Purpose To investigate the relationship between the expression of Syk,VEGF-C and lymph node metastasis in breast carcinoma.Methods Immunohistochemical EnVision and SP methods were used to detect the expression of Syk,NFκB(p65)and VEGF-C in 55 cases of breast carcinoma.Results The positive rates of Syk, VEGF-C and NFκB(p65)in 55 cases of breast carcinoma were 50.9%,56.4% and 81.8%,respectively.Lower positive rate of Syk was obtained in the group of positive lymph-node metastasis than that in the group of non-lymph-node metastasis (P<0.05);Higher positive rate of VEGF-C was obtained in the group of positive lymph-node metastasis than that in the group of non-lymph-node metastasis (P<0.05);But no significant differences was found in p65(P>0.75).Higher positive rate of p65 nuclear expression was obtained in the group of positive lymph-node metastasis than that in the group of non-lymph-node metastasis (P＜0.025).The expression of Syk was negatively associated with VEGF-C (r=-0.620,P=0.000);the nuclear expression of p65 was associated with the low expression of Syk(r=0.448,P=0.002)and the high expression of VEGF-C (r=0.310,P=0.036).Conclusions In breast carcinoma, Syk may downregulate the expression of VEGF-C by inhibiting the activation of NFκB, which suppresses the lymph node metastasis of the cancer.

Objective:This paper designs to analyze compensation patterns and compensation effects of cata-strophic disease insurance in L City, and put forward feasible suggestions to improve the compensation patterns of cat-astrophic disease insurance. Methods:We combined the relevant policy documents to analyze compensation patterns, and used benefit rate, OOP and The effective reimbursement rate to analyze compensation effects of catastrophic dis-ease insurance. Results:Catastrophic disease insurance benefit rate in L city in 2013 was 3. 2%; Rates of NCMS fund unilization was 92%, which diversed from county to county. Patients' OOP decreased significantly after reim-bursement of catastrophic disease insurance;Catastrophic disease insurance and NCMS total effective reimbursement rate reached 84.8%;The NCMS compensation rate reached 68. 9%, while fund incurred a financial deficit at the same time. Conclusion:Set deductibles, compensation rate and compensation range scientifically, and cancel ceiling level,improve the program of catastrophic disease insurance. Take measures to reduce the unfair between the districts and counties at city level. Establish effective link-up between catastrophic disease insurance and NCMS.

10.3969/j.issn.1008-9691.2013.03.015

OBJECTIVETo study the effect of the synthetic peptide RGDSY-CTTHWGFTLC on the biological behavior of breast cancer MCF-7 cells in vitro.

METHODSMCF-7 cells were incubated with different concentrations of the synthesized peptide RGDSY-CTTHWGFTLC (RGDSY-CTT), the positive control peptide CTTHWGFTLC (CTT), or the negative control peptide STTHWGFTLS (STT) in fibronectin-coated 96-well plates for different time lengths, and the changes in cell adhesion, invasiveness, proliferation, apoptosis and cell cycle were detected using Transwell chamber assay, MTT assay, and flow cytometry.

RESULTSIncubation of the cells with 50, 100 and 200 µg/ml of RGDSY-CTT caused a significant concentration- dependent inhibition of the cell adhesion (cell adhesion rates of 85.1%, 74.1% and 63.8%, respectively) with stronger effects than CTT (P<0.05). At 100 and 200 µg/ml, RGDSY-CTT significantly inhibited the invasion (with inhibition rate of 41.8% and 63.9%, respectively) of MCF-7 cells with an effect similar to that by CTT (P>0.05). At 50, 100 and 200 µg/ml, RGDSY-CTT concentration-dependently suppressed MCF-7 cell proliferation (with cell proliferation rates of 98.8%, 82.4% and 63.0%, respectively), and this inhibitory effect was stronger than that of CTT at 100 and 200 µg/ml (P<0.05). The results of flow cytometry also demonstrated a stronger apoptosis-inducing effect of RGDSY-CTT (76.7%) than that in CTT, STT and the blank control groups (P<0.05).

CONCLUSIONSRGDSY-CTT can inhibit cell invasion, suppress adhesion and proliferation, and induce apoptosis in MCF-7 cells.

