Radiofrequency ablation for hepatic hemangioma is safe and effective, and can obtain the same curative effect as traditional surgical resection. For hepatic hemangiomas with large volume, abundant arterial blood supply and long ablation time, systemic inflammatory response syndrome (SIRS) often occurs after radiofrequency ablation, which can lead to injury or dysfunction of important organs. This paper systematically summarizes the mechanism, prevention and treatment of SIRS after radiofrequency ablation of hepatic hemangioma, so as to provide reference for improving the safety of radiofrequency ablation of hepatic hemangioma.
Objective To systematically evaluate the efficacy and safety of dose-dense neoadjuvant chemotherapy (ddNACT) and conventional neoadjuvant chemotherapy (cNACT) for locally advanced breast cancer (LABC). Methods PubMed, Embase, Web of Science, CNKI, Wanfang Data, and VIP databases were searched for randomized controlled trials (RCT) comparing ddNACT regimen with cNACT regimen for breast cancer. The time limit for retrieval was from establishment to March 1st, 2021. Two reviewers independently screened literatures, extracted data and assessed risk bias of included studies; then, meta-analysis was performed by using Stata 15.0 software. Results A total of 13 RCTs were included, including 3 258 patients, of which 1 625 patients received ddNACT and 1 633 patients received cNACT. The results of meta-analysis showed that the ddNACT regimen could improve the pathological complete response rate (pCR, P<0.001), objective response rate (ORR, P<0.001), and disease free survival (DFS, P=0.037) as compared with the cNACT regimen, there was no significant difference in the overall survival (OS) between the two groups (P=0.098). The incidences of grade 3 or 4 oral stomatitis (P=0.005) and neurotoxicity (P<0.001) were higher and the incidence of grade 3 or 4 neutropenia was lower (P=0.025) in the patients with ddNACT regimen, there were no significant differences in grade 3 or 4 thrombocytopenia (P=0.152), grade 3 or 4 anemia (P=0.123), chemotherapy completion rate (P=0.161) and breast conservative surgery rate (P=0.186) between the two groups. Patients with hormone receptor (HR) negative (HR–) were more likely to get pCR after neoadjuvant chemotherapy (P<0.001). ConclusionsCurrent evidence shows that the use of anthracycline/taxane-based ddNACT regimen in LABC patients can improve the pCR, ORR, and DFS as compared with cNACT regimen. The pCR after neoadjuvant chemotherapy in the patients with HR– is higher than that with HR+. Prophylactic use of granulocyte-colony stimulating factor could significantly reduce the incidence of neutropenia, and most patients are tolerant to ddNACT regimen, 2 regimens have similar chemotherapy completion rates.
ObjectiveTo further evaluate the relation between usage of proton pump inhibitor (PPI) and the risk of pancreatic cancer. MethodThe observational studies were systematically searched in the databases of PubMed, Embase, Web of Science, Cochrane Library, ClinicalTrials.gov, CNKI, Wanfang, and VIP. The combined odds ratio (OR) and 95% confidence interval (CI) of pancreatic cancer risk were estimated by the corresponding effect model according to the heterogeneous results, and the subgroup analysis, meta-regression, and sensitivity analysis were performed. In addition, the relation between the defined daily dose (DDD) and usage time of PPI and the pancreatic cancer risk were studied by using restricted cubic spline. ResultsA total of 14 studies were included, including 1 601 430 subjects. The meta-analysis result showed that usage of PPI was positively correlated with the risk of pancreatic cancer [I2=98.9%, OR (95%CI)=1.60 (1.21, 2.11), P<0.001]. The subgroup analysis results showed that usage of PPI would increase the risk of pancreatic cancer in the subgroups of literature published before 2018 [OR (95%CI)=1.88 (1.05, 3.38), P=0.034], non-Asian regions [OR (95%CI)=1.37 (1.04, 1.82), P=0.028], case-control studies [OR (95%CI)=1.59 (1.16, 2.18), P=0.004], cohort studies [OR (95%CI)=1.65 (1.13, 2.39), P=0.009], and high-quality studies [OR (95%CI)=1.62 (1.19, 2.20), P=0.002]. The dose-response curve showed that there was a nonlinear relation