目的:探讨高频喷射通气(HFJV)在胸部创伤后低氧血症的治疗作用。方法:回顾性分析40例胸部创伤引起的低氧血症的抢救治疗措施及其疗效。结果:胸部创伤后低氧血症患者采用无创HFJVV治疗,治疗后24 h PaO2、Pa-CO2、SpO2较治疗前均明显改善...目的:探讨高频喷射通气(HFJV)在胸部创伤后低氧血症的治疗作用。方法:回顾性分析40例胸部创伤引起的低氧血症的抢救治疗措施及其疗效。结果:胸部创伤后低氧血症患者采用无创HFJVV治疗,治疗后24 h PaO2、Pa-CO2、SpO2较治疗前均明显改善,差异有统计学意义(P<0.01),但对血流动力学(MAP、HR、CVP)无明显影响,以PaO2增加>10 mm Hg作为有效的标准,36例(90%)有效。结论:及时应用无创HFJV能改善胸部创伤后低氧血症,同时减轻患者的痛苦,易于患者接受。展开更多
AIM： To investigate the expression of survivin during the early stages of hepatocellular cardnoma （HCC）.METHODS： Immunohistochemical expression of survivin in liver tumor and non-tumor tissue specimens taken from ...AIM： To investigate the expression of survivin during the early stages of hepatocellular cardnoma （HCC）.METHODS： Immunohistochemical expression of survivin in liver tumor and non-tumor tissue specimens taken from 17 patients was compared. In addition, to determine the survivin expression in response to anticancer drugs in early stage HCC, the survivin expression was determined after the treatment of the HCC cells with anti-cancer drugs under hypoxic culture conditions.RESULTS： Survivin proteins were expressed in 64.7% of cells in early HCC specimens. A correlation between the survivin expression rate in the peritumoral hepatocytes and the rate of expression in the HCC specimens （low-rate group vs high-rate group） was observed. The survivin protein concentration in HCC cells was increased by the combination of hypoxia and anti-cancer drugs.CONCLUSION： This study suggests that survivin could be used as a therapeutic target in early HCC.展开更多
AIM: To investigate the combined effects of K-ras antisense oligodeoxynucleotide (K-ras ASODN) specif ic to GTT point mutation at codon 12 and type Ⅰ insulin-like growth factor receptor (IGF-IR) antisense oligodeoxyn...AIM: To investigate the combined effects of K-ras antisense oligodeoxynucleotide (K-ras ASODN) specif ic to GTT point mutation at codon 12 and type Ⅰ insulin-like growth factor receptor (IGF-IR) antisense oligodeoxynucleotide (IGF-IR ASODN) on proliferation and apoptosis of human pancreatic cancer Patu8988 cells in vitro and in vivo. METHODS: K-ras gene point mutation and its style at codon 12 of human pancreatic cancer cell line Patu8988 were detected by using polymerase chain reaction with special sequence primers (PCR-SSP) and sequence analysis. According to the mutation style, K-ras mutation ASODN specifi c to K-ras point mutation at codon 12 was designed and composed. After K-ras ASODN and IGF-IR ASODN treated on Patu8988 cells respectively or cooperatively, the proliferation and morphological change of Patu8988 cells were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony forming assay andtransmission electron microscopy; the expression of K-ras and IGF-IR mRNA and protein in the treated cells was measured by reverse-transcript polymerase chain reaction (RT-PCR) and flow cytometry respectively; apoptosis was determined by flow cytometry. The combined antitumor activity of K-ras ASODN and IGF-IR ASODN was evaluated in BALB/c nude mice bearing human pancreatic cancer inoculated with Patu8988 cells. RESULTS: The results of PCR-SSP and sequence analysis showed that the human pancreatic cancer cell line Patu8988 had point mutation at codon 12, and the mutation style was GGT→GTT. 2-32 μg/mL K-ras ASODN and 2-32 μg/mL IGF-IR ASODN could inhibit Patu8988 cells' growth, induce apoptosis and decrease the expression of K-ras and IGF-IR mRNA and protein alone. However, there was much more effective inhibition of growth and induction of apoptosis by their combination than by each one alone. In tumor bearing mice, the combination of K-ras ASODN and IGF-IR ASODN showed a signif icant inhibitory effect on the growth of transplanted pancreatic cancer, resulting in a statistically signif icant difference compared with each alone. CONCLUSION: It has been found that K-ras ASODN combined with IGF-IR ASODN could cooperatively inhibit the growth of Patu8988 cells, and induce their apoptosis via reinforcing specific down regulation of K-ras and IGF-IR mRNA and protein expression.展开更多
