Objective To explore the change of serum HER2/neu concentration during neoadjuvant chemotherapy for HER2-overexpressed breast cancer and its correlation with the response to the neoadjuvant chemotherapy.Methods The concentration of the serum HER2/neu in 78 cases of HER2-overexpressed advanced breast cancer treated with neoadjuvant chemotherapy were detected with enzyme-linked immunosordent assay(ELISA).The relationship between the serum HER2/neu concentration and the response of neoadjuvant chemotherapy was analyzed.Results The serum HER2/neu concentration of befor and after neoadjuvant chemotherapy was 18.6 ± 10.0ng/ml,11.6 ± 6.lng/ml respectively.The serum HER2/neu concentration decreased significantly(P ＜ 0.001).The response of neoadjuvant chemotherapy was correlated with the change of the serum HER2/neu concentration.The pathologic complete response was correlated with the serum HER2/neu concentration of prechemotherapy and the change of the serum HER2/neu concentration.Conclusion The change of serum HER2/neu concentration may serve as a marker predicting the response of neoadjuvant chemotherapy in HER2-overexpressed breast cancer.

Objective To investigate the effect of immediate breast construction using prosthesi after nipple-areola-sparing mastectomy.Methods The immediate breast construction using prosthesi after nippleareola-sparing mastectomy was performed in 26 cases with breast cancer from January 2008 to December 2011 in Jiangsu Cancer Hospital.The postoperative cosmetic results and the complications were observed.The therapeutic effects were followed up.Results All operations were successful.The s,uperior rate of cosmetic result after one month according to JCRT was 88.5 ％ (23/26).No severe complication was found.After a median follow-up of 26 months (range 3-48 months),there was no recurrence and metastasis.Conclusion The immediate breast construction using prosthesi after nipple-areola-sparing mastectomy is maneuverable with satisfactory aesthetic result and the clinical effect,which deserves the further clinical application.

Objective: To investigate the effect of ribosomal DNA (rDNA) copy number variation caused by hexavalent chromium exposure on DNA damage response in different cell lines, so as to provide insights into the involvement of hexavalent chromium-induced rDNA copy number variation in DNA damage responses. : Methods Human lung epithelial BEAS-2B cells and human embryonic lung MRC-5 cells were treated with 2 μmol/L potassium dichromate for 24 hours, and then cells were transferred to fresh media for further incubation, while cells treated with the same volume of phosphate buffer solution served as controls. Cells treated with potassium dichromate for 24 hours, and 3 and 7 days post-detoxification, were harvested, and rDNA copy number was quantified in cells using a quantitative fluorescent real-time PCR assay. Cell cycle, apoptosis and DNA damage were detected using a Muse cell analyzer, and the DNA damage was evaluated with the proportion of ataxia telangiectasia-mutated (ATM) gene activation, proportion of double-strand DNA breaks and the percentage of the H2A.X variant histone phosphorylatio. : Results The 45S and 5S rDNA copy numbers of were significantly higher in MRC-5 cells than in BEAS-2B cells [(1.54±0.26) vs. (1.02±0.18), P<0.05; (6.97±1.07) vs. (3.00±0.15), P<0.05]. The 45S rDNA copy number was lower in MRC-5 cells 3 days post-detoxification (0.80±0.04) than in controls (P<0.05), and was higher in BEAS-2B cells 3 days post-detoxification (1.43±0.07) than in controls (P<0.05) . G0/G1 phase arrest was found in MRC-5 cells 24 hours post-treatment, and the apoptotic rates were significantly higher in MRC-5 cells 3 and 7 days post-detoxification than in controls [(11.53±1.53)%, (18.33±0.70)% vs. (3.53±0.93)%, P<0.05]. The overall apoptotic rates 24 hours post-treatment and 3 days post-detoxification [(2.80±0.17)%, (3.33±0.57)% vs. (1.53±0.61)%, P<0.05], proportion of ATM gene activation 3 days post-detoxification [(3.37±0.67%) vs. (1.18±0.22)%, P<0.05], proportion of double-strand DNA breaks 3 days post-detoxification [(4.45±0.85)% vs. (0.97±0.21)%, P<0.05] and percentage of the H2A.X variant histone phosphorylation 3 days post-detoxification [(1.68±0.56)% vs. (0.29±0.06)%, P<0.05] in BEAS-2B cells were higher than in controls. Conclusions Hexavalent chromium-induced rDNA copy number variation affects DNA damage response in different cell lines. A stronger DNA damage response is found in BEAS-2B cells with a low rDNA copy number, and a relative stable response is observed in MRC-5 cells with a high rDNA copy number.

