Pulmonary blast injury has become the main type of trauma in modern warfare, characterized by externally mild injuries but internally severe injuries, rapid disease progression, and a high rate of early death. The injury is complicated in clinical practice, often with multiple and compound injuries. Currently, there is a lack of effective protective materials, accurate injury detection instrument and portable monitoring and transportation equipment, standardized clinical treatment guidelines in various medical centers, and evidence-based guidelines at home and abroad, resulting in a high mortality in clinlcal practice. Therefore, the Trauma Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Trauma organized military and civilian experts in related fields such as thoracic surgery and traumatic surgery to jointly develop the Clinical treatment guideline for pulmonary blast injury ( version 2023) by combining evidence for effectiveness and clinical first-line treatment experience. This guideline provided 16 recommended opinions surrounding definition, characteristics, pre-hospital diagnosis and treatment, and in-hospital treatment of pulmonary blast injury, hoping to provide a basis for the clinical treatment in hospitals at different levels.

Objective To investigate the relationship between subgroups of central lymph node metastasis (sCLNM) and lateral lymph node metastasis (LNM) of unilatal papillary thyroid carcinoma (uPTC) with cervical lymph node negative(cN0).Methods The clinical and pathological data of 161 patients with cN0-uPTC who underwent total thyroidectomy+central lymph node dissection+lateral lymph node dissection from Jan.2016 to Dec.2016 were retrospectively analyzed.The relationship between the lymph node metastasis of each subarea in the central area of the affected side and the lymph node metastasis of the affected side was investigated.Results Binary logistic regression analysis of cN0-uPTC subregions in the affected central region showed:pre-laryngeal lymph node metastasis,pre-tracheal lymph node metastasis and paratracheal lymph node metastasis were independent risk factors for lymph node metastasis in the affected lateral region(P=0.008,0.016,0.035,respectively).Prelaryngeal lymph node metastasis was an independent risk factor for lymph node metastasis in the affected area Ⅱ (P=0.015).Pre-tracheal lymph node metastasis was an independent risk factor for lymph node metastasis in affected area Ⅲ (P=0.004).Pre-tracheal and para-tracheal lymph node metastasis were independent risk factors for lymph node metastasis in the affected Ⅳ area (P=0.035,0.011,respectively).Conclusions The lymph node metastasis pathway of thyroid cancer had certain regularity.The pre-laryngeal lymph node metastasis has the prediction value for the lymph node metastasis of the affected area Ⅱ.The pre-tracheal lymph node metastasis has the prediction value for the lymph node metastasis of the affected area Ⅲ.The pre-tracheal and paratracheal lymph node metastasis have the prediction value for lymph node metastasis of the affected area Ⅳ.Lymph node dissection in affected areas Ⅲ and Ⅳ needs to be considered in patients with pre-tracheal or paratracheal lymph node metastases.On this basis,lymph node dissection on the affected areas Ⅱ,Ⅲ,and Ⅳ might be considered if there is pre-laryngeal lymph node metastasis at the same time.

Objective:To analyze the factors related to metastasis of contralateral central lymph node (CLN) in cN0 papillary thyroid car-cinoma (PTC) and discuss the indications for CLN dissection. Methods:We enrolled 149 unilateral PTC patients who underwent total thyroidectomy and prophylactic bilateral (CLN) dissection. This work analyzed the relationship of gender, age, extrathyroidal extension, multifocality, thyroiditis, ipsilateral central lymph nodes, and prelaryngeal lymph node with CLNs. Results:The rates of metastasis to ip-silateral and contralateral central compartments were 73.2%and 23.5%, respectively. In univariate analysis, gender, age, tumor size, multifocality, and thyroiditis were not important in predicting contralateral central compartment lymph node metastasis (P=0.792, 0.097, 0.531, 0.269, and 1.000, respectively);by contrast, extrathyroidal extension (P=0.017), prelaryngeal lymph nodes (P=0.006), and ipsilateral CLNs (P<0.001) are related to CLN metastasis. However, multivariate analysis showed that ipsilateral central metastasis was an independent risk factor for lymph node metastasis in the contralateral central region when the number of ipsilateral central metas-tases is≥3 (P=0.010). Conclusion:Extracapsular invasion, prelaryngeal lymph nodes, and ipsilateral CLN influence the metastases of CLN. Bilateral CLN dissection should be performed when the number of ipsilateral central metastases is≥3 and there is merger of ex-tra-laryngeal lymph nodes or capsule invasion.