between the usage of PPI and the risk of pancreatic cancer (χ2linear=2.27, P=0.132; Pnonlinear=0.039). When the usage of PPI was 800 DDD or less, usage of PPI would increase the risk of pancreatic cancer, but there was no statistical significance when the usage of PPI was more than 800 DDD. The time-effect curve showed that there was a linear relation between the usage time of PPI and the risk of pancreatic cancer (χ2linear=6.92, P=0.009), and the risk of pancreatic cancer would increase by 2.3% if the usage of PPI increased by one month [OR=1.02, 95%CI (1.01, 1.04), P=0.009]. The sensitivity analysis confirmed that the results were stable by gradually eliminating each study, the OR (95%CI) of the risk of pancreatic cancer was 1.37 (1.08, 1.74) to 1.66 (1.22, 2.27), and the publication bias was not found by Egger test (P=0.594).ConclusionsFrom the results of this meta-analysis, usage of PPI will increase the risk of pancreatic cancer, and the dosage of PPI and usage time of PPI may be related to the risk of pancreatic cancer. The clinical usage of PPI should be strictly controlled, and the dosage and usage time should also be carefully considered.
This study aims to clarify host factors of IFN treatment in the treatment of chronic hepatitis B (CHB) patients by screening the differentially expressed genes of IFN pathway CHB patients with different response to interferon (IFN) therapy. Three cases were randomly selected in IFN-responding CHB patients (Rs), non-responding CHB patients (NRs) and healthy participants, respectively. The human type I IFN response RT2 profiler PCR array was used to detect the expression levels of IFN-related genes in peripheral blood monocytes (PBMCs) from healthy participants and CHB patients before and after Peg-IFN-α 2a treatment. The results showed that more differentially expressed genes appeared in Rs group than NRs group after IFN treatment. Comparing with healthy participants, IFNG, IL7R, IRF1, and IRF8 were downregulated in both Rs and NRs group before IFN treatment; CXCL10, IFIT1, and IFITM1 were upregulated in the Rs; IL13RA1 and IFI35 were upregulated in the NRs, while IFRD2, IL11RA, IL4R, IRF3, IRF4, PYHIN1, and ADAR were downregulated. The expression of IL15, IFI35 and IFI44 was downregulated by 4.09 (t = 10.58, P < 0.001), 5.59 (t = 3.37, P = 0.028) and 10.83 (t = 2.8, P = 0.049) fold in the Rs group compared with the NRs group, respectively. In conclusion, IFN-response-related gene array is able to evaluate IFN treatment response by detecting IFN-related genes levels in PBMC. High expression of CXCL10, IFIT1 and IFITM1 before treatment may suggest satisfied IFN efficacy, while high expression of IL13RA1, IL15, IFI35 and IFI44 molecules and low expression of IFRD2, IL11RA, IL4R, IRF3, IRF4, PYHIN1 and ADAR molecules may be associated with poor IFN efficacy.
OBJECTIVE: To investigate the influence of tissue engineered tendon on subgroup of T lymphocytes and its receptor in Roman chickens. METHODS: The flexor digitorum profundus of the third toes of right feet in 75 Roman chickens were resected and made 2.5 cm defects as experimental model. They were randomly divided into five groups according to five repair methods: no operation (group A), autograft (group B), fresh allograft (group C), polymer combined with allogenous tendon cells (group D), derived tendon materials combined with allogenous tendon cells (group E). The proliferation and transformation of lymphocytes and contribution of CD4+, CD8+, CD28 and T cell receptor (TCR) were detected to study the immune response. RESULTS: The CD4+, CD8+ and TCR of group D and E were increased slightly than that of group B after 7 days, while after 14 days, those data decreased gradually and no significant difference between tissue engineered tendon and autografts (P gt; 0.05), and there was significant difference between fresh allograft and tissue engineered tendon (P lt; 0.05). Lymphocytes transformation induced by conA also showed no significant difference between tissue engineered tendon and autografts (P gt; 0.05). CONCLUSION: Tendon cells are hypoantigen cells, there are less secretion of soluble antigen or antigen chips dropped out from cells. Tissue engineered tendon has excellent biocompatibility.
