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 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 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

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

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

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 evaluate the role of homozygosity mapping in the fine mapping of the genes responsible for the rare autosomal recessive diseases.

METHODSPolymerase chain reaction-single sequence length polymorphism was used to genotype the family members from 8 families with osteoporosis-pseudoglioma syndrome(OPS) for 14 polymorphic loci within candidate region. The OPS candidate region was narrowed by searching for homozygous region in affected.

RESULTSThe OPS candidate region was narrowed to a 1 cM interval between D11S1296 and D11S4136.

CONCLUSIONHomozygosity mapping is a powerful method for mapping and narrowing the candidate region of the genes responsible for the rare autosomal recessive diseases.

Abnormalities, Multiple ; genetics ; pathology ; Chromosome Mapping ; methods ; Chromosomes, Human, Pair 11 ; genetics ; Eye Diseases ; pathology ; Family Health ; Female ; Genetic Predisposition to Disease ; genetics ; Homozygote ; Humans ; Male ; Microsatellite Repeats ; Osteogenesis Imperfecta ; pathology ; Pedigree ; Syndrome

BACKGROUNDGenetic factors contribute to the development of coronary artery disease (CAD). Recently, a missense mutation in the low density lipoprotein receptor related protein 6 (LRP6) gene, encoding low density lipoprotein receptor related protein 6, has been implicated in an autosomal dominant form of early-onset CAD. The aim of this study was to determine whether the common variants in LRP6 are associated with sporadic CAD in Chinese.

METHODSA total of 766 CAD patients and 806 healthy controls were included in this study. The presence of angiographic CAD was determined by coronary angiographic analysis. Six signal nucleotide polymorphisms (SNPs) were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique.

RESULTSA significant association was detected between rs11054731 in LRP6 intron 2 and CAD in our cohort (P = 0.001). The CC genotype and C allele frequency in the case group were 52% and 72%. Using a dominant model of inheritance, the C allele of rs11054731 was shown to be an independent risk factor for CAD with an OR of 1.45 (95%CI: 1.19 - 1.77, P = 0.0002). With the stratification according to the number of affected coronary arteries, an association was observed between rs11054731 and CAD (P = 0.0002). No significant association was observed between any other SNPs and the risk of CAD.

CONCLUSIONThe C allele of the rs11054731 within the LRP6 gene was associated with increased risk and extent of CAD in Chinese.

Aged ; Asian Continental Ancestry Group ; genetics ; Coronary Artery Disease ; genetics ; Female ; Genetic Predisposition to Disease ; genetics ; Genotype ; Humans ; Low Density Lipoprotein Receptor-Related Protein-6 ; genetics ; Male ; Middle Aged ; Polymorphism, Genetic ; genetics ; Polymorphism, Restriction Fragment Length ; genetics ; Polymorphism, Single Nucleotide ; genetics

AIMTo investigate the effect of epigallocatechingallate (EGCG) on acute lung injury induced by oleic acid in mice and the possible mechanism.

METHODSAcute lung injury was induced by oleic acid in mice. Light microscopy and electron microscopy were used to examine histological changes and lung index as well as wet to dry weight ratio was calculated. Serum TNF-a level was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of p38 MAPK was determined by Western blotting.

RESULTSPretreatment of EGCG significantly alleviated oleic acid induced lung injury accompanied by reduction of lung index and wet to dry weight ratio, decreased of TNF-a level in serum and inhibition of phosphorylation of p38 MAPK.

CONCLUSIONEGCG showed beneficial effect on acute lung injury induced by oleic acid in mice. The ultimate reduction of TNF-alpha in serum caused by inhibition of phosphorylated p38 MAPK is involved in the mechanism of action of EGCG.

Animals ; Catechin ; analogs & derivatives ; pharmacology ; Lung ; pathology ; ultrastructure ; Male ; Mice ; Oleic Acid ; Phosphorylation ; drug effects ; Protective Agents ; pharmacology ; Respiratory Distress Syndrome, Adult ; chemically induced ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism