Objective:To evaluate therapeutic efficacy and adverse reactions of synchronous chemoradiotherapy combined with gamma knife therapy for pelvic lymph node metastasis of cervical cancers. Methods:Data of 42 cervical cancer patients who suffered from residual pelvic lymph node metastasis and received concurrent chemoradiotherapy were retrospectively analyzed. Intensity-modu-lated radiotherapy was used in the treatment. The prescribed doses of planning target volume and pelvic metastasized lymph node of the planned gross tumor volume were 50.4 Gy/28 F and 59.92 Gy/28 F, respectively. The combined internal irradiation dose was 6 Gy/6 F. Concurrent chemotherapy was administered with 40 mg/m2·w cisplatin. Three months after chemoradiotherapy was completed, the pa-tients with residual pelvic positive lymph node received additional dose ranging from 10 Gy to 15 Gy at three or four fractions by using a gamma knife. Results:Near-term efficacy was 83.3%(35/42) in three months. Local control rates were 88.1%(37/42), 83.3%(35/42), and 76.2%(32/42) in 6, 9, and 12 months, respectively. The 1-and 2-year survival rates were 77.5%(31/40) and 70.0%(28/40), re-spectively. The incidence rates of radiation enteritis, proctitis, cystitis, gut toxicity, and neutrocytopenia were 11.9%(5/42), 38.1%(16/42), 7.1%(3/42), 90.5%(38/42), and 85.7%(36/42), respectively, and the majority of these conditions were classified as grades I and II. Conclusion:Synchronous chemoradiotherapy combined with gamma knife therapy is an effective and feasible treatment method for pelvic lymph node metastasis of cervical cancer;this method exhibits a minimal adverse reaction.

Objective: To evaluate the clinical effect and adverse reactions of radioactive seed interstitial brachytherapy com-bined with etoposide (EP) regimen concurrent chemoradiotherapy treatment for locally advanced non-small cell lung cancer. Methods:All 24 cases of locally advanced non-small cell lung cancer received three-dimensional conformal intensity modulated radiation therapy by using 6 MV X-ray to obtain 95%60-66 Gy/30-33 F planning target volume. All cases received radiation therapy five times a week. EP regimen chemotherapy concurrent with radiotherapy was given to 24 patients. The therapy included VP-16, 60 mg/m2 intravenous in-fusion for 1 d to 5 d, and DDP 50 mg/m2 intravenous infusion on the 1st, 8th, and 28th therapy day. Chemotherapy with EP regimen was given for four cycles, in which two cycles were given during radiotherapy and the remaining cycles were completed after radiotherapy. The patients were reexamined three months after concurrent chemoradiotherapy was completed. Patients with residual tumor, con-firmed via positron emission tomography/computed tomography, underwent 125I radioactive seed implantation interstitial brachytherapy to complement the dose of tumor. Results: The response rate was 83.3% (20/24); the local control rates of 3, 6, 9, 12, 18, and 24 months were 87.5% (21/24), 83.3% (20/24), 75.0% (18/24), 70.8% (17/24), 58.3% (14/24), and 50.0% (12/24). The median survival was 20.2 months. The one-year survival rate was 62.5%, and the two-year survival rate was 37.5%. The following main toxicities were observed:the incidence of radiation-induced lung injury was 25%;the incidence of radiation esophagitis was 33.3%;the incidence of grades Ⅰ to Ⅱ gastrointestinal reactions was 82.3%; the incidence of reducing neutropenia was 87.5%, in which the incidence of gradesⅠtoⅡwas 75.0%, gradeⅢwas 12.5%, and gradeⅣwas 0%. Conclusion:EP regimen concurrent radiotherapy and chemo-therapy combined with radioactive seed interstitial brachytherapy for locally advanced non-small cell lung cancer is effective and has few serious adverse reactions, thus making this approach worthy of promotion.