Objective To detect the effects of cytokines on the expression of early growth response gene-1 (Egr-1) in cultured human retinal pigment epithelial (RPE) cells. Methods Immunofluorescence staining, Western blotting and reverse transcription polymerase chain reaction (RT-PCR) were used to detect and quantitatively analyze the expression of Egr-1 protein and mRNA in cultured human RPE cells which were exposed to stimulants, including 20 mu;g/ml lipopolysaccharide (LPS), 40 ng/ml tumor necrosis factor (TNF)-alpha;, 10 U/ml interferon (IFN)gamma;, 30% supernatant of monocyte/macrophage strain (THP1 cells) and the vitreous humor from healthy human eyeballs, for 0, 10, 20, 30, 40 and 60 minutes, respectively. Results The RPE cells stimulated for 0 minute revealed faint green fluorescence of Egr-1 in the cytoplasm. With exposure to the stimulants, the expressionof Egr-1 increased obviously and b green fluorescence was found in cytoplasm in some nuclei of RPE cells. Compared with the untreated RPE cells, after stimulated by 20 mu;g/ml LPS, 40 ng/ml TNFalpha;, 10 U/ml IFNgamma;, 30% supernatant of THP-1 cells and the vitreous humor, the approximate ultimate amplitudes of Egr-1 mRNA enhanced 1.9, 1.3, 14, 1.2, and 1.4 times, respectively; the greatest amplitudes of Egr-1 protein increased 3.4, 1.2, 1.7, 32, and 1.3 times, respectively. Conclusion LPS, TNF-alpha;, IFN-gamma;, supernatant of THP-1 cells and the vitreous humor can upregulate the expression of Egr-1 mRNA and protein in cultured human RPE cells, and induce its nuclear transposition, which suggests the activation of Egr-1.
Non-small cell lung cancer (NSCLC) accounts for more than 80% of lung cancer. Nowadays, gemcitabine and cisplatin in combination have been adopted as the first-line chemotherapy for patients with NSCLC. This study aimed to monitor early response to combined chemotherapy of gemcitabine plus cisplatin in a mouse model of NSCLC by using 18F-fluorodeoxyglucose and 18F-fluorothymidine small animal positron emission tomography (PET). Lewis lung carcinoma-bearing C57BL/6 mice were treated with gemcitabine-cisplatin or saline. Small animal PET with 18F-FDG and 18F-FLT was performed before (baseline) and after treatment (on Day 3), respectively. Imaging results were confirmed by histopathological studies (hematoxylin and eosin staining, Ki67 staining). Compared to the results in the control group, gemcitabine-cisplatin in the treated group significantly inhibited tumor growth (P<0.05). In the treated group, the maximum standardized uptake value (SUVmax) of 18F-FLT decreased significantly from 0.59±0.05 (baseline) to 0.28±0.05 (Day 3) (P<0.05). There was no significant difference between baseline (4.35±0.46) and that on Day 3 (4.02±0.47) on 18F-FDG SUVmax (P>0.05). The proliferation of tumor assessed by Ki67 staining decreased significantly after treatment of one dose of gemicitabine-cisplatin (P<0.05). The staining of HE showed an increase in necrotic and inflam- matory cells after the treatment. This study demonstrated that the uptake of 18F-FLT reduced more rapidly and signi-ficantly than that of 18F-FDG and was less disturbed by the increase of inflammatory cells after chemotherapy.