文摘目的:探讨高频喷射通气(HFJV)在胸部创伤后低氧血症的治疗作用。方法:回顾性分析40例胸部创伤引起的低氧血症的抢救治疗措施及其疗效。结果:胸部创伤后低氧血症患者采用无创HFJVV治疗,治疗后24 h PaO2、Pa-CO2、SpO2较治疗前均明显改善,差异有统计学意义(P<0.01),但对血流动力学(MAP、HR、CVP)无明显影响,以PaO2增加>10 mm Hg作为有效的标准,36例(90%)有效。结论:及时应用无创HFJV能改善胸部创伤后低氧血症,同时减轻患者的痛苦,易于患者接受。
文摘AIM： To investigate the expression of survivin during the early stages of hepatocellular cardnoma （HCC）.METHODS： Immunohistochemical expression of survivin in liver tumor and non-tumor tissue specimens taken from 17 patients was compared. In addition, to determine the survivin expression in response to anticancer drugs in early stage HCC, the survivin expression was determined after the treatment of the HCC cells with anti-cancer drugs under hypoxic culture conditions.RESULTS： Survivin proteins were expressed in 64.7% of cells in early HCC specimens. A correlation between the survivin expression rate in the peritumoral hepatocytes and the rate of expression in the HCC specimens （low-rate group vs high-rate group） was observed. The survivin protein concentration in HCC cells was increased by the combination of hypoxia and anti-cancer drugs.CONCLUSION： This study suggests that survivin could be used as a therapeutic target in early HCC.
基金Social development foundation of Suzhou, China, No. SZD0614Young teacher foundation of Soochow UniversityFoundation of health department of Jiangsu Province, China, No. Z200622
文摘AIM: To investigate the combined effects of K-ras antisense oligodeoxynucleotide (K-ras ASODN) specif ic to GTT point mutation at codon 12 and type Ⅰ insulin-like growth factor receptor (IGF-IR) antisense oligodeoxynucleotide (IGF-IR ASODN) on proliferation and apoptosis of human pancreatic cancer Patu8988 cells in vitro and in vivo. METHODS: K-ras gene point mutation and its style at codon 12 of human pancreatic cancer cell line Patu8988 were detected by using polymerase chain reaction with special sequence primers (PCR-SSP) and sequence analysis. According to the mutation style, K-ras mutation ASODN specifi c to K-ras point mutation at codon 12 was designed and composed. After K-ras ASODN and IGF-IR ASODN treated on Patu8988 cells respectively or cooperatively, the proliferation and morphological change of Patu8988 cells were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony forming assay andtransmission electron microscopy; the expression of K-ras and IGF-IR mRNA and protein in the treated cells was measured by reverse-transcript polymerase chain reaction (RT-PCR) and flow cytometry respectively; apoptosis was determined by flow cytometry. The combined antitumor activity of K-ras ASODN and IGF-IR ASODN was evaluated in BALB/c nude mice bearing human pancreatic cancer inoculated with Patu8988 cells. RESULTS: The results of PCR-SSP and sequence analysis showed that the human pancreatic cancer cell line Patu8988 had point mutation at codon 12, and the mutation style was GGT→GTT. 2-32 μg/mL K-ras ASODN and 2-32 μg/mL IGF-IR ASODN could inhibit Patu8988 cells' growth, induce apoptosis and decrease the expression of K-ras and IGF-IR mRNA and protein alone. However, there was much more effective inhibition of growth and induction of apoptosis by their combination than by each one alone. In tumor bearing mice, the combination of K-ras ASODN and IGF-IR ASODN showed a signif icant inhibitory effect on the growth of transplanted pancreatic cancer, resulting in a statistically signif icant difference compared with each alone. CONCLUSION: It has been found that K-ras ASODN combined with IGF-IR ASODN could cooperatively inhibit the growth of Patu8988 cells, and induce their apoptosis via reinforcing specific down regulation of K-ras and IGF-IR mRNA and protein expression.