Objective:To retrospectively analyze the regularity and risk factors of skip metastasis (central lymph node negative and lat-eral lymph node positive) in papillary thyroid carcinoma (PTC). Methods:A total of 521 PTC patients underwent total thyroidectomy and central plus lateral lymph node dissection at The First Affiliated Hospital of Chongqing Medical University from January 2013 to De-cember 2016. Clinicopathological characteristics of the patients were collected and analyzed. Results:Skip metastasis rate of PTC was 8.3％(43/521). Tumors in the upper lobe (OR=3.401, 95％CI:1.770-6.536;P=0.001) and in the lateral part (OR=3.424, 95％CI:1.182-9.920;P=0.023) of the thyroid, as well as age above 45 (OR=2.856, 95％CI:1.488-5.482;P=0.002), were independent risk factors for skip metastases for this disease. Clinically node-negative (cN0) PTC patients with tumors in the upper lobe had higher possibility of skip metastases than those with clinically involved lateral neck nodes(cN1b) (P=0.022). Conclusion:Skip metastasis of PTC is not un-common. Thus, preoperative clinical assessment and imaging examination for lateral lymph node is necessary, especially for PTC pa-tients who are above 45 years old and with tumors in the upper lobe and/or unilateral area of thyroid. The lateral lymph node dissec-tion should be performed when necessary.

Objective: To explore influence of tanshinone on rabbit malignant arrhythmias and calmodulin signal transduction pathway after myocardial infarction. Methods: A total of 30 rabbits were randomly and equally divided into sham operation group (sham group), model group and tanshinone group. Acute myocardial infarction model was established through ligating left anterior descending branch of coronary. After modeling, the rabbits were randomly and equally divided into model group and tanshinone group. Incidence rate of malignant arrhythmias, action potential duration (APD) of three myocardial layers (namely endocardium layer, myocardium layer and epicardium layer), transmural dispersion of repolarization, Ca2+ concentration, compared among three groups. Results: Incidence rate of malignant arrhythmias in tanshinone group was significantly lower than that of model group (20.0% vs. 70.0%, P<0.01); compared with sham group, there were significant rise in transmural dispersion of repolarization, 90% APD, Ca2+ concentration, expression levels of calmodulin and calmodulin kinase Ⅱ of three layers in model group and tanshinone group (P<0.01 all) ; compared with model group, there were significant reductions in transmural dispersion of repolarization[(46.2±10.9) ms vs.(35.5±8.8) ms], 90% APD [epicardium layer, (231.5±17.4) ms vs.(211.0±16.3) ms], Ca2+ concentration [epicardium layer, (132.0±12.3) mmol/L vs.(102.3±10.3) mmol/L], expression levels of calmodulin [epicardium layer, (0.724±0.014) vs. (0.563±0.014)] and calmodulin kinase Ⅱ[epicardium layer, (0.759±0.019) vs. (0.589±0.017)] in tanshinone group, (P<0.05～0.01). Conclusion: Tanshinone possesses anti-malignant arrhythmias effect after myocardial infarction. Its mechanism may be regulating calmodulin and calmodulin kinase Ⅱ signal transduction pathway.