ObjectiveTo observe the accuracy of magnetic resonance imaging (MRI) for predicting pathologic complete response (pCR) after neoadjuvant chemotherapy (NAC) in breast cancer, and to analyze the cause of the prediction error.MethodsData from 157 breast cancer patients who underwent NAC before surgery in Mianyang Central Hospital from January 2017 to January 2019 were analyzed. MRI parameters before and after NAC and pCR conditions were collected to analyze the parameters that produced false positives and false negatives.ResultsOf the 157 patients, 37 (23.6%) achieved pCR after NAC, and 33 (21.0%) achieved radiation complete remission (rCR) after NAC. The accuracy of MRI prediction was 70.7% (111/157), the sensitivity was 82.5% (99/120), and the specificity was 32.4% (12/37). A total of 25 cases did not achieve rCR, but postoperative evaluation achieved pCR (false positive), 21 cases achieved rCR, but postoperative evaluation did not achieve pCR (false negative). Diameter of tumor, peritumoral oedema, and background parenchymal enhancement were associated with MRI false positive prediction (P<0.05); gland density and tumor rim enhancement were associated with MRI false negative prediction (P<0.05).ConclusionMRI can be used as an important method to predict pCR after NAC in breast cancer patients, and its accuracy may be related to diameter of tumor, peritumoral oedema, background parenchymal enhancement, gland density, and tumor rim enhancement.
ObjectiveTo evaluate the effect of different doses of dexmedetomidine on hemodynamics during endotracheal extubation of laparoscopic cholecystectomy in patients with hypertension. MethodsA total of 120 hypertension patients ready to undergo laparoscopic cholecystectomy under general anesthesia between December 2013 and December 2014 were chosen to be our study subjects. They were randomly divided into 4 groups with 30 patients in each:saline control group (group C), low-dose dexmedetomidine hydrochloride injection group (group D1), moderate-dose dexmedetomidine hydrochloride injection group (group D2), and high-dose dexmedetomidine hydrochloride injection group (group D3). The anesthesia methods and drugs were kept the same in each group, and 20 mL of saline, 0.25, 0.50, 1.00 μg/kg dexmedetomidine (diluted to 20 mL with saline) were given to group C, D1, D2, and D3 respectively 15 minutes before the end of surgery. Time of drug administration was set to 15 minutes. We observed and recorded each patient's mean arterial pressure (MAP) and heart rate (HR) in 5 particular moments:the time point before administration (T1), immediately after administration (T2), extubation after administration (T3), one minute after extubation (T4), and 5 minutes after extubation (T5). Surgery time, recovery time, extubation time and the number of adverse reactions were also detected. ResultsCompared at with, MAP and HR increased significantly at the times points of T3, T4, T5 compared with T1 and T2 in Group C and group D1 (P<0.05), while the correspondent difference was not statistically significant in group D2 and D3 (P>0.05). Compared with group C, MAP and HR decrease were not significantly at the time points of T3, T4, T5 in group D1 (P>0.05). However, MAP and HR decrease at times points of T3, T4, T5 in group D2 and D3 were significantly different from group C and D1 (P<0.05). After extubation, there were two cases of dysphoria in group C and two cases of somnolence in group D3, but there were no cases of dysphoria, nausea or shiver in group D1, D2, D3. ConclusionIntravenously injecting moderate dose of dexmedetomidine 15 minutes before the end of surgery can effectively reduce patients' cardiovascular stress response during laparoscopic cholecystectomy extubation for patients with hypertension, and we suggest a dose of 0.5 μg/kg of dexmedetomidine.
Acute lung injury is a kind of common complication after cardiopulmonary bypass. Acute lung injury is attributed to the ischemia-reperfusion injury and systemic inflammatory response syndrome. Several factors common in cardiac surgery with cardiopulmonary bypass may worsen the risk for acute lung injury including atelectasis, transfusion requirement, older age, heart failure, emergency surgery and prolonged duration of bypass. Targets for prevention of acute lung injury include mechanical, surgical and anesthetic interventions that aim to reduce the contact activation, systemic inflammatory response, leukocyte sequestration and hemodilution associated with cardiopulmonary bypass. We aim to review the etiology, risk factors and lung protective strategies for acute lung injury after cardiopulmonary bypass.