The accumulation of fatigue during military operations may lead to decreased operational efficiency and non-combat attrition,which can impact combat effectiveness.On-site monitoring and evaluation of fatigue during military operations,as an important means to keep track of military operations and bring about quick changes in training,underlie the combat effectiveness of military personnel.Focusing on the on-site monitoring and evaluation methods of fatigue during military operations,this paper reviews the determinants of such fatigue as well as on-site monitoring and comprehensive evaluation methods so as to provide reference for accurate and efficient evaluation of fatigue during military operations and for early warning of such fatigue.

Objective:To investigate the perioperative alterations and management of coagulation function in patients of massive blood transfusion during retroperitoneal tumor (RT)resection.Methods:Fourty-seven RT patients at Peking University International Hospital from Jan 2016 to Dec 2021 undergoing resection with massive blood transfusion more than 20 U within 24 h were reviewed for coagulation function before and after surgery.Results:Intraoperative bleeding was 3 000-25 800 ml, 10 patients had blood loss ≥10 000 ml. During the operation, (25.3±9.9) U of red blood cells were transfused, (2 720±1 369) ml plasma transfused, and (2.4±3.3) U platelets were transfused in 6 patients. Fourty-five patients received intraoperative albumin of (79.5±46.5) g; All 47 patients received fibrinogen of (2.3±1.3) g; Prothrombin complex was given in 45 patients (1 205±807) U. Preoperative hemoglobin was statistically different compared to postoperatively and days 1, 3 and 5 ( W=1 790, P<0.001; W=1 672, P<0.001; W=1 704, P<0.001; W=1 486, P=0.004);As with platelets, the difference was also statistically significant compared to postoperative days 1, 3, and 5 ( W=2 153, P<0.001; W=2 092, P<0.001; W=1 732, P<0.001); Preoperative albumin was different compared to postoperative days 1 and 3 ( W=1 568, P<0.001; W=1 578, P<0.001,); Preoperative fibrinogen was different compared to postoperative day 1 ( W=1 964, P<0.001). PT and APTT were prolonged on postoperative days 1 and 3 ( W=628, P<0.001, W=804, P=0.023) ( W=661, P<0.001, W=796, P=0.02). Patient's preoperative fibrin degradation products and D-dimer were above the normal value and were higher on postoperative days 3 and 5 ( W=498, P<0.001, W=345, P<0.001). Conclusions:Coagulation disorders occur perioperatively in patients with massive transfusion while undergoing surgery for RT.The implementation of ratiional transfusion strategy and close postoperative survey and management of coagulation dysfunction help avoid the coagulation related morbidities.

Objective To investigate the expression of hsa_circ_0018574 in colorectal cancer tissues and human colon cancer HT29 cell line, as well as its effect on the proliferation and apoptosis of colorectal cancer cells. Methods The circPrimer 1.2 software was used to draw the circRNA sequence structure. Meanwhile, the circRNA microarray was used to screen differentially-expressed circRNA in colorectal cancer tissues and adjacent tissues, and RNA was extracted from tissue samples. The expression of hsa_circ_0018574 in human colorectal tumors was detected by RT-qPCR. The si-circ_0018574 was transfected into HT29 cells, and the expression of CDK2, CDK4, CDK6, cyclinD1, and cyclinE cyclins were detected by colony formation assay, flow cytometry, and Western blot, respectively. Results The expression of hsa_circ_0018574 in human colorectal tumor tissues was significantly higher than that in adjacent tissues (P < 0.01). Meanwhile, the si-circ_0018574 in HT29 cells could significantly inhibit the proliferation of cancer cells, reduce clone formation and colony formation ability (P < 0.01), and induce tumor cell apoptosis (P < 0.01). The expressions of CDK2, CDK4, CDK6, cyclinD1 and cyclinE cyclins were decreased. Conclusion The hsa_circ_0018574 is highly expressed in colorectal tumors, and si-circ_0018574 could significantly inhibit the proliferation of HT29 cells, reduce cell division, and induce apoptosis.

Objective To investigate the correlation between the expression of Hsa_circ_0026352 and the clinical characteristics of breast cancer(BC) patients, to evaluate the value of Hsa_circ_0026352 as a diagnostic marker of breast cancer. Methods Human circRNA microarray was used to screen the different expression of circRNAs in BC tissues. qRT-PCR was used to verify the expression of Hsa_circ_0026352 in BC tissue and peripheral blood. CircRNA structure were performed by circPrimer1.2 software. T-test, ANOVA analysis, curve regression analysis and ROC curve analysis were performed to determine the diagnostic values of Hsa_circ_0026352. Results Hsa_circ_0026352 was significantly down-regulated in both breast cancer tissues and peripheral blood (P < 0.01). The AUC of Hsa_circ_0026352 were 0.881 in tissues and 0.826 in peripheral blood (both P < 0.01). The relative expression of Hsa_circ_0026352 in peripheral blood of BC cancer patients was negatively correlated with CA153 level (P < 0.05). The AUC of Hsa_circ_0026352 in peripheral blood of patients with ER positive, early stage breast cancer and breast neoplasm metastasis were 0.710, 0.771 and 0.722 (all P < 0.01), respectively. Conclusion Hsa_circ_0026352 could be a novel predictive biomarker for diagnosis of BC.