Objective: To explore the expression level of serum interleukin (IL)-7 in patients with acute coronary syndrome (ACS) and analyze the relationship between IL-7 level and prognosis. Methods: A total of 130 ACS patients [ACS group, including 70 cases with acute myocardial infarction (AMI) and 60 cases with unstable angina pectoris (UAP)], 33 cases with stable angina pectoris (SAP，SAP group) and 89 healthy subjects (healthy control group) were selected. IL-7 level was measured using enzyme linked immunosorbent assay (ELISA) and compared among all groups. The 130 ACS patients were followed up, and Logistic regression analysis was used to analyze the relationship between IL-7 level and prognosis. Results: Compared with healthy control group and SAP group, there was significant rise in IL-7 level in UAP group and AMI group [(1.84±0.47) pg/ml, (2.11±0.63) pg/ml vs. (4.87±0.52) pg/ml, (5.15±0.71) pg/ml, P<0.05 or P<0.01]. There were no significant difference in IL-7 level between healthy control group and SAP group, UAP group and AMI group (P>0.05 both); Logistic regression analysis indicated that expression level of serum IL-7 was an independent risk factor for adverse cardiovascular events in ACS patients (OR=1.212, 95%CI:1.061-1.418). Conclusion: Interleukin-7, as an important inflammatory cytokines, its serum level abnormally elevated in patients with acute coronary syndrome, it may have important prognostic value.

This study examined the effect of tanshinone II A (TSN II A) on the cardiac fibrosis induced by transforming growth factor β1 (TGF-β1) and the possible mechanisms. Cardiac fibroblasts were isolated from cardiac tissues of neonatal Sprague-Dawley (SD) rats by the trypsin digestion and differential adhesion method. The cells were treated with 5 ng/mL TGF-β1 alone or pretreated with TSN II A at different concentrations (10(-5) mol/L, 10(-4) mol/L). Immunocytochemistry was used for cell identification, RT-PCR for detection of the mRNA expression of connective tissue growth factor (CTGF) and collagen type I (COL I), Western blotting for detection of the protein expression of Smad7 and Smad3, and immunohistochemistry and immunofluorescence staining for detection of the protein expression of phosphorylated Smad3 (p-Smad3), CTGF and COLI. The results showed that TGF-β1 induced the expression of CTGF, COL I, p-Smad3 and Smad7 in a time-dependent manner. The mRNA expression of CTGF and COL I was significantly increased 24 h after TGF-β1 stimulation (P<0.01 for all). The protein expression of p-Smad3 and Smad7 reached a peak 1 h after TGF-β1 stimulation, much higher than the baseline level (P<0.01 for all). Pretreatment with high concentration of TSN A resulted in a decrease in the expression of p-Smad3, CTGF and COL I (P<0.01). The protein expression of Smad7 was substantially upregulated after pretreatment with two concentrations of TSN II A as compared with that at 2 h post TGF-β1 stimulation (P<0.05 for low concentration of TSN I IA; P<0.01 for high concentration of TSN II A). It was concluded that TSN II A may exert an inhibitory effect on cardiac fibrosis by upregulating the expression of Smad7, suppressing the TGF-β1-induced phosphorylation of Smad3 and partially blocking the TGF-β1-Smads signaling pathway.
Animals ; Diterpenes, Abietane ; pharmacology ; Fibrosis ; metabolism ; Heart ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; metabolism

