ObjectiveTo evaluate the efficacy, feasibility and safety of CT guided percutaneous 125Ⅰ seeds implantation in elderly patients of stage Ⅰperipheral non-small cell lung cancer ( NSCLC ).MethodsClinical data of 16 elderly peripheral stage Ⅰ NSCLC patients ( 10 squamous carcinoma and 6adenocarcinoma;13 stage ⅠA and 3 stage ⅠB ) who received radioactive 125Ⅰ seeds implantation because of refusal or being unsuited to operation or external radiotherapy were retrospectively analyzed. Prescribed dose was 140 - 160 Gy. Under CT guidance, 125Ⅰ seeds were implanted percutaneously into tumors for interstitial radiotherapy according to treatment plan system. ResultsMean number of 125Ⅰ seeds each patient received was21.1. 12 complete response (CR) and 4 partial response (PR) were achieved. Total response rate ( CR + PR) was 100％. 100％ patients completed 10 to 56 months of follow-up, 15, 13, 8 and 6 patients completed 1-, 2-, 3-and 4-years'follow-up, respectively. The median local progression free time was 14months. The 1-,2-,3-and 4-year overall survival rate were 60％, 54％, 50％ and 33％, respectively (median:14 months). 7 cases died of non-tumor disease and 5 died of metastasis. No severe complications were observed. ConclusionsCT guided 125Ⅰ seeds implantation is a safe, reliable and effective radical treatment method for elderly stage Ⅰ peripheral NSCLC patients, who refuse to or are unsuitable to operation or external radiotherapy.

Objective　To evaluate the methods of surgical treatment for tumors of brain stem and their curative effects. Methods: 25 cases of tumors of brain stem were analysed retrospectively. Results: There were 18 cases of astrocytomas, 2 cases of cavernous angioma, 1 cases of hemangioblastoma, 1 cases of dermoid cyst, 1 cases of syringopontia, 1 cases of inflammatory granuloma accompanied with hecrosis and 1 cases of AVM of brain stem in 25 cases. Four patients died after operation. Conclusion: Extrinsic tumors of brain stem could be resected totally or subtotally, resulting in good outcome.

Objective To observe the effect of heat shock protein 70 (HSP70) expression induced by Herba Hedyotis Diffusae (HHD) on the apoptosis of H22 hepatoma cells.Methlds Mice were immunized with H22 hepatoma cells from in-vivo ascites of the mice pretreated by HHD and Radix Codonopsis (RC).Mice were divided into five groups after being blocked with HSP70 monoclonal antibody:non-HHD blocking group,HHD blocking group,non-RC blocking group,RC blocking group and the blank control group,10 mice in each groups.Then the mice were attacked with cultured H22 hepatoma cells to induce transplanted tumor.The apoptosis in the transplanted tumor was detected by a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) method.Results Large amount of brown particles can be observed in the cell nucleus of transplanted tumor mice from HHD groups.Compared with RC groups,number of apoptotic cells and the staining intensity were increased in HHD groups.The apoptosis in HHD groups and RC groups differed from that in the blank control group,and was obvious in HHD groups.The apoptosis exerted a increasing tend in non-HHD blocking group,but the difference was insignificant between non-HHD blocking group and HHD blocking group,and between non-RC blocking group and RC blocking group.Conclusion HHD can promote the apoptosis of H22 hepatoma cells in transplated tumor through inducing the expression of HSP70 to some extent,and the related mechanism of inducing apoptosis needs further research.

This study aimed to investigate the effect and underlying mechanism of Poria cocos polysaccharides(PCP) on myocardial cell apoptosis in the rat model of myocardial ischemia-reperfusion injury(MI/RI). Male SPF-grade SD rats were randomly divided into a sham group(saline), a model group(saline), low-and high-dose PCP groups(100 and 200 mg·kg~(-1)), and a fasudil group(10 mg·kg~(-1)), with 16 rats in each group. Except for the sham group, the other four groups underwent left anterior descending coronary artery ligation for 30 min followed by reperfusion for 2 h to establish the MI/RI model. The myocardial infarct area was assessed by TTC staining. Histological changes were observed through HE staining. Myocardial cell apoptosis was evaluated using TUNEL staining. Serum lactate dehydrogenase(LDH), creatine kinase MB(CK-MB), interleukin-1β(IL-1β) and IL-18 levels, myocardial superoxide dismutase(SOD) activity and malondialdehyde(MDA) levels were detected by ELISA. Protein expression of B-cell lymphoma 2(Bcl-2), Bcl-2 associated X protein(Bax), cleaved caspase-3, Ras homolog gene A(RhoA), myosin phosphatase target subunit 1(MYPT-1), phosphorylated MYPT-1(p-MYPT-1), and Rho-associated coiled-coil forming kinase 1(ROCK 1) were measured by Western blot. Pathological staining of myocardial tissue revealed that in the model group, there was focal necrosis of myocardial tissue, myocardial cell swelling, unclear boundaries, and neutrophil infiltration. These pathological changes were alleviated in the low-and high-dose PCP groups and the fasudil group. Compared with the model group, the low-and high-dose PCP groups and the fasudil group showed significantly reduced myocardial infarct area and myocardial cell apoptosis rate. Compared with the sham group, the model group exhibited elevated serum LDH, CK-MB, IL-1β and IL-18 levels, increased MDA levels, relative protein expression of Bax, cleaved caspase-3, RhoA, ROCK1 and p-MYPT-1, and decreased myocardial SOD levels and Bcl-2 protein expression. Compared with the model group, the PCP groups and the fasudil group showed lowered serum LDH, CK-MB, IL-1β and IL-18 levels, decreased MDA levels, relative protein expression of Bax, cleaved caspase-3, RhoA, ROCK1 and p-MYPT-1, and increased myocardial SOD levels and Bcl-2 protein expression. PCP exhibited a certain preventive effect on myocardial tissue pathological damage and myocardial cell apoptosis in MI/RI rats, possibly related to the inhibition of the Rho-ROCK signaling pathway activation, thereby reducing oxidative stress and inflammatory responses.
Rats ; Male ; Animals ; Myocardial Reperfusion Injury/drug therapy* ; bcl-2-Associated X Protein/metabolism* ; Rats, Sprague-Dawley ; Caspase 3/metabolism* ; Interleukin-18 ; Wolfiporia ; Signal Transduction ; Myocardial Infarction/drug therapy* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Creatine Kinase, MB Form ; Apoptosis ; Polysaccharides/pharmacology* ; Superoxide Dismutase/metabolism* ; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives*

