RESUMO
We investigated the relationship between claudin-1 and micro-lymphatic vessel density (MLVD) by detecting claudin-1 and protein D2-40 expression in cancer tissue specimens obtained from 97 patients with hypopharyngeal squamous cell carcinoma (HSCC). We also explored the correlation between the expression of these proteins and clinical tumor stage, pathological grading, and clinical prognosis in the patients. Moreover, we studied the mechanism of lymph node metastasis in HSCC, thereby providing information for treating HSCC and inhibiting lymph node metastasis. We detected levels of claudin-1 and protein D2-40 expression in cancer tissue from 97 patients with HSCC and para-tumor tissue from 90 patients by immunohistochemistry; we analyzed the correlation between markers and clinicopathological features by using the Pearson chi-square test and conducted survival analysis by the log-rank test. Claudin-1 expression was high in HSCC and was related to tumor differentiation and lymph node metastasis; Kaplan-Meier analysis showed that claudin-1 expression was related to patient survival rate (P = 0.012). There was a significant relationship between MLVD in the tissues adjacent to the carcinoma and the indices of histopathological grade, clinical stage, and lymph node metastasis. There was also a positive correlation between claudin-1 expression and MLVD. High expression of claudin-1 might induce the generation of tumor lymphatic vessels, which increases metastasis in the lymph node. Because claudin-1 is related to patient survival rate, it may be useful as a monitoring index for postoperative HSCC and might be a new target for treating the disease.
Assuntos
Biomarcadores Tumorais/genética , Carcinoma de Células Escamosas/diagnóstico , Claudina-1/genética , Neoplasias Hipofaríngeas/diagnóstico , Hipofaringe/metabolismo , Vasos Linfáticos/metabolismo , Idoso , Anticorpos Monoclonais Murinos/química , Biomarcadores Tumorais/metabolismo , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/mortalidade , Carcinoma de Células Escamosas/cirurgia , Claudina-1/metabolismo , Feminino , Expressão Gênica , Humanos , Neoplasias Hipofaríngeas/genética , Neoplasias Hipofaríngeas/mortalidade , Neoplasias Hipofaríngeas/cirurgia , Hipofaringe/patologia , Hipofaringe/cirurgia , Linfonodos/metabolismo , Linfonodos/patologia , Metástase Linfática , Vasos Linfáticos/patologia , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Estadiamento de Neoplasias , Prognóstico , Análise de SobrevidaRESUMO
We studied the activity of matrix metalloproteinases (MMP) 2 and 9 generated by cultured rabbit corneal epithelium cells that had been stimulated with tumor necrosis factor alpha (TNF-α), to investigate the possible regulative mechanisms of MMP-2/9 and their potential effect on corneal inflammatory diseases. The rabbit corneal epithelium cells were cultured in vitro and incubated with different concentrations of TNF-α (0, 1, 10, and 100 ng/mL) for 24 h. The activity of MMP-2/9 was examined using gelatin zymography. The results were analyzed by computer image analysis and statistical tests. TNF-α stimulated the secretion of MMP-2/9 in a dose-dependent manner, and MMP-2 was activated by TNF-α. Inflammatory factors such as TNF-α can stimulate MMP-2/9 activity in corneal epithelium cells. This may be a potential manipulating mechanism of MMP expression in the pathogenesis of corneal diseases, and could play an important role in the prevention and treatment of corneal inflammatory diseases.
Assuntos
Doenças da Córnea/genética , Epitélio Corneano/metabolismo , Metaloproteinase 2 da Matriz/biossíntese , Metaloproteinase 9 da Matriz/biossíntese , Fator de Necrose Tumoral alfa/biossíntese , Animais , Células Cultivadas , Doenças da Córnea/metabolismo , Doenças da Córnea/patologia , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Epitélio Corneano/patologia , Regulação da Expressão Gênica , Humanos , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 9 da Matriz/genética , Coelhos , Fator de Necrose Tumoral alfa/genéticaRESUMO
Isoflurane can induce widespread cytotoxicity. We hypothesized that isoflurane induces apoptosis partly by causing excessive calcium release from the endoplasmic reticulum (ER) via direct activation of inositol 1,4,5-trisphosphate receptors (IP3R). Rat pheochromocytoma cells cultured for seven days with nerve growth factor were divided into four groups: control group (C), IP3R antagonist group (X), isoflurane group (I) and isoflurane + IP3R antagonist group (I+X). Groups I and I+X were treated with 1 MAC isoflurane for 12 h. Groups X and I+X were pretreated with IP3R antagonist. Annexin V/PI apoptosis and TUNEL assays were performed to evaluate cell apoptosis. TEM was used to observe changes in cell ultrastructure. Changes in calcium concentration ([Ca(2+)]i) in the cytoplasm were measured by flow cytometry. RT-PCR was performed to evaluate IP3R mRNA expression. TEM showed that isoflurane treatment altered cell ultrastructure. Compared to group C, cell apoptosis rate and [Ca(2+)]i increased in groups I and I+X (P < 0.05). Compared to group C, IP3R mRNA expression was lower in group X and higher in group I (P < 0.05). Compared to group X, cell apoptosis rate, [Ca(2+)]i and IP3R mRNA expression increased in groups I and I+X (P < 0.05). Compared to group I, cell apoptosis rate, [Ca(2+)]i and IP3R mRNA expression decreased in group I+X (P < 0.05). These results suggest that exposure to 1 MAC isoflurane for 12 h causes excessive calcium release partly by direct activation of IP3R on the ER membrane and triggers cell apoptosis.
