Objective According to the changes of microcirculation in the pulmonary cancers, the treatment effect was evaluated after the vascular interventional therapy.Methods Angiography of 138 primary pulmonary carcinomas, and the feeding arteries were performed. Areas of mass blush were measured for 81 cases before and after therapy. The tumour blush was considered to be the imaging appearance of the microcirculation of the lung carcinoma. The angiographic images were collected by digital image system (DSA and movie). Results (1) The rate of the tumour blush appearance was 88.8% in this group. (2) The areas of the lung carcinoma blush in 81 cases before and after therapy were (941.4?73.2)mm 2 and (427.9? 93.8 )mm 2( P

Adult ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Medicine, Chinese Traditional ; Phytotherapy ; Pre-Eclampsia ; drug therapy ; Pregnancy ; Research Design

Adolescent ; Case-Control Studies ; Child ; Child, Preschool ; Heart Defects, Congenital ; blood ; immunology ; Humans ; Infant ; Lymphocyte Subsets ; Th1 Cells ; immunology ; Th2 Cells ; immunology

Objective To study the localization of Smad 2 and Smad 4 proteins, which are intracellular signaling molecules of transforming growth factor ? family in adult rat testis. Method Immunohistochemical ABC method with glucose oxidase DAB nickel enhancement technique was used in the present study. Results Smad 2 immunoreactivity was mainly located in the spermatogonia, spermatocytes, spermatids, Sertoli cells in the seminiferous tubule and Leydig cells in the interstitial tissue. The reactive substance distributes in cytoplasm with negative nuclei. While Smad 4 is mainly expressed in cytoplasm of Leydig cells, and Sertoli cells is weak stained. Conclusion Our findings of Smad 2 expression in spermatogenic cells and Smad 4 expression in Leydig cells provide direct evidence for the molecular mechanism of TGF ? action during spermatogenesis.

Child ; Encephalitis, Viral ; pathology ; Enterovirus A, Human ; Enterovirus Infections ; complications ; Heart Failure ; etiology ; Humans ; Respiratory Insufficiency ; etiology

Epilepsy ; genetics ; Humans ; Mutation ; NAV1.1 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins ; genetics ; Sodium Channels ; genetics

Drugs, Chinese Herbal ; chemistry ; Humans ; Isoflavones ; isolation & purification ; pharmacology ; Phytoestrogens ; Plant Preparations ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Platelet Aggregation Inhibitors ; isolation & purification ; pharmacology ; Pueraria ; chemistry ; Scutellaria baicalensis ; chemistry

Adult ; Chronic Periodontitis ; diagnosis ; diagnostic imaging ; therapy ; Combined Modality Therapy ; Dental Implantation ; Dental Scaling ; Female ; Follow-Up Studies ; Guided Tissue Regeneration, Periodontal ; Humans ; Orthodontics, Corrective ; Radiography, Panoramic ; Tooth Loss ; diagnosis ; diagnostic imaging ; surgery ; Toothbrushing

Acrylonitrile ; poisoning ; Adult ; Female ; Humans ; Male ; Middle Aged ; Young Adult

Objective:To investigate the mechanism of endoplasmic reticulum (ER) stress-induced chemoresistance to cisplatin in gastric cancer cells. Methods:ER stress models were established in both BGC823 and SGC7901 gastric cancer cells. The expression of GRP78, an ER stress marker, was examined by Western blot analysis. Moreover, whether ER stress can decrease the sensitivity of gastric cancer cells to cisplatin and activate P38 was explored by flow cytometry and Western blot analysis, respectively. Whether ER stress-induced chemoresistance to cisplatin can be abrogated by blocking P38 activity in gastric cancer was also elucidated using flow cytometry. Results:GRP78 protein expression markedly increased after treating BGC823 and SGC7901 gastric cancer cells with tunica-mycin (TM) or thapsigargin (TG) for 8, 16, and 24 h (P<0.05), compared with that in the group treated for 0 h. The apoptotic rates of TM-(or TG)-, cisplatin-, and TM (or TG) plus cisplatin-treated groups significantly increased (P<0.05) in both BGC823 and SGC7901 gastric cancer cells compared with the rate in the control group. The apoptotic rate of TM (or TG) plus cisplatin-treated group signifi-cantly decreased (P<0.05) in both BGC823 and SGC7901 gastric cancer cells compared with that of the cisplatin-treated group. Com-pared with the group treated for 0 h, phospho-P38 expression markedly increased after treating BGC823 and SGC7901 gastric cancer cells with TM (or TG) for 8, 16, and 24 h (P<0.05). No difference in P38 protein expression was observed between each group in both BGC823 and SGC7901 gastric cancer cells (P>0.05). Both P38 inhibitors, either SB203580 or PD169316, can inhibit the activation of P38. The inhibition of P38 activity can overcome ER stress-induced chemoresistance to cisplatin in gastric cancer cells (P<0.05). Con-clusion:ER stress can trigger the chemoresistance to cisplatin by activating P38 in gastric cancer cells.