Apoptosis ; drug effects ; Cell Adhesion ; Cell Proliferation ; drug effects ; Female ; Humans ; MCF-7 Cells ; Peptides, Cyclic ; chemical synthesis ; pharmacology

Objective To study the effect of the synthetic peptide RGDSY-CTTHWGFTLC on the biological behavior of breast cancer MCF-7 cells in vitro. Methods MCF-7 cells were incubated with different concentrations of the synthesized peptide RGDSY-CTTHWGFTLC (RGDSY-CTT), the positive control peptide CTTHWGFTLC (CTT), or the negative control peptide STTHWGFTLS (STT) in fibronectin-coated 96-well plates for different time lengths, and the changes in cell adhesion, invasiveness, proliferation, apoptosis and cell cycle were detected using Transwell chamber assay, MTT assay, and flow cytometry. Results Incubation of the cells with 50, 100 and 200 μg/ml of RGDSY-CTT caused a significant concentration-dependent inhibition of the cell adhesion (cell adhesion rates of 85.1%, 74.1% and 63.8%, respectively) with stronger effects than CTT (P<0.05). At 100 and 200μg/ml, RGDSY-CTT significantly inhibited the invasion (with inhibition rate of 41.8%and 63.9%, respectively) of MCF-7 cells with an effect similar to that by CTT (P>0.05). At 50, 100 and 200 μg/ml, RGDSY-CTT concentration-dependently suppressed MCF-7 cell proliferation (with cell proliferation rates of 98.8%, 82.4% and 63.0%, respectively), and this inhibitory effect was stronger than that of CTT at 100 and 200 μg/ml (P<0.05). The results of flow cytometry also demonstrated a stronger apoptosis-inducing effect of RGDSY-CTT (76.7%) than that in CTT, STT and the blank control groups (P<0.05). Conclusions RGDSY-CTT can inhibit cell invasion, suppress adhesion and proliferation, and induce apoptosis in MCF-7 cells.

Objective To study the effect of the synthetic peptide RGDSY-CTTHWGFTLC on the biological behavior of breast cancer MCF-7 cells in vitro. Methods MCF-7 cells were incubated with different concentrations of the synthesized peptide RGDSY-CTTHWGFTLC (RGDSY-CTT), the positive control peptide CTTHWGFTLC (CTT), or the negative control peptide STTHWGFTLS (STT) in fibronectin-coated 96-well plates for different time lengths, and the changes in cell adhesion, invasiveness, proliferation, apoptosis and cell cycle were detected using Transwell chamber assay, MTT assay, and flow cytometry. Results Incubation of the cells with 50, 100 and 200 μg/ml of RGDSY-CTT caused a significant concentration-dependent inhibition of the cell adhesion (cell adhesion rates of 85.1%, 74.1% and 63.8%, respectively) with stronger effects than CTT (P<0.05). At 100 and 200μg/ml, RGDSY-CTT significantly inhibited the invasion (with inhibition rate of 41.8%and 63.9%, respectively) of MCF-7 cells with an effect similar to that by CTT (P>0.05). At 50, 100 and 200 μg/ml, RGDSY-CTT concentration-dependently suppressed MCF-7 cell proliferation (with cell proliferation rates of 98.8%, 82.4% and 63.0%, respectively), and this inhibitory effect was stronger than that of CTT at 100 and 200 μg/ml (P<0.05). The results of flow cytometry also demonstrated a stronger apoptosis-inducing effect of RGDSY-CTT (76.7%) than that in CTT, STT and the blank control groups (P<0.05). Conclusions RGDSY-CTT can inhibit cell invasion, suppress adhesion and proliferation, and induce apoptosis in MCF-7 cells.

Background: and Purpose CGG repeat expansion in the 5' untranslated region (5'UTR) of the Notch 2 N-terminal-like C gene (NOTCH2NLC) has been associated with neuronal intranuclear inclusion disease (NIID) and oculopharyngodistal myopathy type 3 (OPDM3). Few OPDM3 patients have been reported. This report describes two OPDM3 patients with novel imaging findings who presented the typical features of NIID, and reviews all OPDM3 cases available in the literature. Methods: The available clinical, imaging, and pathological information was reviewed and investigated. CGG repeat expansion in the 5'UTR of NOTCH2NLC was tested using the repeatprimed polymerase chain reaction (PCR), followed by the fluorescence amplicon-length PCR to determine the number of CGG repeats. Results: Our two OPDM3 patients and most patients reported in the literature developed the typical clinical characteristics of NIID, including leukoencephalopathy, peripheral neuropathy, cognitive deterioration, pigmentary retinopathy, ataxia, tremor, acute encephalitis-like episodes, pigmentary retinopathy, miosis, and sensorineural hearing loss. In addition to typical imaging findings of NIID, our two patients exhibited diffusion weighted imaging (DWI) hyperintensities in the middle cerebellar peduncles, which have not been described previously. Muscle biopsies revealed rimmed vacuoles and p62-positive intranuclear inclusions in the myofibers in both patients. The skin biopsy performed in one patient detected typical eosinophilic intranuclear inclusions. Genetic analysis identified CGG repeat expansion in NOTCH2NLC as the causative mutation in the two patients. Conclusions Our two patients with OPDM3 had clinical characteristics of NIID and exhibited DWI abnormality in the cerebellum. Our results indicate that OPDM3 is within the spectrum of NIID and that DWI hyperintensities in the cerebellum are helpful for diagnosing NIID or OPDM3.

