This study is to investigate the effect of total flavonoids of Uygur medicine bugloss (BTF) on rats with myocardial ischemia/reperfusion injury, and to explore the mechanisms by which it acts. Left anterior descending (LAD) coronary artery in rats was occluded for 30 min followed by 4 h reperfusion. Meanwhile, BTF dissolved in saline was administered intraperitoneally at dosage of 10, 30 and 50 mg x kg(-1). Electrocardiograph, infarction index, serum myocardial enzymes and heart function were determined to evaluate the effect of BTF. Some other observations were carried out to explore whether inhibiting inflammation and apoptosis is involved in the mechanisms underlying BTF. Our results showed that in ischemia/reperfusion injured rats BTF could dose-dependently reduce myocardial infarction index and myocardial enzyme leakage, and enhance heart function, indicating that it possesses significant cardio protection. ELISA analysis showed that BTF could decrease the content of myocardial inflammatory cytokines such as IL-1beta, IL-6 and TNF-alpha. Western-blotting confirmed that BTF could increase the expression of anti-apoptotic protein Bcl-2 and reduce the expression of proapoptosis protein Bax. Further more, the phosphorylation level of PI3K and Akt was upregulated by BTF treatment. BTF can protect rat against myocardial ischemia/reperfusion injury. Anti-inflammation and inhibition of apoptosis through upregulating PI3K/Akt signal pathway may contribute to the protective effect of BTF.

Neuroendocrine carcinoma of the breast is a rare malignant tumor which, with the features of Merkel cells is even rarer. Herein, we report a case of small cell carcinoma with Merkel cell features in a 52-year-old female. Microscopically, the tumor was characterized by diffuse and consistent small round cells that were de-adherent. The tumor cells had round or oval nuclei with delicate chromatin and small nucleoli, the cytoplasm was sparse and eosinophilic. Additionally, the tumor was accompanied by high-grade ductal carcinoma in situ. Immunohistochemical staining showed that infiltrating tumor cells were positive for neuroendocrine markers, and punctately positive for CK20. The patient underwent modified radical mastectomy, axillary lymph node dissection, and postoperative adjuvant chemotherapy. No recurrence or metastasis was observed during follow-up period. Primary breast small cell carcinoma with Merkel cell features is rare and easily misdiagnosed as Merkel cell carcinoma. Early diagnosis and treatment may improve patient prognosis.

Objective To explore the influence of family history of diabetes and central obesity on prediabetes(Pre-DM)and their interaction.Methods Based on the REACTION studyduring August December 2011 in Dalian,2587 individuals aged≥40 with normal blood glucose(BG)were divided into newly diagnosed Pre-DM(n=522)and BG normal group(NC,n=2065)during follow-up.The influence of family history of DM and central obesity on prediabetes and their interaction were analyzed.Results The age,SBP,DBP,BMI,WC,HDL-C,LDL-C,TG,ALT,GGT,FPG,2 hPG,HbA1c,FIns,HOMA-IR,SUA and the incidence of hypertension,fatty liver disease,dyslipidemia,overweight/obesity and central obesity in Pre-DM group were all higher than those in NC group(P＜0.05).Multivariate logistic regression analysis showed that family history of diabetes and central obesity were risk factors for Pre-DM.After adjustment,no significant multiplicative interaction was shown between diabetes family history and central obesity on the risk of Pre-DM(P=0.764).Quantitative analysis of interaction showed that RERI=0.110,S=1.112 and AP=0.053,suggesting that DM family history and central obesity have no significant additive interaction on the risk of Pre-DM.Conclusion The family history of DM and central obesity are both associated with the occurrence of Pre-DM,but there is no significant interaction.

