Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; CD2 Antigens ; metabolism ; Child, Preschool ; Chromosome Breakage ; Cyclophosphamide ; therapeutic use ; Doxorubicin ; therapeutic use ; Female ; Follow-Up Studies ; Humans ; Ki-1 Antigen ; metabolism ; Lymphoma, Large-Cell, Anaplastic ; drug therapy ; metabolism ; pathology ; Mucin-1 ; metabolism ; Prednisone ; therapeutic use ; Receptor Protein-Tyrosine Kinases ; genetics ; metabolism ; Vincristine ; therapeutic use

Blood Cell Count ; Bone Marrow Cells ; metabolism ; Child ; Cord Blood Stem Cell Transplantation ; Cytokines ; therapeutic use ; Histocompatibility Testing ; Humans ; Male ; Myelodysplastic Syndromes ; blood ; therapy ; Treatment Outcome

AIM:To explore the effect of microRNA-221 (miR-221) on the proliferation of lung cancer A549 cells, and to investigate its mechanism .METHODS: The A549 cells were transfected with miR-221 mimics by Lipo-fectamine 2000.The expression of miR-221 was detected by RT-qPCR.The expression of PTEN at mRNA and protein le-vels was detected by RT-qPCR and Western blot , respectively .The cell proliferation was examined by CCK-8 assay and colony formation assay.The 3'-UTR of PTEN was cloned into luciferase reporter vector and its enzymatic activity was detec-ted to verify whether miR-221 targeted to PTEN.RESULTS:The expression level of miR-221 in the A549 cells was sig-nificantly increased after transfection with miR-221 mimics as compared with negative control group and blank group ( P<0.01).The mRNA and protein levels of PTEN were significantly down-regulated compared with control group and blank group ( P <0.05 ) .In addition , miR-221 over-expression significantly promoted the proliferation of A 549 cells ( P <0.05).Moreover, miR-221 inhibited the enzymatic activity of luciferase reporter vector of PTEN.CONCLUSION:Over-expression of miR-221 significantly promotes the proliferation ability of human lung cancer A 549 cells by down-regulation of PTEN.

OBJECTIVETo investigate the correlation of serum sex hormones and parathyroid hormone (PTH) with the biochemical markers of bone turnover in aged men.

METHODSWe collected the laboratory data of 465 men aged 60- 93 (73. 1 +/- 8. 3) years old, who came for routine physical examinations in our hospital. We obtained the levels of serum follicle- stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), testosterone (T), sex hormone binding globulin (SHBG), PTH, 25-hydroxy-vitamin D3 (25(OH) D3), and bone turnover markers C-terminal telopeptide of type I collagen (CTX), osteocalcin (OC) and amino-terminal propeptide of type I procollagen (PINP). We also determined free testosterone (FT) , bioactive testosterone (BT) , testosterone secretion index (TSI) and FT index (FTI), and analyzed the correlation of each index with the biochemical markers of bone turnover.

RESULTSThe concentrations of serum FSH, LH, and SHBG increased, while the levels of FT, BT, TSI, FTI, PTH, CTX, OC and PINP decreased with age, especially in those over 80 years old (P <0.05). PTH was positively correlated with CTX, OC and PINP (r =0. 227, 0. 269 and 0. 162, P <0. 01), even after the adjustment for age, while SHBG negatively correlated with OC (r = -0. 100, P <0.05). The bone turnover markers increased with the elevation of the PTH quartiles, with significant differences between the first and the fourth quartile (P <0. 01). Multiple stepwise regression analysis showed that age was correlated inversely with CTX, OC and PINP ( beta = -0. 126, -0. 141 and -0. 122, P <0.05) , PTH positively with the three markers (beta = 0. 196, 0.279 and 0.189; P <0. 001), and SHBG negatively with OC ( beta = -0. 100, P <0.05) .

CONCLUSIONAging is the fundamental cause of reduced bone turnover in aged men. The levels serum PTH and SHBG are significantly associated with the biochemical markers of bone turnover.

Aged ; Aged, 80 and over ; Aging ; Bone Density ; Bone Remodeling ; physiology ; Bone and Bones ; metabolism ; Estradiol ; blood ; Follicle Stimulating Hormone ; blood ; Gonadal Steroid Hormones ; blood ; Humans ; Male ; Middle Aged ; Parathyroid Hormone ; blood ; Testosterone ; blood

