were higher than those in TMJID group (P<0.05), and the expression levels were the highest in TMJOA Ⅱ group. Compared with control group, the expressions of MIF, COX2 and PGE2 in serum and synovial fluid at UAC-4 weeks, 8 weeks and 12 weeks were slightly higher, and significantly higher at UAC-8 weeks in rat TMJOA model (P<0.05). In addition, the expression trend of protein levels in temporomandibular joint tissues was similar, which showed higher expression levels of IL-1β, IL-18, MIF, COX2 and PTGER2 (P<0.05). In the cell model where FFSS interfered with FLSs, with the increase of FFSS, cell with deformation, incomplete cell membrane and reduced number. Compared with control group, the expression levels of IL-1β, IL-18, MIF, COX2 and PGE2 (PTGER2) of FLSs were increased in 1, 3, 5 and 10 dyn/cm² intervention groups (P<0.05). Conclusion MIF, COX2 and PGE2 were highly expressed in temporomandibular joint synovial fluid of TMJOA patients with malocclusion. And these three factors were also highly expressed in serum and synovial fluid of UAC rats. The abnormal fluid shear stress promotes the secretion of MIF, COX2 and PGE2 by FLSs to participate in joint microenvironment inflammation and accelerate disease progression.

With the continuous development and progress of medicine, the total number of general anesthetic surgery is increasing, and postoperative complications are also on the rise, especially postoperative pulmonary complications (PPCs) caused by perioperative lung injury. PPCs are the main cause of prolonged hospitalization, increased morbidity and mortality, poor prognosis, and increased medical burden in patients undergoing general anesthesia. With the enhancement of awareness of mechanical ventilation and the implementation of the enhanced recovery after surgery (ERAS) concept, lung-protective ventilation strategies (LPVS) are receiving more and more attention. However, the debate continues on how to apply the LPVS effectively. The recent introduction of diaphragm-protective ventilation as a novel concept has led to the realization that the application of protective ventilation strategies should limit the adverse effects of mechanical ventilation on diaphragm function within the context of lung protective ventilation. How to apply protective ventilation strategies effectively to prevent the development of ventilator-induced lung injury (VILI) and ventilator-induced diaphragm dysfunction (VIDD), reduce the incidence of PPCs, improve patient prognosis, and reduce the medical burden is an important challenge in the management of mechanically ventilated patients. In this paper, we will focus on ventilation strategies of lung and diaphragm combined with the latest progress of LPVS, to elaborate the research on the application of individualized ventilation strategies and the mechanisms of VILI and VIDD occurrence. Finally, prospecting the future research direction of protective ventilation strategies.

Objective To evaluate the clinical value to characterize abdominal lymphadenopathy in autoimmune liver diseases (AILD) patients using computed tomography (CT). Methods We recruited 136 AILD patients (set as AILD group) from January 2015 to December 2019 and 65 patients with other liver diseases (set as control group). We assessed the volume and number of the enlarged lymph nodes in different lymph centers using CT. To evaluate the diagnosis value of abdominal lymphadenopathy for AILD, we calculated the area under the receiver operating characteristic curve (AUROC) of abdominal lymphadenopathy. We further employed logistic regression to analyze the risk factors associated with perihepatic lymph node enlargement. Results The abdominal lymph nodes in AILD group had significantly increased average volume and number than those in control group [(0.47±0.61) cm³ vs. (0.25±0.20) cm³;8.10±4.97 vs. 4.26±3.25, P<0.001]. The combination of the number of hepatic lymph nodes and the volume of mesenteric lymph nodes showed well diagnostic value for AILD (AUROC=0.816, P<0.001). Within 77 AILD patients, who underwent liver biopsy, patients with positive hepatic lymphadenopathy showed a significantly higher proportion of interface hepatitis in liver tissues than patients with negative hepatic lymphadenopathy (52.31% vs. 16.67%, χ²=5.169, P<0.05). Multivariate analysis showed that the serum IgG level is a risk factor for perihepatic lymph node enlargement (OR=1.012, 95%CI 1.000-1.024, P<0.05). Conclusions The enlargement of hepatic and mesenteric lymph nodes is of value in the differential diagnosis of AILD. Enlargement of hepatic lymph nodes is correlated with the disease activity in AILD.