Objective To investigate the effect of sevoflurane preconditioning on lung injury induced by limb ischemia-reperfusion in rats and the relationship with endoplasmic reticulum stress.Methods Forty-five healthy male Sprague-Dawley rats,aged 6-8 weeks,weighing 250-300 g,were randomly allocated into 3 groups (n =15 each) using a random number table:sham operation group (group S),limb ischemia-reperfusion group (group LIR),and sevoflurane preconditioning group (group SP).Limb ischemia-reperfusion was induced by clamping bilateral femoral arteries for 3 h followed by 3 h reperfusion in LIR and SP groups.In group SP,2.5％ sevoflurane was inhaled for 30 min,and 15 min later the model was established.Before ischemia and at 3 h of reperfusion (at the corresponding time point in group S),arterial blood samples were collected for blood gas analysis,and arterial oxygen partial pressure (PaO2) and arterial carbon dioxide partial pressure (PaCO2) were recorded.The rats were sacrificed at 3 h of reperfusion,and lung specimens were obtained for determination of wet to dry lung weight ratio (W/D ratio) and total lung water content (TLW) and for microscopic examination of the pathological changes,and index of quantitative evaluation for alveolar damage (IQA) was calculated.The expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) protein and mRNA in lung tissues was detected by Western blot and real-time polymerase chain reaction,respectively.Results Compared to group S,the PaO2was significantly decreased at 3 h of reperfusion,the W/D ratio,TLW and IQA were significantly increased,the expression of GRP78 and CHOP protein and mRNA was significantly up-regulated (P＜0.05),and no significant change was found in PaCO2 in group LIR (P＞0.05).Compared to group LIR,the PaO2 was significantly increased at 3 h of reperfusion,the W/D ratio,TLW and IQA were significantly decreased,the expression of GRP78 and CHOP protein and mRNA was significantly down-regulated (P＜ 0.05),and no significant change was found in PaCO2 in group SP (P＞0.05).Conclusion Sevoflurane preconditioning can ameliorate lung injury induced by limb ischemia-reperfusion in the rats,and the mechanism is related to inhibition of endoplasmic reticulum stress.

OBJECTIVE To study the clinical characteristics of invasive pulmonary aspergillosis(IPA).METHODS Based on the clinical data from 14 IPA cases identified by pathologic examination in the 454th Hospital,the characteristics of IPA were discussed,including the underlying diseases,symptoms,X-ray,CT,the treatment methods and the curative effect.The related literatures were also reviewed.RESULTS All of the 14 patients had underlying diseases.From them 5 were with pulmonary cancer(35.7%),3 with chronic obstructive pulmonary disease(21.4%),2 with pulmonary abscess(14.3%),2 were after chemotherapy for leukemia(14.3%),1 with pulmonary tuberculosis(7.1%)and 1 with diabetes(7.1%).The common symptoms of the 14 cases were febricity,productive cough and hemoptysis.Some of them also suffered with short of breath,night sweat,fatigue,chest pain and losing weight.The air crescent sign showed on X-ray and CT.Soft tissue masses with halo-sign on the margin,dense shadow of small masses within the alveoli,and multi-nodular shadows were also observed.Among 10 patients treated by antifungal medications,only 4 treated otherwise with operation were cured,4 patients died,and 2 patients did not complete the treatment scheme.CONCLUSIONS The patients with immunodeficiency are susceptible to IPA.The clinical manifestations of IPA are non-specific.The final diagnosis depends on the pathologic examination.The only medication is not sufficient for IPA patients.Pulmonary resection should be considered if the prolonged illness or frequent hemoptysis exist.

Objective To explore the differentially expressed genes (DEG) involved in the pathogenesis of preeclampsia(PE). Methods The gene expression profiles of placental tissues from 7 severe PE patients and 7 preterm controls from June to December 2012 were assessed using microarray. Gene ontology(GO)enrichment analysis and pathway analysis were performed to explore the genes and pathways involved in the pathogenesis of PE. Four DEG involved in these biological processes were further verified by quantitative real-time PCR. Results A total of 308 transcripts were significantly differentially expressed. Of these DEG,81 genes(LEPTIN,PAPPA2,CRH,PLIN2,INHA,BCL6,FLT1,CCR7,etc)were up-regulated,and 227 genes(CXCL12,CXCL9,etc)were down-regulated. GO enrichment analysis indicated that the top 3 GO molecular functions were immune response(GO: 0006955,17 DEG),positive regulation of apoptosis(GO: 0043065,11 DEG)and inflammatory response(GO: 0006954,11 DEG). Pathway analysis showed that the top 3 pathways were cell adhesion molecules(11 DEG),cytokine-cytokine receptor interaction(11 DEG),chemokine signaling pathway(8 DEG). Many genes(LEP,FLT1,TFRC,SH3PXD2A, CYP11A1,SEPP1,and so on)involved in oxidative stress were found to be significantly changed. Of these genes,LEP were significantly up-regulated with a fold change of 61.5. The fold changes of FLT1, SH3PXD2A,SEPP1,CYP11A1,TFRC were 8.6,2.2,-2.0,2.7 and-2.8. Four DEG involved in oxidative stress were further verified by quantitative real-time PCR. Conclusions A DEG signature was identified in severe preeclampsia placentas compared with normal controls. The DEG mainly involved in the molecular mechanisms of immune response,oxidative stress and inflammatory response,and were closely associated with the pathogenesis of PE.