OBJECTIVETo investigate the association of the ATP-binding cassette sub-family G member 1 (ABCG1) gene polymorphisms with coronary atherosclerotic disease (CAD) in Chinese Han population.

METHODSA population based case-control association study was carried out in 541 patients with CAD and 649 healthy controls from Chinese Han population. Two single nucleotide polymorphisms (SNPs) of the ABCG1 gene were genotyped using polymerase chain reaction-restriction fragment length polymorphism. Logistic regression was used to compare the genotypic and allelic frequency difference.

RESULTSThe frequency of allele C of rs225374 was significantly higher in the CAD patients than that in the healthy controls (OR=1.186, 95%CI: 1.009-1.394, P=0.039), while the difference was also significant in the male subgroup (OR=1.236, 95%CI: 1.014-1.506, P=0.036). A statistically higher frequency of rs1044317 allele A was found in the CAD patients in comparison to the healthy controls (OR=1.187, 95%CI: 1.009-1.397, P=0.039). In case-only association study, rs225374 showed significant association in the high Gensini score group compared with the low Gensini score group (OR=1.303, 95%CI: 1.024-1.657, P=0.031).

CONCLUSIONThe two SNPs of the ABCG1 gene might be associated with the susceptibility and severity of CAD in Chinese Han population.

ATP Binding Cassette Transporter, Sub-Family G, Member 1 ; ATP-Binding Cassette Transporters ; genetics ; Aged ; Asian Continental Ancestry Group ; ethnology ; genetics ; Case-Control Studies ; Coronary Artery Disease ; ethnology ; genetics ; pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide

OBJECTIVETo investigate the expressions of chemokine receptors and interleukin (IL) receptors on the peripheral blood mononuclear cells (PBMCs) from systemic lupus erythematosus (SLE) patients and their correlations with clinical features as well as SLE disease activity index (SLEDAI).

METHODSThe mRNA expressions of chemokine receptors and IL receptors on PBMCs of 93 SLE patients and 30 healthy controls were detected by reverse transcription-polymerase chain reaction, including CCR2, CCR3, CCR4, CCR5, CCR6, CCR8, CXCR3, CXCRS, CX3CR1, XCR1, IL-4R, and IL-10R. The clinical features of SLE patients were recorded. The correlations of chemokine receptors and IL receptors mRNA expressions with clinical features as well as SLEDAI were assayed using linear regression analysis.

RESULTSThe level of CCR5 mRNA in SLE patients (including active and inactive SLE) was significantly higher than that in healthy controls (P < 0.05), and there was no significant difference between active and inactive patients in this respect (P > 0.05). CX3CR1 mRNA expression significantly increased from healthy control to inactive SLE to active SLE in sequence. The others (except for CCR8, CXCR3, and IL-10R) in active SLE patients were significantly higher than those in both inactive SLE patients and healthy controls (all P < 0.05). There were positive correlations between SLEDAI and CCR2 (r = 0.424, t = 4.313, P < 0.001), CCR3 (r = 0.518, t = 5.410, P < 0.001), CCR4 (r = 0.376, t = 3.851, P < 0.001), CCR6 (r = 0.457, t = 4.513, P < 0.001), CXCR5 (r = 0.455, t = 4.629, P < 0.001), CX3CR1 (r = 0.445, t = 4.523, P < 0.001), as well as XCR1 (r = 0.540, t = 5.445, P < 0.001). And CCR5 mRNA expression level was positively correlated with IL-4R mRNA (r = 0.313, t = 2.353, P < 0.05). The patients with myositis and cutaneous vasculitis simultaneously showed lower levels of CCR5 and CX3CR1, and CCR5 expression was negatively correlated with the scores of SLEDAI in SLE cases accompanied by photosensitivity (r = 0.426, t = -2.155, P < 0.05).