Assuntos
Anestésicos Inalatórios/toxicidade , Cálcio/metabolismo , Receptores de Inositol 1,4,5-Trifosfato/metabolismo , Isoflurano/toxicidade , RNA Mensageiro/metabolismo , Animais , Anexina A5/metabolismo , Apoptose/efeitos dos fármacos , Retículo Endoplasmático/efeitos dos fármacos , Retículo Endoplasmático/metabolismo , Expressão Gênica , Marcação In Situ das Extremidades Cortadas , Receptores de Inositol 1,4,5-Trifosfato/agonistas , Receptores de Inositol 1,4,5-Trifosfato/antagonistas & inibidores , Receptores de Inositol 1,4,5-Trifosfato/genética , Transporte de Íons , Compostos Macrocíclicos/farmacologia , Fator de Crescimento Neural/farmacologia , Oxazóis/farmacologia , Células PC12 , RNA Mensageiro/agonistas , RNA Mensageiro/antagonistas & inibidores , RNA Mensageiro/genética , RatosRESUMO
This study aimed to analyze the clinical application value of computed tomography (CT)-guided hook-wire positioning before thoracoscopic surgery. Eighty-four patients who had received a thoracoscopic wedge resection of pulmonary nodules between January and December 2013 were selected. Group A consisted of 38 cases where the hook-wire positioning technique was not used, and the positioning approaches were intraoperative observation and palpation. Group B consisted of 46 cases where the hook-wire positioning technique was used. The diameter of each nodule was less than 2 cm, and all patients underwent the operation within 2 h of invasive positioning. The evaluation indexes included positioning success rate, positioning-related complications, and rate of conversion to thoracotomy. In Group A, nine patients (23.68%) underwent conversion to thoracotomy; in Group B, three patients (6.52%) did. This difference was statistically significant (P < 0.05). The average operation duration was 118 ± 21 min in Group A and 53 ± 18 min in Group B. The difference between both groups was statistically significant (P < 0.05). The average length of hospital stay of patients who underwent conversion to thoracotomy was 8.7 ± 2.2 days, and of patients who underwent thoracoscopic pulmonary wedge resection was 4.5 ± 1.6 days. This difference was statistically significant (P < 0.05). Therefore, CT-guided hook-wire positioning of pulmonary nodules before thoracoscopic surgery has clinical application value. It helps to accurately locate the pulmonary nodules, effectively lowers the rate of conversion to thoracotomy, and reduces the operation duration.
Assuntos
Neoplasias Pulmonares/cirurgia , Adulto , Idoso , Feminino , Humanos , Tempo de Internação , Neoplasias Pulmonares/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Período Pré-Operatório , Cirurgia Assistida por Computador , Tomografia Computadorizada por Raios XRESUMO
Hyperglycemia is common in critical patients and high blood glucose levels have a negative effect on their prognosis. The aim of this study was to investigate the effect of hyperglycemia and glycosylated hemoglobin (GHb) in critical patients. A total of 648 critical patients were enrolled in the study and received a random blood glucose test when they entered the emergency department. If blood glucose was more than 11.1 mM, a GHb test was followed within 24 h. All patients were followed up for 28 days. According to diabetes mellitus (DM) history, GHb value, and outcome of follow-up, patients were divided into different groups, and mortality rates were calculated, respectively. Hyperglycemia was found in 67.44% (437/648) of patients, and 51.49% (225/437) and 48.51% (212/437) had normal and elevated GHb levels, respectively. At the end of the follow-up period, 14 of the normal GHb patients and 32 of the elevated GHb patients died (6.22 and 15.09%, respectively). In the normal GHb group, 53 had a DM history, 23 were newly diagnosed with DM, and 149 had hospital-related hyperglycemia (HRH); the mortality rates were 11.32% (6/53), 8.70% (2/23), and 4.03% (6/149), respectively. In the elevated GHb group, 114 had a DM history, 83 were newly diagnosed with DM, and 15 had HRH; the mortality rates were 13.16% (15/114), 19.27% (16/83), and 6.67% (1/15), respectively. Hyperglycemia and GHb might play important roles in the prognosis and assessment for critical patients, and the prognosis would vary according to the different causes of hyperglycemia.