Severe pneumonia associated with sepsis-induced myopathy: one case report and literature review / 中国感染控制杂志

Clinical data of one patient with sepsis-induced myopathy (SIM) who was successfully treated were reviewed retrospectively, analysis was conducted combined with the relevant literatures. Patient was a middle-aged woman without underlying disease, she was admitted to hospital because of fever, cough, chest tightness and shortness of breath, during the treatment period, type II respiratory failure occurred repeatedly, and it was difficult in withdrawing respirator, patient was finally diagnosed with SIM. After anti-infective treatment and rehabilitation training, she was successfully withdrawn respirator, muscle strength was recovered. This case suggests that SIM can be completely cured through early identification, neuromuscular nutrition therapy, graded rehabilitation training and lung rehabilitation therapy.

Inhibition of nuclear factor-κB activity enhanced chemosensitivity to cisplatin in human lung adeno-carcinoma A549 cells under chemical hypoxia conditions / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tumor hypoxia, one of the features of solid tumors, is associated with chemo-resistance. Recently, nuclear factor-κB (NF-κB) was found to be activated during hypoxia. However, the impact of NF-κB activation on chemo-resistance during hypoxia remains unknown.</p><p><b>METHODS</b>Human lung adenocarcinoma A549 cells were transfected with NF-κB p65siRNA and treated with cobalt chloride (CoCl2) to mimic hypoxia in the presence or absence of cisplatin. NF-κB expression was measured by Western blotting, immune-fluorescence and real-time PCR. Hypoxia-inducible factor-1α (HIF-1α) and Bcl-2 expression were determined by Western blotting. Cell apoptosis and survival with half-maximum inhibitory concentration (IC50) of cisplatin were determined by Annexin V-FITC/PI and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), respectively.</p><p><b>RESULTS</b>Exposure of A549 cells to CoCl2 increased nuclear HIF-1a protein expression, and enhanced NF-κB p65 protein nuclear accumulation (the mark of NF-κB activation) in a time and dose dependant manner. CoCl2 did not promote apoptosis in A549 cells; on the contrary, it reduced cisplatin-induced apoptosis and increased the IC50 of cisplatin. However, when we inhibited CoCl2-induced activation of NF-κB through NF-κB p65siRNA, cisplatin-induced apoptosis was increased and IC50 of cisplatin was reduced to levels similar to those in control cells. Meanwhile, CoCl2-induced Bcl-2 overexpression was down-regulated in the presence of cisplatin when NF-κB activity was inhibited.</p><p><b>CONCLUSION</b>Up-regulating Bcl-2 might be involved in NF-κB activation induced resistance to cisplatin in A549 cells under CoCl2-induced chemical hypoxia.</p>

Study on the relationship between the polymorphism of p53 gene intron 7 and non-small cell lung cancer (NSCLC) and p53 mutation in NSCLC tissues / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between p53 gene intron 7 polymorphism and non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>One hundred and five patients with NSCLC and 100 controls were selected with case-control analysis. Polymerase chain reaction (PCR), Apa I restriction enzyme digestion and agarose gel electrophoretic separation were used to identify genotypes of p53 intron 7 in peripheral blood. Then, NSCLC biopsy tissues (n=64) and NSCLC paraffin-embedded tissues (n=40) were selected for mutation analysis. PCR products of p53 exons 5-8 were sequenced on an automated sequencer following the identification of intron 7 genotypes as previously described.</p><p><b>RESULTS</b>In NSCLC patients, the homozygote positive for ApaI site in p53 intron 7 was 23.8%, the homozygote negative was 12.34%, and the heterozygote was 63.8%. Whereas in control group, the homozygote positive, the homozygote negative and the heterozygote were 44.0%, 11.0% and 45.0%, respectively (P<0.01). In the second part, mutation rate of p53 exons 5-8 was 20.0%, 50.0% and 52.9% in samples with ApaI positive, negative and heterozygotes, respectively (P<0.05).</p><p><b>CONCLUSION</b>p53 intron 7 ApaI polymorphism may be associated with human NSCLC.</p>

p53 gene intron 7 polymorphism and its association with oral neoplasms / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the association between oral neoplasm genetic susceptibility and genetic polymorphism of p53 intron 7.</p><p><b>METHODS</b>The intron 7 ApaI polymorphism of p53 was analyzed in 95 oral neoplasm patients and 105 healthy individuals by utilizing polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping assay technique, and direct sequencing was performed in 30 cases which were selected from the patients and controls by random sampling.</p><p><b>RESULTS</b>In oral neoplasms cases, haplotype combinations were T-G 43.2%, C-T 56.8%, and frequencies of genotype were T-G/T-G 15.8%, C-T/T-G 54.7%, C-T/C-T 29.5%, while in controls they were T-G 30.9%, C-T 69.1% and T-G/T-G 10.5%, C-T/T-G 41.0%, C-T/C-T 48.5%. There was a significant difference in the allelic frequency and the genotypical distributions between the oral neoplasm patients and the controls. The individuals with the T-G allele had a slight increasing neoplasm risk than individuals with C-T allele; the OR for T-G versus C-T was 1.69 (95% CI, 1.12 - 2.51). The risk of suffering from oral neoplasms was higher in the individuals of T-G/T-G genotype and of T-G/C-T genotype than in individuals of C-T/CT genotype with odds ratio of 2.48 versus 2.20.</p><p><b>CONCLUSIONS</b>There are two polymorphic points in the 7th intron of human p53 gene, which could be associated with genetic susceptibility of oral neoplasms. T-G allele may be the risk factor of oral neoplasms.</p>