Objective:To explore application of quantitative goal exercise (QGE) combined with whole-process refined nutrition management (WP-RNM) in rehabilitation quality management after chemotherapy for hematologic diseasespatients.Methods:By the convenient sampling method, a total of 125 patients with hematologic diseases who underwent chemotherapyand were admitted to Beijing Chaoyang Hospital, Capital Medical University from January 2017 to January 2019 were selected as research objects. The patients were divided into groups A, B, C and D according to the difference of intervention methods, with 31, 32, 31 and 31 cases in every group in turn. Group A was given routine intervention, group B was given QGE, group C was givenWP-RNM and group D was given QGE combined withWP-RNM. The nutritional status and quality of life of the 4 groups before and after intervention were compared.Results:The nutritional indexes such as prealbumin, albumin, transferrin and hemoglobin of four groups after intervention were improved, group D was higher than those of groups A, B, and C, and the differences were statistically significant ( P<0.05) . Scored Patient-Generated Subjective Global Assessment scores of group D were lower than other groups, and the differences were statistically significant ( P<0.05) . The scores of all dimensions of Quality of Life Questionnaire-C30 after intervention of 4 groups were declined, the scores of each dimension of group D were lower than those of groups A, B, and C, and the differences were statistically significant ( P<0.05) . Conclusions:The scientific and rational implementation of QGE combined with f WP-RNM for hematologic diseases after chemotherapy can effectively improve the nutritional intake quality of patients and improve the immune function and quality of life of patients, which has good auxiliary application value. It can be targeted for promotion and application during chemotherapy for hematologic diseases.

This study was purposed to investigate the biological effect of vinblastine (VLS), usually known as inductor of mitotic arrest, on MOLT-4 of ALL cells and to evaluate its significance. The cell arrest in M phase and/or cell apoptosis were induced by treatment of MOLT-4 cells with 0.05 microg/ml VLS for 0 - 12 hours; the DNA histogram was detected by flow cytometry; the morphological changes of cells were observed by confocal microscopy; the cell cycle distribution, cell apoptosis and morphological changes of cells before and after arrest were analyzed by using arrest increasing rate (AIR), arrest efficiency (AE), apoptosis rate (AR) and morphologic parameters respectively. The results indicated that the cell arrest did not accompanied by significant increase of apoptosis rate; the DNA histogram of cell arrest showed dynamic change of cell cycle in time-dependent manner; the arrest efficiency could be quantified. The cell arrest at M phase was accompanied by cell stack in S phase, the cell proliferation rate dropped after cell arrest occurred. The cells arrested at M phase possessed of characteristic morphologic features in cell mitosis. It is concluded that the vinblastine can solely induce arrest of MOLT-4 cells at M phase. This study provides experimental basis for further investigating the relation of cell cycle arrest to apoptosis, mechanism of checkpoint and development of new anticancer drugs.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Flow Cytometry ; Humans ; Tumor Cells, Cultured ; Vinblastine ; pharmacology

OBJECTIVETo evaluate the accuracy of sentinel lymph node mapping(SLM) in patients with rectal cancer by single-photon emission computed tomography (SPECT-CT) lymphoscintigraphy and carbon nanoparticles suspension injection.

METHODSTwelve patients with clinical T(1-2)N(0)M(0) rectal cancer were selected and locally injected with technetium-(99m)sulfur-colloid and carbon nanoparticles suspension by endoscope one day before surgery, followed by SPECT-CT scanning 1, 3 and 5 hours later. Radioactive isotope(RI) uptake of each sentinel node(SN) basin with location preoperatively determined by SPECT-CT was postoperatively calculated using gamma probe. Nodes with the highest RI uptake, the number of which was also pre-determined by SPECT-CT, was defined as SNs. Immunohistochemical cytokeratin staining was performed for all the SNs and non-SNs.

RESULTSThe rate of sentinel node detection was 91.7%(11/12) with at least one SN(1-3) per patient. Ten cases showed metastasis-negative in SNs as well as all the resected regional nodes by immunohistochemical cytokeratin staining. Only one patient had positive nodes in both SN and non-SNs. The accuracy of SLM was 100%.

CONCLUSIONSPECT-CT lymphoscintigraphy and carbon nanoparticles suspension injection can effectively detect the anatomic location and number of sentinel nodes, and improve the accuracy of SLM for rectal cancer.

Adult ; Aged ; Carbon ; Female ; Humans ; Male ; Middle Aged ; Nanostructures ; Rectal Neoplasms ; diagnosis ; diagnostic imaging ; pathology ; Sentinel Lymph Node Biopsy ; methods ; Tomography, Emission-Computed, Single-Photon ; methods ; Tomography, X-Ray Computed ; methods

OBJECTIVETo assess the effect of surgical reconstruction of congenital aural atresia via the mastoid antrum approach and investigate method for preventing postoperative atresia of the reconstructed aural canal.

METHODSFrom 2000 to 2008, aural canal reconstruction and tympanoplasty was performed via the mastoid antrum approach. In 48 patients with congenital aural atresia (54 ears, including 45 ears of type II, 9 ears of type III). All the patients were followed-up for 18 months to assess the therapeutic effect.