This study examined the effect of tanshinone II A (TSN II A) on the cardiac fibrosis induced by transforming growth factor β1 (TGF-β1) and the possible mechanisms. Cardiac fibroblasts were isolated from cardiac tissues of neonatal Sprague-Dawley (SD) rats by the trypsin digestion and differential adhesion method. The cells were treated with 5 ng/mL TGF-β1 alone or pretreated with TSN II A at different concentrations (10(-5) mol/L, 10(-4) mol/L). Immunocytochemistry was used for cell identification, RT-PCR for detection of the mRNA expression of connective tissue growth factor (CTGF) and collagen type I (COL I), Western blotting for detection of the protein expression of Smad7 and Smad3, and immunohistochemistry and immunofluorescence staining for detection of the protein expression of phosphorylated Smad3 (p-Smad3), CTGF and COLI. The results showed that TGF-β1 induced the expression of CTGF, COL I, p-Smad3 and Smad7 in a time-dependent manner. The mRNA expression of CTGF and COL I was significantly increased 24 h after TGF-β1 stimulation (P<0.01 for all). The protein expression of p-Smad3 and Smad7 reached a peak 1 h after TGF-β1 stimulation, much higher than the baseline level (P<0.01 for all). Pretreatment with high concentration of TSN A resulted in a decrease in the expression of p-Smad3, CTGF and COL I (P<0.01). The protein expression of Smad7 was substantially upregulated after pretreatment with two concentrations of TSN II A as compared with that at 2 h post TGF-β1 stimulation (P<0.05 for low concentration of TSN I IA; P<0.01 for high concentration of TSN II A). It was concluded that TSN II A may exert an inhibitory effect on cardiac fibrosis by upregulating the expression of Smad7, suppressing the TGF-β1-induced phosphorylation of Smad3 and partially blocking the TGF-β1-Smads signaling pathway.

BACKGROUND: One of important mechanisms underlying myocardial fibrosis is that transforming growth factor β1(TGF-β1) stimulates the proliferation and differentiation of cardiac fibroblasts via Smads signaling pathway.Previous studies have confirmed that tanshinone ⅡA can effectively inhibit myocardial fibrosis.But whether blockage of TGF-β1/Smads signaling pathway is involved in this process remains unclear. OBJECTIVE: To investigate the effects of tanshinone ⅡA on TGF-β1 signal transduction in rat cardiac fibroblasts. METHODS: Neonatal rat cardiac fibroblasts were harvested by trypsin digestion and differential attachment and treated with 5 μg/L TGF-βI and different concentrations of tanshinone Ⅱ A(106,10-5 and 10-4 mol/L).At 6,12,and 24 hours after TGF-β1 application,fibronectin expression was detected by reverse transcription-polymerase chain reaction and Western blot analysis.At 15,30,60,and 120 minutes after TGF-β1 application,Smads protein expression was determined by Western blot analysis. RESULTS AND CONCLUSION: Fibronectin mRNA and protein expression began to increase at 6 hours after TGF-β1 application and was 1.3 and 1.8 times higher than initial level,respectively(P < 0.01),at 24 hours after TGF-β1 application.Phosphorylated Smad2/3 protein expression began to increase at 15 minutes after TGF-β1 application,peaked at 1 hour,decreased at 2 hours,but it was still 3.9 times higher than initial level(P < 0.01).Tanshinone ⅡA(10-5 and 10-4 mol/L)pretreatment downregulated fibronectin and phosphorylated Smad2/3 expression(P < 0.05 or P < 0.01)in a dose-dependent manner.These findings demonstrate that TGF-β1 induced fibronectin protein and mRNA expression and Smad2/3 protein expression in a time-dependent manner.Tanshinone ⅡA against myocardial fibrosis was likely related to its inhibition of TGF-β1-induced Smad2/3 phosphorylation and blockage of TGF-β1/Smads signaling pathways within cardiac fibroblasts.

Summary: The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ (Ang Ⅱ)-induced hypertrophy and effects of sodium tanshinone Ⅱ A sulfonate (STS) in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction (RT-PCR). It was found after cardiomyocytes were treated with Ang Ⅱ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly (P<0.01). After treatment with Ang Ⅱ for 24 h, the rate of protein synthesis in Ang Ⅱ group was significantly increased as compared with control group (P<0.01). After treatment with Ang Ⅱ for 7 days, the size of cardiomyocytes in Ang Ⅱ group was increased obviously as compared with control group (P<0.05). After pretreatment with STS or Valsartan before Ang Ⅱ treatment, both of them could inhibit the above effects of Ang Ⅱ (P<0.05 or P<0.01). It was suggested that STS could ameliorate Ang Ⅱ-induced cardiomyocyte hypertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.