Objective To explore the effect and mechanism of acid-sensitive ion channel 3 (ASIC3) expression on visceral sensitivity in irritable bowel syndrome (IBS) rats and the possible regulatory mechanisms of signalling pathways. Methods From the 2nd day postpartum, 6 neonatal rats and their mother were kept in their original cages as control group; the rest of the neonatal rats were separated from their mother to make IBS models. After the neonatal rats grow into rats, use abdominal withdrawal reflex (AWR) score to screen 16 rats that were successful in IBS modeling, and they were randomly divided into neonatal maternal separation (NMS) group and NMS+APETx2 group, with 8 rats in each group. NMS+APETx2 group was given the ASIC3-specific blocker APETx2 100 μg/kg intraperitoneally for 1 week while NMS group and control group were intraperitoneally injected with same amount of normal saline. Visceral pain response was measured by abdominal withdraw reflex (AWR) score, the intestinal transmission rate was measured by ink staining, the 5-hydroxytrgptamine (5-HT) level in colonic tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the expression levels of 5-HT4 receptor and ASIC3 in colonic tissue were measured by immunohistochemistry. Results Compared with control group, rats in NMS group showed significantly increased AWR scores at colorectal pressures of 40, 60, 80 mmHg, decreased intestinal transmission rate, intestinal 5-HT, ASIC3 and 5-HT4 receptor expression increased, all with statistically significant differences (P<0.01). There was no significant difference in AWR score and intestinal propulsion rate in NMS+APETx2 group compared with control group (P>0.05), but the expression levels of 5-HT, ASIC3 and 5-HT4 receptors increased compared with control group with significant difference (P<0.01). Compared with NMS group, the application of ASIC3-specific blocker APETx2 in NMS+APETx2 group resulted in lower AWR scores, enhanced intestinal transmission rate, and the expression levels of 5-HT, ASIC3 and 5-HT4 receptor decreased, and the differences were statistically significant (P<0.05 or P<0.01). Conclusion ASIC3 expression takes part in the generation of high sensitivity in viscera of IBS rat, which may be related to the enhance of 5-HT pathway activation.

Objective To investigate the clinical diagnostic value of peripheral white blood cell count (WBC) and neutrophil-to-lymphocyte ratio (NLR) in obesity with gastroesophageal reflux disease (GERD). Methods The clinical data of 118 patients of obesity admitted to People's Hospital of Xinjiang Uygur Autonomous Region from January 2020 to January 2022 were retrospectively analyzed. Based on the medical history and examination results, the patients were divided into obesity with GERD group (n=57) and obesity without GERD group (n=61). Univariate and multivariate logistic regression were used to analyze the risk factors of obesity combined with GERD. Receiver operating characteristic (ROC) curve was used to evaluate the clinical diagnostic value of peripheral WBC and NLR testing alone vs. combined testing for obesity combined with GERD. Results The obesity with GERD group had a higher proportion of smoking history (31.6% vs. 14.8%, P=0.030), family history of GERD (43.9% vs. 24.6%, P=0.027), and WBC of peripheral blood [(10.25±1.81)×10⁹/L vs. (8.72±2.11)×10⁹/L, P<0.001], NLR (3.55±0.71 vs. 3.00±0.64, P<0.001), and fasting plasma glucose [(6.39±2.21) mmol/L vs. (5.76±0.85) mmol/L, P=0.041] were higher in obesity without GERD group. The results of multivariate logistic regression analysis showed that peripheral WBC and NLR were independent risk factors for the obesity combined with GERD (P<0.05). ROC curve analysis showed that peripheral WBC (AUC=0.707) and NLR (AUC=0.722) had high clinical diagnostic values for obesity combined with GERD (P<0.001), and the combination of them improved the diagnostic efficacy (AUC=0.786). Conclusion Peripheral WBC and NLR are independent risk factors for the obesity combined with GERD, and are of great diagnostic value for obesity combined with GERD, and the combination of the two can improve the diagnostic efficacy and have a certain clinical value.

Parkinson's disease (PD) is a common neurodegenerative disease, and its incidence increases with age. The incorrect folding and abnormal aggregation of α-synuclein are the key neuropathological markers of PD. Recent studies have shown that exosomes may also promote the pathological α-synuclein spreads in brain through their transport and transfer functions, further promoting the development of PD, thus participating in the pathogenesis of PD. Exosomes are nanoscale extracellular vesicles, the advantage of its smaller diameter is expected to play a significant role in treatment of PD. This article reviews the related research progress on the role of exosome and its potential clinical application in PD.

Breast reconstruction is an important cosmetic repair after total mastectomy. Nipple-areola complex-sparing mastectomy (NSM) avoids such problems as nipples loss, poor nipple reconstruction, and complicated surgical procedures during breast reconstruction after total mastectomy, resulting in higher patient satisfaction. Prosthetic breast reconstruction is the most widely used breast reconstruction method with no donor injury, little trauma, low complication rate and re-operation rate. NSM combined with prosthetic breast reconstruction is safe, aesthetically pleasing, highly satisfied after surgery, and can significantly improve the patient's social mental health and quality of life. This article reviews NSM, implant breast reconstruction and the effects of adjuvant therapy on NSM combined with prosthetic breast reconstruction.