Background: and Purpose CGG repeat expansion in the 5' untranslated region (5'UTR) of the Notch 2 N-terminal-like C gene (NOTCH2NLC) has been associated with neuronal intranuclear inclusion disease (NIID) and oculopharyngodistal myopathy type 3 (OPDM3). Few OPDM3 patients have been reported. This report describes two OPDM3 patients with novel imaging findings who presented the typical features of NIID, and reviews all OPDM3 cases available in the literature. Methods: The available clinical, imaging, and pathological information was reviewed and investigated. CGG repeat expansion in the 5'UTR of NOTCH2NLC was tested using the repeatprimed polymerase chain reaction (PCR), followed by the fluorescence amplicon-length PCR to determine the number of CGG repeats. Results: Our two OPDM3 patients and most patients reported in the literature developed the typical clinical characteristics of NIID, including leukoencephalopathy, peripheral neuropathy, cognitive deterioration, pigmentary retinopathy, ataxia, tremor, acute encephalitis-like episodes, pigmentary retinopathy, miosis, and sensorineural hearing loss. In addition to typical imaging findings of NIID, our two patients exhibited diffusion weighted imaging (DWI) hyperintensities in the middle cerebellar peduncles, which have not been described previously. Muscle biopsies revealed rimmed vacuoles and p62-positive intranuclear inclusions in the myofibers in both patients. The skin biopsy performed in one patient detected typical eosinophilic intranuclear inclusions. Genetic analysis identified CGG repeat expansion in NOTCH2NLC as the causative mutation in the two patients. Conclusions Our two patients with OPDM3 had clinical characteristics of NIID and exhibited DWI abnormality in the cerebellum. Our results indicate that OPDM3 is within the spectrum of NIID and that DWI hyperintensities in the cerebellum are helpful for diagnosing NIID or OPDM3.

Background: and Purpose CGG repeat expansion in the 5' untranslated region (5'UTR) of the Notch 2 N-terminal-like C gene (NOTCH2NLC) has been associated with neuronal intranuclear inclusion disease (NIID) and oculopharyngodistal myopathy type 3 (OPDM3). Few OPDM3 patients have been reported. This report describes two OPDM3 patients with novel imaging findings who presented the typical features of NIID, and reviews all OPDM3 cases available in the literature. Methods: The available clinical, imaging, and pathological information was reviewed and investigated. CGG repeat expansion in the 5'UTR of NOTCH2NLC was tested using the repeatprimed polymerase chain reaction (PCR), followed by the fluorescence amplicon-length PCR to determine the number of CGG repeats. Results: Our two OPDM3 patients and most patients reported in the literature developed the typical clinical characteristics of NIID, including leukoencephalopathy, peripheral neuropathy, cognitive deterioration, pigmentary retinopathy, ataxia, tremor, acute encephalitis-like episodes, pigmentary retinopathy, miosis, and sensorineural hearing loss. In addition to typical imaging findings of NIID, our two patients exhibited diffusion weighted imaging (DWI) hyperintensities in the middle cerebellar peduncles, which have not been described previously. Muscle biopsies revealed rimmed vacuoles and p62-positive intranuclear inclusions in the myofibers in both patients. The skin biopsy performed in one patient detected typical eosinophilic intranuclear inclusions. Genetic analysis identified CGG repeat expansion in NOTCH2NLC as the causative mutation in the two patients. Conclusions Our two patients with OPDM3 had clinical characteristics of NIID and exhibited DWI abnormality in the cerebellum. Our results indicate that OPDM3 is within the spectrum of NIID and that DWI hyperintensities in the cerebellum are helpful for diagnosing NIID or OPDM3.

Small cell lung cancer (SCLC) is a neuroendocrine tumor with fast progression, high malignancy, easy recurrence, and extremely poor prognosis. In the past 30 years, the clinical treatment strategy of SCLC has been mainly chemotherapy and radiotherapy, but the curative effect is not significant; the current immunotherapy of SCLC has gradually entered the clinic and has made certain progress. Tumor immunotherapy includes immune checkpoint inhibitors, tumor vaccines, cytokines, chimeric antigen receptor T-cell immunotherapy (CAR-T) therapy, etc. Currently, immune checkpoint inhibitors are the most widely used. This article summarizes the principles of immune checkpoint inhibitors and related drugs, summarizes their domestic and foreign clinical trials progress in SCLC treatment, reviews the biomarkers used in the therapy, and discusses its future development direction.
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Cancer Vaccines/therapeutic use* ; Clinical Trials as Topic ; Humans ; Immune Checkpoint Inhibitors ; Immunotherapy ; Lung Neoplasms/drug therapy* ; Small Cell Lung Carcinoma/drug therapy*