Myelodysplastic syndrome (MDS) is a malignant hematologic tumor, which is currently difficult to cure. The theory of Xuanfu was proposed by Liu Wansu, which is unique in the clinical evidence of Chinese medicine and is less frequently applied to hematological diseases. The application of Xuanfu theory in myelodysplastic syndrome provides new ideas for the treatment of the disease. The abnormal flow of Qi, blood and fluids caused by the occlusion of the Xuanfu is the cause of toxic stasis obstruction, which is the pathogenesis of toxic stasis obstruction. Thus, the method of dispersion of Bone from Xuanfu, the external treatment of Xuanfu, and regulation of liver qi and Xuanfu help to return to normal of opening and closing function of Xuanfu, and release toxic stasis. In this paper, we analyzed the evidence of toxin-stasis obstruction in myelodysplastic syndrome from the theory of Xuanfu, aiming to provide a feasible theoretical basis for clinical treatment of the disease.

BACKGROUND: Simultaneity multiple primary lung cancer always is a rare disease, but in recent years due to the progress of the diagnosis and treatment means detection rate increased. This study summarized the clinical data of 31 cases of synchronous multiple primary lung cancer (sMPLC) analysis, further to explore the diagnosis, treatment and prognosis of MPLC. METHODS: Sum up the clinical data of 31 cases of simultaneous multiple primary lung cancer, the diagnostic method, surgical methods, pathology, were retrospectively analyzed. RESULTS: All the patients are thoracoscope surgery, no deaths. Thin high resolution computed tomography (CT) in preoperative found multiple lung nodules. Lesions located in the same side of the same period surgical treatment, the operation method is given priority to with under the thoracoscope lung + the lobectomy; Lesions located in bilateral, all staged operation, the time interval for 3 months-4 months. CONCLUSIONS Thin layer distinguish CT preoperative diagnosis is the best way to simultaneous multiple primary lung cancer. Multiple primary lung cancer incidence of ipsilateral lung at the same time higher than that of bilateral lung (23:8), type, around 94%, the most common histology to adenocarcinoma, 80.6% (25/31). Primary lesions under thoracoscope lobectomy plus the lobectomy of secondary lesions is the most commonly used.
Adult ; Aged ; Female ; Humans ; Lung Neoplasms ; diagnosis ; diagnostic imaging ; surgery ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; diagnosis ; diagnostic imaging ; surgery ; Retrospective Studies ; Tomography, X-Ray Computed

BACKGROUND: Colorectal carcinogenesis and progression are related to the gut microbiota and the tumor immune microenvironment. Our previous clinical trial demonstrated that berberine (BBR) hydrochloride might reduce the recurrence and canceration of colorectal adenoma (CRA). The present study aimed to further explore the mechanism of BBR in preventing colorectal cancer (CRC). METHODS: We performed metagenomics sequencing on fecal specimens obtained from the BBR intervention trial, and the differential bacteria before and after medication were validated using quantitative polymerase chain reaction. We further performed ApcMin/+ animal intervention tests, RNA sequencing, flow cytometry, immunohistochemistry, and enzyme-linked immunosorbent assays. RESULTS: The abundance of fecal Veillonella parvula ( V . parvula ) decreased significantly after BBR administration ( P = 0.0016) and increased through the development from CRA to CRC. Patients with CRC with a higher V. parvula abundance had worse tumor staging and a higher lymph node metastasis rate. The intestinal immune pathway of Immunoglobulin A production was activated, and the expression of TNFSF13B (Tumor necrosis factor superfamily 13b, encoding B lymphocyte stimulator [BLyS]), the representative gene of this pathway, and the genes encoding its receptors (interleukin-10 and transforming growth factor beta) were significantly upregulated. Animal experiments revealed that V. parvula promoted colorectal carcinogenesis and increased BLyS levels, while BBR reversed this effect. CONCLUSION: BBR might inhibit V. parvula and further weaken the immunomodulatory effect of B cells induced by V. parvula , thereby blocking the development of colorectal tumors. TRIAL REGISTRAION ClinicalTrials.gov, No. NCT02226185.
Animals ; Humans ; Berberine/therapeutic use* ; Carcinogenesis ; Veillonella ; Colorectal Neoplasms/genetics* ; Tumor Microenvironment