CONCLUSIONIncreased expressions of CCR5 and CX3CR1 on PBMCs may be indicators in clinical survey for SLE.

Adolescent ; Adult ; CX3C Chemokine Receptor 1 ; Child ; Female ; Humans ; Leukocytes, Mononuclear ; immunology ; Lupus Erythematosus, Systemic ; etiology ; immunology ; Male ; Middle Aged ; RNA, Messenger ; blood ; Receptors, CCR5 ; genetics ; Receptors, Chemokine ; genetics ; Receptors, Interleukin-10 ; genetics ; Receptors, Interleukin-4 ; genetics

OBJECTIVETo identify potential mutation responsible for synpolydactyly (SPD) in a large Chinese kindred and to offer genetic counseling and prenatal diagnosis for the members of the family.

METHODSAll family members were examined clinically, and blood samples were obtained for linkage analysis and mutation screening. Ultrasound examinations were conducted at 16-21 weeks. Amniotic fluid sample was obtained by ultrasound-guided amniocentesis at 18 weeks of gestation.

RESULTSA large kindred affected with SPD was identified and characterized. With two short tandem repeat (STR) markers (D2S1238 and D2S1245) flanking the HOXD13 gene, the disease was mapped to 2q31. A heterozygous 27 bp expansion within the imperfect GCN triplet-repeat of exon 1, c. 184_210dup, was identified. The mutation resulted in a gain of 9 alanine residues between the 14th and 15th alanine of the normal 15-amino-acid-long polyalanine tract. On ultrasound examination, all fingers and toes of the fetus appeared to be normal. Linkage analysis and mutation detection confirmed that the fetus did not inherit the mutant allele from his affected mother.

CONCLUSIONHOXD13 gene mutation was responsible for the SPD phenotype in this family. Accurate prenatal diagnosis of SPD was achieved with combined ultrasound and molecular analysis.

Adolescent ; Adult ; Base Sequence ; China ; DNA Mutational Analysis ; Female ; Fingers ; abnormalities ; Genetic Linkage ; Homeodomain Proteins ; genetics ; Humans ; Male ; Middle Aged ; Pedigree ; Pregnancy ; Syndactyly ; diagnosis ; genetics ; Toes ; abnormalities ; Transcription Factors ; genetics ; Ultrasonography, Prenatal ; Young Adult

AIMTo compare the antagonistic effects of 6 beta-naltrexol and naltrexone against morphine analgesia.

METHODSThe effects of 6 beta-naltrexol and naltrexone against morphine analgesia were observed in mouse heat radiant tail-flick assay and in mouse (55 +/- 1) degrees C hot plate test. The displacement of 6 beta-naltrexol and naltrexone on binding to CHO-mu receptor was observed by radioligand binding study.

RESULTS6 beta-naltrexol antagonized morphine analgesia but the potency was (6.1 +/- 1.7)% that of naltrexone. The effective duration of 6 beta-naltrexol was 3-4 times that of naltrexone and the peak time of the response was about 0.5-1 h after s.c. equivalent efficacy dose (ED95) in two models. Like naltrexone, 6 beta-naltrexol was effective by oral administration and the potency ratio of p.o./s.c. was 1/3. As an antagonist to opioid receptor, the displacement of 6 beta-naltrexol was about 12.5% that of naltrexone, which was almost in agreement with the efficacies against morphine analgesia in mouse.

CONCLUSIONCompared with naltrexone, 6 beta-naltrexol was less potent but duration was longer.