OBJECTIVETo study the state of oxidative stress in patients with acute coxsackie virus myocarditis (ACM), and to investigate the pathological chain reactions of a series of free radicals and oxidative and lipoperoxidative damages in their bodies.

METHODSEighty ACM patients and 80 healthy adult volunteers (HAV) were enrolled in a case-control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and LPO in erythrocytes (RBC), vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in RBC were determined by using spectrophotometric assays.

RESULTSCompared with the average values (AV) of the above biochemical parameters (BP) in the HAV group, the AV of NO in plasma, and LPO in plasma and RBC in the ACM group were significantly increased (P = 0.0001), while the AV of VC, VE, beta-CAR, SOD, CAT and GSH-Px in the ACM group were significantly decreased (P = 0.0001). The values of the above BP were used to estimate the relative risk ratio (RR) between the ACM group and the HAV group; the RR and its 95% confidence interval were 12.467 (5.745-27.051), 4.333 (2.126-8.834), 6.517 (3.225-13.618), 3.310 (1.598-6.858), 31.000 (12.611-76.201), 4.663 (2.228-9.759), 11.769 (5.440-25.462), 3.043 (1.486-6.229) and 6.594 (3.045-14.281) respectively, and their P levels ranged from 0.002 to 0.0001. The results were as follows: D = 22.143 - 0.017SOD + 0.008NO + 0.244LPO in RBC, Eigenvalue = 13.659, Canonical correlation = 0.965, Wilks' lambda = 0.068, chi 2 = 420.212, P = 0.0001. The correct rate of discrimination to the ACM group and to the HAV group was 87.5% and 95.0%, respectively, and 91.3% of originally grouped cases was correctly classified.

CONCLUSIONThe findings in this study suggested that the oxidative stress in bodies of ACM patients was severely aggravated, and marked high oxidative constituents and low antioxidants and antioxidases in the human body might increase the relative risk of inducing acute coxsackie virus myocarditis, and measuring the values of NO in plasma, SOD and LPO in RBC might increase the correct rates of discriminatory analysis of the ACM.

Adolescent ; Adult ; Antioxidants ; analysis ; pharmacology ; Case-Control Studies ; Coxsackievirus Infections ; physiopathology ; Female ; Free Radicals ; Humans ; Lipid Peroxidation ; Male ; Middle Aged ; Myocarditis ; pathology ; virology ; Oxidative Stress

Objective To investigate the reliability and feasibility of spectral entropy in evaluate the effectiveness of analgesic sedation in patients with ischemic stroke.Methods A total of 64 patients with acute ischemic stroke admitted to Hongqi Hospital Affiliated to Mudanjiang Medical University from July 2021 to November 2022 were selected as study objects,and the included patients were divided into control group and experimental group according to random number table method,with 32 cases in each group.Patients in control group adjusted analgesia and sedation regimen according to Richmond agitation-sedation scale(RASS)score and critical-care pain observation tool(CPOT)score.Patients in experimental group adjusted the analgesic and sedation regimen according to the results of spectral entropy.The vital signs,C-reactive protein(CRP),dose of sedative and analgesic drugs and incidence of adverse reactions were compared between two groups.The correlation between spectral entropy and RASS score and CPOT score was used Spearman correlation analysis.Results The spectral entropy values were positively correlated with the RASS score and CPOT score,respectively(r=0.719,0.556,P<0.001).There were no significant differences in mean arterial pressure and percutaneous arterial oxygen saturation between two groups at different time points(P>0.05).The heart rate at T3 in experimental group was significantly lower than that in control group(P<0.05).At T1,T2 and T3,CRP levels in experimental group were significantly lower than those in control group(P<0.05).The dosage of sufentanil and midazolam in experimental group were significantly lower than those in control group(P<0.05).The incidence of adverse reactions in experimental group was significantly lower than that in control group(12.50%vs.34.38%,χ2=4.267,P=0.039).Conclusion Spectral entropy can be used as an objective method to monitor the depth of analgesia and sedation in patients with ischemic stroke,and has a good correlation with RASS score and CPOT score,which can reduce the incidence of adverse reactions,effectively avoid stress reactions,and reduce the application of analgesia and sedation drugs.