RESULTSThe mastoid antrum was located uneventfully for all the 54 ears, all showing ossicular chain anomalies involving most frequently the malleus and the incus followed by the upper structures of the stapes. Facial nerve abnormalities were seen in 23 ears (42.6%). Hearing improvement to over 20 dB was achieved in 45 ears (83.3%) and to over 25 dB in 25 ears (46.2%) one year later.

CONCLUSIONThe mastoid antrum approach for surgical reconstruction of congenital aural atresia is safe and reliable. Maintenance of the width of the aural canal and prevention of lateral healing of the transplanted tympanic membrane are crucial in the treatment of congenital aural atresia.

Child ; Child, Preschool ; Ear Canal ; abnormalities ; surgery ; Ear, External ; abnormalities ; surgery ; Ear, Middle ; abnormalities ; surgery ; Female ; Humans ; Male ; Mastoid ; surgery ; Reconstructive Surgical Procedures ; methods ; Tympanoplasty

Objective To better understand the prevalence and geographic distribution of genotypes/subtypes on HCV and the relationship between HCV genotypes/subtypes and HIV infection disease progression in the HIV-1/HCV co-infected individuals living in high HIV-1 prevalent areas in China. Methods 186 plasma samples were collected from HIV-1 seropositive individuals infected through paid blood donors (PBD), injecting drug users (IDUs) or sexual contact, living in most severely affected provinces, Henan, Yunnan, Xinjiang, Jilin and Liaoning provinces. Samples with HCV viral load >1000 cop/ml were amplified by RT-nested PCR, sequenced and phylogenetically analyzed for genotyping/subtyping of HCV. HIV-1, HCV viral loads and CD4 T lymphocytes were measured for all subjects. Results (1) HCV were identified as 1 a (1.7%), 1 b (39.9%), 2a (17.9%), 3a (10.4%), 3b (15.6%), 6a (1.2%), 6n (6.4%), and a newly unclassified subtype (7.5%). HCV 2a and lb subtypes predominated in PBD in Henan, 3a and 3b in IDUs in Xinjiang and Yunnan, and 6 genotype/subtypes in IDU in Yunnan. (2) There were no significant differences in CD4 T cell counts among the different HCV subtypes. (3) The viral load of HCV RNA in lb subtype was higher than that of non-1b subtype, however, no significant differences in HIV-1 viral loads and CD4 T cell counts were found between Ib and non-1b subtype. Both HIV and HCV viral loads were lower in 2a than non-2a subtype. Conclusion The prevalence of HCV genotype/subtype in HIV-1/FICV co-infected individuals was associated with geographic areas and transmission routes. HCV subtypes had no direct correlation with HIV infection disease progression.

OBJECTIVETo explore the intrinsic connection between activation of classical nuclear factor-κB (NF-κB) pathway and gefitinib resistance in human lung adenocarcinoma H1650 cells.

METHODSHuman lung adenocarcinoma H1650 cells were exposed to gefitinib continuously for 60 days to obtain resistant H1650 cells. The expressions of P-IκBα, P-p50 and P-p65 in the cytoplasm or nuclei were detected using Western blotting in human lung adenocarcinoma HCC827 cells, parental H1650 cells and gefitinib-resistant H1650 cells. The effects of gefitinib alone or in combination with PDTC on the survival rate and expressions of NF-κB P-p50 and P-p65 were compared among the 3 cell lines.

RESULTSGefitinib-resistant H1650 cells showed increased cytoplasmic and nuclear P-IκBα expressions. The expressions of P-p50 and P-p65 differed significantly among the 3 cell line, decreasing in the order of resistant H1650 cells, parental H1650 cells, and gefitinib sensitive HCC827 cell lines (P<0.05 or 0.01). Treatment with gefitinib alone resulted in a significantly lower cell inhibition rate in resistant H1650 cells than in the parental H1650 cells (P<0.05) and HCC827 cells (P<0.01). The resistant H1650 cells had a significantly higher expression of P-p50 and P-p65 than other two cell lines (P<0.05). In both the resistant and parental H1650 cells, gefitinib significantly lowered P-p50 and P-p65 expressions (P<0.05 or 0.01), and the combined treatment with gefitinib and PDTC significantly decreased the cell survival rate and further lowered the cytoplasmic and nuclear expressions of P-p50 and P-p65 (P<0.01 or 0.01).

CONCLUSIONThe activation of classical NF-κB pathway is a key factor contributing to transformation of the parental H1650 cells into gefitinib-resistant cells. Gefitinib combined with PDTC can inhibit P-IκBα production and NF-κB P-p50 and P-p65 activation to suppress the survival of residual H1650 cells and the generation of gefitinib-resistant cells.