Objective To analyze the changes of ultrasonography and Ki-67 before and after neoadjuvant chemotherapy for breast cancer ,and to assess the value of ultrasonography and Ki-67 in the evaluation of neoadju-vant chemotherapy for breast cancer. Methods The focus changes of 122 cases of breast cancer before and after neoadjuvant chemotherapy were observed by Color Doppler ultrasonography. The therapeutic effect was evaluated by RECIST standard,and the changes of Ki-67 before and after chemotherapy were observed. Results There were significant differences in size and internal blood flow signal of breast cancer before and after chemotherapy (P <0.05). The sensitivity of ultrasonography in the evaluation of neoadjuvant chemotherapy for breast cancer was 89.3%and specificity 53.8%. The clinical efficiency of neoadjuvant chemotherapy for breast cancer with high Ki-67 expression was higher than that with low Ki-67 expression. Conclusion Ultrasonography shows high clinical value in the evaluation of neoadjuvant chemotherapy for breast cancer ,and the expression of Ki-67 could predict the effi-cacy of neoadjuvant chemotherapy.

Objective To investigate the impact of 1,25(OH)2D3 on histological changes and activation of STAT3 in BLM?induced pulmonary fibrosis mice. Methods 30 male C57BL/6 mice were randomly divided into control group ,BLM group and BLM+VD group. Mice in BLM group and BLM+VD group received intratracheal injection of BLM(3 U/kg). Control group were intratracheally injected equal volume of sterile saline. From the first day after the surgery,mice in BLM+VD group received intraperitoneal injection of VD (5μg/kg·d). After 21 days, H&E and Masson′s trichrome staining were carried out. Aschroft score were used to evaluate histological changes in lungs. IL?6,IL?4 and INF?γin BALF were assessed by Elisa. p?STAT3,α?SMA and Collagen I were detected by western blot (WB) and immunohistochemistry. Results Fibrosis score and level of α?SMA,Collagen I in BLM group were significantly higher than that in control group (P < 0.05). However ,treatment with VD effectively at?tenuated fibrosis (P<0.05). IL?6 and IL?4 increased while INF?γwas decreased in BALF of BLM group (P<0.05). VD could ameliorate these changes. Upregulation and neuclear translocation of p?STAT3 were observed in BLM group,while VD intervention could inhibit phosphorylation of STAT3. Conclusions VD attenuate BLM?induced pulmonary fibrosis and regulate inflammatory cytokines probably by blocking STAT3 activation.

Objective To explore the role of MKK34 (a peptide spanning a C-terminal α-helical region in TSLP) on airway inflammation and β-catenin of airway epithelium in a HDM-induced mouse asthma.Methods 32 male BALB/c mice were randomly divided into control,MKK34,asthma and MKK34 + HDM groups.The mice in the asthma group were exposed to HDM for five consecutive days and the MKK34 + HDM group was pretreated with MKK34 1 h prior to the HDM intranasally treated.After 8 weeks' treatment,animal lung function test and pathological staining were performed to evaluate the asthma situation,IL-4,IFN-γin bronchoalveolar lavage fluid and IgE in the serum were detected,immunohistochemistry and western blot were used to assess β-catenin and p-ERK,t-ERK levels.Results Airway reactivity,IL-4 and IgE in the asthma group were significantly higher than that in the control group.Treatment with MKK34 significantly decreased airway hyperresponsiveness,IL-4 and IgE.HE staining demonstrated the chronic bronchitic inflammation in the lungs of asthma group.β-catenin in the control group was distributed evenly at the cytomembrane of epithelial cells.In the asthma group,β-catenin was disordered in epithelial cells and its expression was decreased.Treatment with MKK34 ameliorated the damage of β-catenin and chronic bronchitic inflammation.The protein levels of p-ERK1/2 increased obviously in the asthma group.The pretreated group significantly decreased the expression of p-ERK1/2.Conclusions MKK34 can ameliorate the airway inflammation and the destruction of β-catenin of airway epithelium in a HDM-induced mouse asthma.The ERK pathway may play a role in this process.

OBJECTIVETo assess the clinical value of contrast-enhanced ultrasonography (CEUS) in early diagnosis of breast cancer.

METHODSCEUS was performed in 107 cases of ultrasound BI-RADS(®) category 3 or category 4 small breast tumors (diameter no greater than 10 mm) before surgery. The range, type and patter of enhancement of the tumor and the surrounding tissues were observed, and the time-intensity curve (TIC) was analyzed for TIC curve type, basic and peak intensity, enhancement intensity, rising slope, and enhancement intensity. The results were analyzed comparatively between benign and malignant tumors.

RESULTSThe peak intensity, enhancement intensity index and peak time in CEUS were statistically significant between benign and malignant breast tumor (t=-2.310, -2.592, -2.127, P=0.021, 0.010, 0.033), and the intensity difference and rising slope also differed significantly (t=-3.422, -3.388, P=0.001, 0.001). TIC curve type, enhancement pattern, enhancement types and enhancement range were statistically significantly between benign and malignant breast tumor (P<0.001).