OBJECTIVE:To investigate the early changes of ECG,cTnⅠ,LDH,α-HBDH and CKMB in patients with anthra-cyclines chemotherapy-induced heart damage after breast cancer surgery,and to explore their significances in the diagnosis of early heart damage. METHODS:Medical information of 152 cases of anthracyclines chemotherapy after breast cancer surgery in our hos-pital during Jan. 2015-Jun. 2016 were analyzed retrospectively. According to diagnosis criteria of drug-induced cardiotoxicity,the occurrence of heart damage was evaluated during hospitalization and 1-year follow-up. According to evaluation results,those pa-tients were divided into heart damage group(50 cases)and control group(102 cases). The early changes of ECG,cTnⅠ,LDH, CKMB and α-HBDH were analyzed before chemotherapy(T0),24 h after first chemotherapy(T1),24 h after second chemothera-py(T2),24 h after forth chemotherapy. RESULTS:At T1,T2,T3,the proprotion of ECG abnormalities in heart damage group was significantly higher than control group;the serum levels of cTnⅠ,LDH,CKMB andα-HBDH in heart damage group were signifi-cantly higher than control group, with statistical significance (P<0.01). CONCLUSIONS:For anthracyclines chemotherapy drugs-induced heart damage after breast cancer surgery,early regular monitoring of ECG,cTnⅠ,LDH,CKMB and α-HBDH can improve the efficiency of early diagnosis of heart damage,and improve prognosis.

Objective To investigate the association between SLCO1B1/ApoE gene polymorphisms and lipid-lowering efficacy and safety of rosuvastatin.Methods DNA samples were extracted from blood using nano paramagnetic particle method.The SLCO1B1 521T＞C and ApoE gene polymorphisms were screened by PCR-pyrophosphate sequencing method.Totally 152 patients received rosuvastatin orally at a dose of 10 mg/d.The lipidlowering efficacy was evaluated through detecting serum low-density lipoprotein cholesterol (LDL-C) level before and 8 weeks after the treatment.The incidence of myopathic adverse effect was assessed by follow-up of the occurrence of myalgia.Results The gene distribution of SLCO1B1 521T＞C was 73.7％,23.7％ and 2.6％ respectively for TT,TC and CC in 152 patients,and the distribution of ApoE gene was 65.8％,13.2％ and 21.0％ respectively for ε3/ε3,ε3/ε2 and ε4/ε3.The genotype ε4/ε4,ε2/ε2 and ε4/ε2 were not detected.After orally receiving rosuvastatin 10 mg daily for 8 weeks,the decreased LDL-C levels showed significant differences (P＜0.05) among ApoE genotype ε3/ε2,ε3/ε3 and ε4/ε3 groups,and the frequencies of myalgia showed significant differences in the three genotype groups of SLCO1B1 521T＞C (P＜0.05).Conclusion The gene polymorphism of SLCO1B1/ApoE was correlated with efficacy and safety of rosuvastatin.The combined detection of SLCO1B1/ApoE genes can be utilized to predict efficacy and risk,and then realize individualized medication.