Tripartite motif (TRIM) family proteins are important effectors of innate immunity against viral infections. Here we identified TRIM35 as a regulator of TRAF3 activation. Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon (IFN) in response to viral infection. Trim35-deficient mice were more susceptible to influenza A virus (IAV) infection than were wild-type mice. TRIM35 promoted the RIG-I-mediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1. IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3. TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2, thereby antagonizing its suppression of TRAF3 activation. Our in vitro and in vivo findings thus reveal novel roles of TRIM35, through catalyzing Lys63- or Lys48-linked polyubiquitination, in RIG-I antiviral immunity and mechanism of defense against IAV infection.
A549 Cells ; Animals ; Apoptosis Regulatory Proteins/immunology* ; DEAD Box Protein 58/immunology* ; Dogs ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/immunology* ; Madin Darby Canine Kidney Cells ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/pathology* ; Proteolysis ; RAW 264.7 Cells ; Signal Transduction/immunology* ; THP-1 Cells ; TNF Receptor-Associated Factor 3/immunology* ; Ubiquitination/immunology* ; Viral Proteins/immunology*

The progression of hyperuricemia disease is often accompanied by damage to renal function. However, there are few studies on hyperuricemia nephropathy, especially its association with intestinal flora. This study combines metabolomics and gut microbiota diversity analysis to explore metabolic changes using a rat model as well as the changes in intestinal flora composition. The results showed that amino acid metabolism was disturbed with serine, glutamate and glutamine being downregulated whilst glycine, hydroxyproline and alanine being upregulated. The combined glycine, serine and glutamate could predict hyperuricemia nephropathy with an area under the curve of 1.00. Imbalanced intestinal flora was also observed. , , , , and other conditional pathogens increased significantly in the model group, while and , the short-chain fatty acid producing bacteria, declined greatly. At phylum, family and genus levels, disordered nitrogen circulation in gut microbiota was detected. In the model group, the uric acid decomposition pathway was enhanced with reinforced urea liver-intestine circulation. The results implied that the intestinal flora play a vital role in the pathogenesis of hyperuricemia nephropathy. Hence, modulation of gut microbiota or targeting at metabolic enzymes, , urease, could assist the treatment and prevention of this disease.

Objective:To explore the clinical effect of bi-layered artificial dermis combined with autologous skin graft in the repair of wounds with exposed bone and/or tendon.Methods:The medical records of 25 patients (aged 3 to 79 years, including 21 males and 4 females) with bone and/or tendon exposed wounds caused by various reasons, admitted to Nanfang Hospital of Southern Medical University from May 2014 to December 2018 were analyzed retrospectively. Of the 25 patients, 7 patients had exposed bone only, 13 patients had exposed tendon only, and 5 patients had exposure of both bone and tendon. The total wound area was 78.0 (53.4, 103.2) cm 2. The widths of bone exposure and tendon exposure were 3.2 (3.0, 3.6) cm and 2.0 (1.7, 2.4) cm, respectively. All wounds were implanted with bi-layered artificial dermis in the first stage after thorough wound debridement. After 2 to 3 weeks of vascularization of artificial dermis, autologous thin-to-medium-thickness skins or split-thickness skins were grafted to repair the wounds in the second stage. The vascularization of artificial dermis and its time, whether or not producing hematoma, the skin graft survival rate on day 7 post autologous skin grafting, whether or not repeating skin grafting, and the time of complete wound healing were observed and recorded. The patients were further followed up and observed for 3 or more months after discharge. Results:The vascularization of artificial dermis was achieved in 24 patients after the first transplantation with vascularization time being 11-21 (16±4) days. No hematoma was observed in the transplanted artificial dermis. Failed vascularization of grafted artificial dermis was observed in one patient who was later treated with negative pressure drainage and skin grafting alone, and was discharged with wound healing. The skin graft survival rate on day 7 post autologous skin grafting was 92.2%-100.0% ( (99.3±1.3)%), with the remaining wound areas recovered later by themselves or healed by dressing changes without repeated skin grafting. The complete wound healing time was 7-19 (11.9±2.8) days after autologous skin grafting. The patients were followed up for 3 to 60 months after discharge. Except for the pigmentation in skin graft area, the skin grafts survived well, being soft in texture and with no repeated ulceration, obvious hypertrophic scar, or contracture deformity.Conclusions:Artificial dermis combined with autologous skin grafting can effectively repair wounds with bone and/or tendon exposure, providing a repair strategy for this type of wounds.

Gastric cancer highly expressed transcript 1 (GHET1) is first found in gastric cancer and is a long non-coding RNA (lncRNA). GHET1 is located on chromosome 7q36.1, and is highly expressed in many tumors. High expression of GHET1 is closely related to poor prognosis. Studies have found that GHET1 is involved in regulating many physiological and pathological processes of the body through interaction with microRNAs (miRNAs) or proteins, especially in digestive system tumors, and is expected to become a valuable tumor marker and therapeutic target in the future.