Analgesia ; Analgesics, Opioid ; antagonists & inhibitors ; Animals ; Female ; Male ; Mice ; Morphine ; antagonists & inhibitors ; Naltrexone ; analogs & derivatives ; pharmacology ; Narcotic Antagonists ; pharmacology ; Pain Threshold ; drug effects ; Receptors, Opioid, mu ; metabolism

AIM:To investigate the inhibitory effect of allicin on apoptosis and caspase-12 activation of macro-phage-derived foam cells,and to elucidate the underlying molecular mechanisms. METHODS:RAW264.7 macrophages were pretreated with allicin (12.5,25 and 50 mg/L) or 4-phenylbutyric acid(PBA,4 mmol/L) for 1 h and then treated with oxidized low-density lipoprotein(ox-LDL,100 mg/L) or tunicamycin(TM,4 mg/L) for 24 h. The cell viability and apoptosis were examined by MTT assay and flow cytometry with Annexin V-FITC/PI staining,respectively. The activities of caspase-3 in the cells and lactic dehydrogenase (LDH) in the medium were measured. The protein levels of caspase-12 were determined by Western blot. The intracellular lipid accumulation was measured with oil red O staining and the content of intracellular total cholesterol was determined by enzymatic colorimetry. RESULTS:Similar to the endoplasmic reticulum stress (ERS) inhibitor PBA, allicin inhibited ox-LDL-induced injury of RAW264.7 macrophages in a concentration-de-pendent manner,as determined by the increased cell viability and the decreased LDH leakage,apoptosis and caspase-3 ac-tivity. The decrease in cell viability and increases in LDH leakage and apoptosis induced by TM (an ERS inducer) were also suppressed by allicin. Moreover, similar to PBA, allicin remarkably inhibited ox-LDL- or TM-induced activation of caspase-12. Furthermore, allicin remarkably attenuated ox-LDL-induced lipid accumulation in the RAW264.7 cells and foam cells formation in a concentration-dependent manner. CONCLUSION:Allicin may inhibit macrophage-derived foam cell apoptosis induced by ox-LDL,and the mechanism is partially related to suppressing the activation of caspase-12.

OBJECTIVETo investigate the CpG methylation locus and frequency pattern on p16 INK4a gene promoter in epidermis of p16 INK4a methylated patients with psoriasis vulgaris.

METHODSThe DNA specimens were obtained from epidermal lesion of 50 plaque psoriatic patients. Methylation specific PCR and DNA sequencing were used to detect the frequency and locus of methylation in p16 INK4a gene promoter region.

RESULTSApproximately 50% CpG was methylated in p16 INK4a methylated patients, methylation was found in specifical locus of p16 INK4a gene promoter.

CONCLUSIONThe distinct methylation pattern is showed on the p16 INK4a gene promoter region in patients with psoriasis.

Adolescent ; Adult ; Aged ; Base Sequence ; CpG Islands ; genetics ; Cyclin-Dependent Kinase Inhibitor p16 ; genetics ; metabolism ; DNA Methylation ; genetics ; Epidermis ; metabolism ; Female ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Polymerase Chain Reaction ; Promoter Regions, Genetic ; genetics ; Psoriasis ; genetics ; Sequence Alignment ; Tumor Suppressor Protein p14ARF ; genetics ; Young Adult

OBJECTIVETo study the association of the OX40 gene rs2298212G/A polymorphism with coronary atherosclerotic disease (CAD) in Chinese Han population.

METHODSFive hundred and thirty six CAD patients and 544 age and ethnic matched controls of Chinese Han population were recruited from Qilu Hospital, Shandong University. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to genotype the selected single nucleotide polymorphism. Distributions of genotypic and allelic frequencies were analyzed by Chi-square test.

RESULTSThe distribution of genotypic and allelic frequencies have no significant differences between the CAD cases and controls(P> 0.05), even after adjusting for age, gender, body mass index, systolic blood pressure, diastolic blood pressure, glucose, total cholesterol, and triglyceride. However, when substratification analysis of the involved coronary artery vessels was performed, significant difference was found between single-vessel and triple-vessel (P= 0.02, OR = 1.56, 95% CI: 1.08-2.26) involvement.

CONCLUSIONThe rs2298212G/A polymorphism in OX40 gene may be associated with the severity of coronary atherosclerotic disease.

Asian Continental Ancestry Group ; ethnology ; genetics ; Base Sequence ; Coronary Artery Disease ; genetics ; Ethnic Groups ; genetics ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Receptors, OX40 ; genetics