CONCLUSIONBenign and malignant BI-RADS(®) category 3 or 4 small breast tumors differ in the peak intensity, enhancement intensity index and peak time in CEUS. More nodular hyperplasia showed no enhancement in CEUS, and 97.8% of the lesions without enhancement are benign. In enhanced breast nodules, malignant breast lesions show more quick wash-in and wash-out type and quick wash-in and slow wash-out type, and the latter is more common; benign lesions often show a slow wash-in and slow wash-out type. In CEUS, the range of enhancement in malignant nodules is wider than that in two-dimensional ultrasound.

Breast Neoplasms ; diagnostic imaging ; Contrast Media ; Early Detection of Cancer ; Female ; Humans ; Ultrasonography

Objective To assess the clinical value of contrast-enhanced ultrasonography (CEUS) in early diagnosis of breast cancer. Methods CEUS was performed in 107 cases of ultrasound BI-RADS? category 3 or category 4 small breast tumors (diameter no greater than 10 mm) before surgery. The range, type and patter of enhancement of the tumor and the surrounding tissues were observed, and the time-intensity curve (TIC) was analyzed for TIC curve type, basic and peak intensity, enhancement intensity, rising slope, and enhancement intensity. The results were analyzed comparatively between benign and malignant tumors. Results The peak intensity, enhancement intensity index and peak time in CEUS were statistically significant between benign and malignant breast tumor (t=-2.310,-2.592,-2.127, P=0.021, 0.010, 0.033), and the intensity difference and rising slope also differed significantly (t=-3.422,-3.388, P=0.001, 0.001). TIC curve type, enhancement pattern, enhancement types and enhancement range were statistically significantly between benign and malignant breast tumor (P<0.001). Conclusion Benign and malignant BI-RADS? category 3 or 4 small breast tumors differ in the peak intensity, enhancement intensity index and peak time in CEUS. More nodular hyperplasia showed no enhancement in CEUS, and 97.8%of the lesions without enhancement are benign. In enhanced breast nodules, malignant breast lesions show more quick wash-in and wash-out type and quick wash-in and slow wash-out type, and the latter is more common;benign lesions often show a slow wash-in and slow wash-out type. In CEUS, the range of enhancement in malignant nodules is wider than that in two-dimensional ultrasound.

Objective To assess the clinical value of contrast-enhanced ultrasonography (CEUS) in early diagnosis of breast cancer. Methods CEUS was performed in 107 cases of ultrasound BI-RADS? category 3 or category 4 small breast tumors (diameter no greater than 10 mm) before surgery. The range, type and patter of enhancement of the tumor and the surrounding tissues were observed, and the time-intensity curve (TIC) was analyzed for TIC curve type, basic and peak intensity, enhancement intensity, rising slope, and enhancement intensity. The results were analyzed comparatively between benign and malignant tumors. Results The peak intensity, enhancement intensity index and peak time in CEUS were statistically significant between benign and malignant breast tumor (t=-2.310,-2.592,-2.127, P=0.021, 0.010, 0.033), and the intensity difference and rising slope also differed significantly (t=-3.422,-3.388, P=0.001, 0.001). TIC curve type, enhancement pattern, enhancement types and enhancement range were statistically significantly between benign and malignant breast tumor (P<0.001). Conclusion Benign and malignant BI-RADS? category 3 or 4 small breast tumors differ in the peak intensity, enhancement intensity index and peak time in CEUS. More nodular hyperplasia showed no enhancement in CEUS, and 97.8%of the lesions without enhancement are benign. In enhanced breast nodules, malignant breast lesions show more quick wash-in and wash-out type and quick wash-in and slow wash-out type, and the latter is more common;benign lesions often show a slow wash-in and slow wash-out type. In CEUS, the range of enhancement in malignant nodules is wider than that in two-dimensional ultrasound.

OBJECTIVETo study the signaling pathways associated with lipopolysaccharide (LPS)-induced inflammation in islet micro-endothelial cells (IMECs) and the mechanism of pravastatin intervention.

METHODSIMECs exposed to LPS, SB203580, pravastatin, or SB203580+pravastatin were examined for cell apoptosis with Hoechst staining and flow cytometry and for expression levels of total-p38, photophosphorylation-p38 (p-p38) and iNOS with Western blotting.

RESULTSThe apoptosis rate and expression levels of total-p38, p-p38, iNOS in IMECs all increased after LPS exposure. Pravastatin, SB203580, and their combination significantly attenuated LPS-induced enhancement of cell apoptosis and total-p38, p-p38, and iNOS expressions in IMECs.

CONCLUSIONLPS-induced inflammatory toxicity in IMECs is associated with the activation of P38MAPK and iNOS/NO signaling pathways. Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve the cell inflammatory injuries.

Animals ; Apoptosis ; Endothelial Cells ; drug effects ; metabolism ; Endothelium, Vascular ; cytology ; Inflammation ; Islets of Langerhans ; blood supply ; MAP Kinase Signaling System ; drug effects ; Mice ; Nitric Oxide Synthase Type II ; metabolism ; Phosphorylation ; Pravastatin ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; metabolism