278 research outputs found
Metformin promotes apoptosis of A549 cells via regulation of p-AMPK protein expression, bax/bcl-2 ratio and ROS levels
Purpose: To investigate the influence of metformin on apoptosis of pulmonary carcinoma cells (A549), and the associated mode of action.Methods: Pulmonary carcinoma cells in logarithmic growth phase were treated with graded concentrations of metformin, and the anti-proliferative and apoptotic effects of the drug were measured using MTT assay and flow cytometry, respectively. The levels of reactive oxygen species (ROS) in A549 cell suspension were determined with 2, 7- dihydrodichlorofluorescein diacetate (DCFH-DA) assay. The expression levels of phosphorylated AMP-activated protein kinase (p-AMPK), mammalian target of rapamycin (mTOR), and bax/bcl-2 ratio were measured using Western blotting and real-time fluorescence quantitative polymerase chain reaction (qRT-PCR).Results: Metformin significantly promoted A549 cell apoptosis, but suppressed its proliferative potential in a dose- and time-based fashion. The levels of ROS, superoxide anion and MDA in A549 cells were significantly and dose-dependently increased by metformin (p < 0.05). Moreover, metformin markedly upregulated the mRNA and protein expressions of p-AMPK as well as bax/bcl-2 ratio, but had no impact on the expression level of mTOR (p < 0.05).Conclusion: Metformin promotes apoptosis in A549 cells via regulation of p-AMPK protein expression, bax/bcl-2 ratio, and ROS levels, and hence may play a role in lung cancer therapy
Metastatic Renal Cell Carcinoma to the Parotid Gland in the Setting of Chronic Lymphocytic Leukemia
Renal cell carcinoma (RCC) is infamous for its unpredictable behavior and metastatic potential. We report a case of a patient with a complex history of multifocal renal cell carcinoma and chronic lymphocytic leukemia (CLL), who subsequently developed a parotid mass. Total parotidectomy revealed this mass to be an additional site of metastasis which had developed 19 years after his initial diagnosis of RCC
Placental Chorangiosis: Increased Risk for Cesarean Section
We describe a patient with Class C diabetes who presented for nonstress testing at 36 weeks and 4 days of gestation with nonreassuring fetal heart tones (NRFHT) and oligohydramnios. Upon delivery, thrombosis of the umbilical cord was grossly noted. Pathological analysis of the placenta revealed chorangiosis, vascular congestion, and 40% occlusion of the umbilical vein. Chorangiosis is a vascular change of the placenta that involves the terminal chorionic villi. It has been proposed to result from longstanding, low-grade hypoxia in the placental tissue and has been associated with such conditions such as diabetes, intrauterine growth restriction (IUGR), and hypertensive conditions in pregnancy. To characterize chorangiosis and its associated obstetric outcomes we identified 61 cases of chorangiosis on placental pathology at Henry Ford Hospital from 2010 to 2015. Five of these cases were omitted due to lack of complete records. Among the 56 cases, the cesarean section rate was 51%, indicated in most cases for nonreassuring fetal status. Thus, we suggest that chorangiosis, a marker of chronic hypoxia, is associated with increased rates of cesarean sections for nonreassuring fetal status because of long standing hypoxia coupled with the stress of labor
Effects of different extracts of Cremastra appendiculata (D. Don) Makino Cremastra appendiculata (D. Don) Makino on apoptosis of A549 cells
Purpose: To investigate the effect of different extracts of Cremastra appendiculata (D. Don) Makino onapoptosis of A549 cells, and the underlying mechanism.Methods: The contents of colchicine in ethyl acetate and n-butanol extracts of Cremastra appendiculata(D. Don) Makino were determined using high performance liquid chromatography (HPLC). Lung cancerA549 cells cultured in vitro were divided into blank control, standard colchicine and Cremastra appendiculata (D. Don) Makino extract groups. The effect of different extract concentrations on proliferation of the cells was determined using methyl thiazolyl diphenyl-tetrazolium (MTT) assay, while apoptosis of A549 cells induced by the extracts was evaluated by flow cytometry (FC).Results: Compared with the standard colchicine group, there was no colchicine in the n-butanol and ethyl acetate extracts of Cremastra appendiculata. Results from MTT assay showed that the extract inhibited the proliferation of A549 cells (p < 0.05). Flow cytometry results showed that ethyl acetate extract significantly enhanced apoptosis in A549 cells (p < 0.05). However, n-butanol extract had no significant effect on the apoptosis of A549 cells (p < 0.05).Conclusion: The ethyl acetate extract of Cremastra appendiculata (D. Don) Makino induces apoptosis in lung cancer A549 cells. Therefore, there is a need for further research and development of antitumor drugs from the extract of Cremastra appendiculata (D. Don) Makino.
Keywords: Cremastra appendiculata (D. Don) Makino, Colchicine, A549 cells, Apoptosi
New Insights into Interfacial Passivation on 3D Graphene–CuInS<sub>2</sub> Composites-Based Perovskite Solar Cells
Immunohistochemical identification of primary peritoneal serous cystadenocarcinoma mimicking advanced colorectal carcinoma: a case report
Primary peritoneal cystadenocarcinoma is a rare tumor of similar histogenic origin as primary ovarian carcinoma. We present a case of primary peritoneal serous cystadenocarcinoma mimicking advanced colorectal cancer in a 68 yr-old African American female. Radiology, endoscopy and cytology yielded only inconclusive findings. Immunohistochemical analysis of percutaneously obtained ascitic fluid provided a correct diagnosis of primary peritoneal cystadenocarcinoma. The discovery of serous ascites at the time of laparotomy confirmed a diagnosis of primary peritoneal serous cystadenocarcinoma. Final surgical pathology reconfirmed the diagnosis of primary peritoneal cystadenocarcinoma. This case demonstrates the utility of immunohistochemistry for accurately diagnosing patients with inconclusive findings in the setting of peritoneal carcinomatosis and primary peritoneal cystadenocarcinoma
Activation of Sirtuin 3 by Silybin Attenuates Mitochondrial Dysfunction in Cisplatin-induced Acute Kidney Injury
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