Objective To investigate the expression change and their clinical role of triggering receptor expressed on myeloid cells-1 (TREM-1) in patients with severe thoracic trauma.Methods A prospective cohort study was conducted to analyze the clinical data of 52 patients with severe thoracic trauma (trauma group) hospitalized from October 2016 to May 2017.The peripheral anticoagulant blood samples were collected at days 1,3,5,7 and 14 after trauma.Meanwhile,10 healthy volunteers were enrolled in control group and their blood samples were collected once.According to injury severity score (ISS),the patients were divided into ISS low-score group (＜ 20 points,n =15) and high-score group (≥20 points,n =37).The patients were assigned to traumatic non-sepsis group (n =34) and traumatic sepsis group (n =18) by the latest definition and standard of sepsis 3.0 issued by the Society of Critical Care Medicine (SCCM)/European Society of Intensive Care Medicine (ESICM).The expressions of TREM-1 on neutrophils and monocytes were measured by flow cytometry.Pairwise comparisons were done between trauma group and healthy volunteers,ISS low-score group and ISS high-score group,and traumatic sepsis group and non-sepsis group,respectively.The accuracy of traumatic sepsis prediagnosis by TREM-1 was evaluated by the area under receiver operating characteristic curve (AUC).Results Trauma group had 41 males and 11 females,with age of (45.9 ± 12.4) years,Abbreviated Injury Scale (AIS) of (3.5 ± 0.6) points and Injury Severity Score (ISS) of (23.6 ± 8.5) points.Control group had eight males and two females,with the age of(29.1 ± 2.8) years.Compared to control group,trauma group had slightly lower TREM-1 expressions in neutrophils and significantly higher expressions in monocytes at days 1 to 14 (all P ＜ 0.01).ISS high-score group had slightly lower TREM-1 expressions in neutrophils than ISS low-score group at days 1 to 7,with significant difference at day 1 (P ＜ 0.05).ISS high-score group had slightly higher TREM-1 expressions in monocytes than ISS lowscore group at days 1 to 14,with significant difference at day 14 (P ＜ 0.05).Compared to traumatic non-sepsis group,traumatic sepsis group had significantly lower TREM-1 expressions in neutrophils at days 1 to 14 (all P ＜ 0.05).Traumatic sepsis group had slightly lower expressions in monocytes than traumatic non-sepsis group at days 1 to 7,with significant difference at day 3 (P ＜ 0.05).AUC and 95％ CI evaluating the role of neutrophils TREM-1 in traumatic sepsis prediagnosis were 0.852 (0.738,0.966) at day 1,0.835 (0.721,0.948) at day 3,0.797 (0.654,0.939) at day 5,0.756 (0.599,0.914) at day 7,and 0.707 (0.525,0.888) at day 14,respectively.Conclusions After severe thoracic trauma,the expressions of TREM-1 are decreased in neutrophils but increased in monocytes.TREM-1 might be used to assess the injury severity and has certain value in prediagnosis for traumatic sepsis.

Tumor-associated macrophages (TAMs), one of the dominating constituents of tumor microenvironment, are important contributors to cancer progression and treatment resistance. Therefore, regulation of TAMs polarization from M2 phenotype towards M1 phenotype has emerged as a new strategy for tumor immunotherapy. Herein, we successfully initiated antitumor immunotherapy by inhibiting TAMs M2 polarization via autophagy intervention with polyethylene glycol-conjugated gold nanoparticles (PEG-AuNPs). PEG-AuNPs suppressed TAMs M2 polarization in both in vitro and in vivo models, elicited antitumor immunotherapy and inhibited subcutaneous tumor growth in mice. As demonstrated by the mRFP-GFP-LC3 assay and analyzing the autophagy-related proteins (LC3, beclin1 and P62), PEG-AuNPs induced autophagic flux inhibition in TAMs, which is attributed to the PEG-AuNPs induced lysosome alkalization and membrane permeabilization. Besides, TAMs were prone to polarize towards M2 phenotype following autophagy activation, whereas inhibition of autophagic flux could reduce the M2 polarization of TAMs. Our results revealed a mechanism underlying PEG-AuNPs induced antitumor immunotherapy, where PEG-AuNPs reduce TAMs M2 polarization via induction of lysosome dysfunction and autophagic flux inhibition. This study elucidated the biological effects of nanomaterials on TAMs polarization and provided insight into harnessing the intrinsic immunomodulation capacity of nanomaterials for effective cancer treatment.