Objective To evaluate the effect of dexmedetomidine combined with erector spinae plane block on inflammatory responses and cellular immune function after thoracic interbody fusion in patients.Methods Ninety American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes,aged 18-60 yr,with body mass index of 19-25 kg/m2,scheduled for elective thoracic interbody fusion with the vertebral segments involved in the operation ＜6,were divided into 3 groups (n =30 each) using a random number table method:general anesthesia group (group G),dexmedetomidine group (group D) and dexmedetomidine plus erector spinae plane block group (group DE).In group D and group DE,dexmedetomidine was intravenously infused over 10 min at a loading dose of 0.5 μg/kg starting from 30 min before anesthesia induction,followed by continuous infusion of 0.5 μg · kg-1 · h-1 until 15 min before the end of operation.In group DE,bilateral erector spinae blocks were performed under ultrasound guidance at 20 min before anesthesia induction,and 0.25％ ropivacaine 30 ml was injected into each side.Patients received patient-controlled analgesia (PCA) after operation.The consumption of propofol was recorded.The patients were followed up for 48 h after operation,and the pressing times of PCA and consumption of sufentanil were recorded.The emergence time,extubation time and volume of blood loss were also recorded.Blood samples were collected from the radial artery immediately before induction (T1),at 30 min of operation (T2),and at 1 h and 1,3 and 5 days after operation (T3-6) for determination of plasma CD42+,HLA-DR+ and CD14+ concentrations,white blood cell (WBC) count (by electrical impedance method) and plasma C-reactive protein (CRP) concentrations (by latex-enhanced scattering turbidimetry assay).CD42+/CD14+ and HLA-DR+/CD14+ ratios were calculated.Results Compared with group G,the pressing times of PCA and consumption of sufentanil were significantly decreased,CD42+/CD14+ ratio was decreased,and HLA-DR+/CD14+ ratio was increased at T3-6 in group D,and the emergence time,extubation time,pressing times of PCA and consumption of sufentanil and propofol were significantly decreased,CD42+/CD14+ ratio was decreased,HLA-DR+/CD14+ratio was increased at T3-6,and the plasma CRP concentrations and WBC count were decreased at T2-6 in group DE (P ＜0.05).Compared with group D,the emergence time,extubation time,pressing times of PCA and consumption of sufentanil and propofol were significantly decreased,CD42+/CD14+ ratio was decreased at T5,HLA-DR+/CD14+ratio was increased at T3.4,and the plasma CRP concentrations and WBC count were decreased at T3-6 in group DE (P ＜0.05).Conclusion Dexmedetomidine combined with erector spinae plane block can reduce inflammatory responses and improve cellular immune function after thoracic interbody fusion in patients.

Objective To evaluate the effect of sevoflurane on unfolded protein response-related cell apoptosis during acute lung injury in rats undergoing cardiopulmonary bypass ( CPB) . Methods For-ty-eight clean-grade healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 250-300 g, were allocated into 3 groups ( n=16 each) using a random number table method: sham operation group ( Sham group) , CPB group and sevoflurane group ( Sev group) . Left common carotid artery and right internal jugu-lar vein were only cannulated in group Sham. After establishing CPB, the flow rate was gradually adjusted to the maximum (100 ml·kg-1·min-1) and maintained for 60 min in group CPB. Two percent sevoflurane was inhaled for 30 min, and 15 min later the model of CPB was established in Sev group. Rats were sacri-ficed at 1 h after the end of CPB, lungs were removed and lung tissues were obtained. The pathological changes and ultrastructure of lung tissues were examined with a light microscope and with an electron micro-scope, respectively. The wet to dry weight ratio ( W∕D ratio) , apoptosis in lung cells ( by TUNEL assay) , expression of glucose-regulated protein 78 ( GRP78) , CCAAT∕enhancer-binding protein homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and caspase-12 mRNA was determined by real-time polymerase chain reaction. The expression of GRP78, CHOP, phosphorylated JNK (p-JNK) and caspase-12 was de-tected by Western blot. The index of quantitative assessment of histologic lung injury ( IQA) was measured, and apoptotic index ( AI) was calculated. Results Compared with Sham group, the W∕D ratio, IQA and AI were significantly increased, the expression of GRP78, CHOP, JNK and caspase-12 was up-regulated ( P<0. 05) , and the pathological changes of lung tissues were accentuated in CPB group. Compared with CPB group, the W∕D ratio, IQA and AI were significantly decreased, the expression of GRP78, CHOP, JNK and caspase-12 was down-regulated ( P<0. 05) , and the pathological changes of lung tissues were sig-nificantly attenuated in Sev group. Conclusion The mechanism by which sevoflurane mitigates acute lung injury induced by CPB is related to inhibiting unfolded protein response related cell apoptosis in lung tissues of rats.