Objective To analyze the regulation of estrogen receptor α (ERα) on truncated neurokinin-1 receptor (NK1R-Tr), and the influence of this regulation on cell proliferation in estrogen receptor-positive breast cancer cell lines. Methods The chromatin immune coprecipitation (CHIP) was used to observe the transcriptional regulation function of ERαon NK1R-Tr in breast cancer cells. Luciferase reporter gene assay was used to verify whether ERα played a positive regulatory role in the expression of NK1R-Tr. Western blot assay and real-time-PCR were used to detect the expression of ERα and NK1R-Tr in breast cancer cells, MCF-7 and T47D, as well as the expression of NK1R-Tr protein and mRNA level. NK1R-Tr levels were also detected after using estradiol (E2, ERα agonist) and small interfering RNA (knock out ERα). CCK-8 and clone formation experimen were used to detect the proliferation ability of breast cancer cells after knocking out NK1R-Tr with small interfering RNAs. Results CHIP test and Luciferase reporter gene assay proved that ERα can positively regulate the expression of NK1R-Tr via the ERα sequences in the upstream of the NK1R-Tr gene promoter. The expression of NK1R-Tr at both protein level and mRNA level dropped in the estrogen receptor-positive breast cancer cell line MCF-7 upon knocking out ERα. After knocking out NK1R-Tr, the proliferation ability of estrogen receptor-positive breast cancer cells was lower than that of the control group. Conclusion The ERα positively regulates the expression of NK1R-Tr, resulting in the increased cell proliferation in estrogen positive breast cancer cells.

Objective To explore the characteristics of polysomnography (PSG) of depressed patients and the correlation between rapid eye movement (REM) and severity degree of depression. Methods Polysomnography was used to assess patients'sleep condition and Montgomery-Asberg depression scale (MADRS) was used to assess the severity degree of depression. 90 patients and 30 healthy controls were included. Results Compared to healthy controls,sleep progress of depressed patients changed as follow:prolonged sleep latency((25.2 ±15.25) minutes) ,lowered sleep efficiency(0.853 ±0.11) ;the architecture of sleep also changed:percentage of stage 1 increased( (27.7 ± 16.38) % ),percentage of REM sleep increased( (22. 8 ± 6. 1 ) % ) , percentage of stage 2 decreased ((40.2±11.3)%), percentage of slow wave sleep decreased ((11.8 ±9. 32)%); REM sleep significantly changed; decreased REM latency((79. 27 ±30. 44) minutes) , increased REM activity((129. 0 ±53. 12) u) .increased intensity of REM((36.7 ±14.0)u/min), increased REM density((159.2 ±57.2)u/min) were observed in depressed patients. There was no obvious correlation between the variance of REM and severity degree of depression. Conclusion There are a series of changes in sleep progress, architecture and REM sleep of depression and the change of REM sleep can be specified to diagnose depression. However,there is no causality between REM variance and severity of depression.

Objective:To determine the expression of the full-length (NK1R-FL) and truncated (NK1R-Tr) neurokinin-1 receptor (NK1R) and the neurokinin-2 receptor (NK2R) in breast cancer tissues and cell lines, as well as to study the effects of the NK1R and NK2R antagonists on the growth of breast cancer cells. Methods:Immunohistochemistry and Western blot assays were used to detect NK1R, NK1R-FL, and NK2R expression in clinical samples of primary breast cancer tissue, benign lesions, and normal breast tissue, as well as in different breast cancer cell lines. Cell proliferation and soft agar growth tests were performed on cells treated with the NK1R and NK2R antagonists to study the ectopic overexpression of NK1R-FL and NK1R-Tr in breast cancer cell lines. Results:Total NK1R expression was detected in the breast cancer tissues, benign lesions, and normal breast tissues. Compared with the normal breast epithe-lia and benign breast lesions, the expression levels of NK1R-FL and NK2R decreased in the carcinoma. These changes were also relat-ed to the carcinoma type, histological grade, lymph node metastasis, HER2 and Ki-67 expression, and estrogen and progesterone recep-tors in breast cancer. The expression levels of NK1R-FL and NK2R were high in the HBL-100 breast cell lines of para-neoplastic tis-sues, but NK1R-Tr expression was low. The MDA-MB-231, T-47D, and MCF-7 cells only expressed NK1R-Tr. NK1R-Tr or NK1R-FL overexpression caused the decreased inhibition rate or increased levels of the NK1R and NK2R antagonists in the breast cancer cells. Conclusion:NK1R-FL and NK2R are co-expressed in normal cells. NK1R-Tr is highly expressed in breast cancer cells and exerts nega-tive feedback to regulate NK1R-FL and NK2R expression in all cells, especially cancer cells.