BACKGROUND:Recent years, fiber posts and resin cores have been widely used in repairing the endodonticaly treated teeth with satisfactory effect. Erbium:yttrium aluminum garnet (Er:YAG) laser is a new type of water power laser system, which can be used for surface treatment of fiber posts. But studies on the effect of Er:YAG laser surface treatment on the bond strength of fiber posts are rarely reported. OBJECTIVE: To evaluate the effect of surface treatment utilizing Er:YAG laser irradiation with different parameters on the bond strength of fiber posts to root canal dentin. METHODS: Fifty human maxilary central incisors that had similar dimensions were used. After endodontic treatment, removal of the crown and canal preparation, ParaPost FIBER LUX glass fiber posts were cemented into the root canals. According to the method of surface treatment, 50 teeth were randomly divided into: no surface treatment as control group; four groups undergoing surface preparation with Er:YAG laser with four different power settings (150, 250, 350 and 450 mJ at 10 Hz for 60 s at 100-μs pulse duration), named 1.5, 2.5, 3.5, and 4.5 W Er:YAG laser irradiation groups, respectively. RESULTS AND CONCLUSION: The mean bond strength values reduced from the cervical to the apical root canal, and the bond strength of the dental cervix was significantly different from that of middle and apical thirds (P < 0.05), but there was no difference between the middle and apical thirds (P> 0.05). Regardless of the different part of the root slices, the bond strength was highest in the 4.5 W Er:YAG laser irradiation group, showing significant difference from other groups (P < 0.05). These findings indicate that 4.5 W Er:YAG laser irradiation significantly increases the bond strength of the fiber posts to root canal dentin.

Objective To evaluate the differential diagnostic value of 18F-FDG PET/CT between pancreatic lymphoma (PL) and pancreatic carcinoma (PC).Methods The 18 F-FDG PET-CT data of 16 patients who were pathological diagnosed with PL were retrospectively reviewed and compared with those of 32 consecutive pancreatic cancer patients who were pathologically diagnosed and randomly enrolled.The age,location,diameter and the maximum standard uptake values (SUVmax) of pancreatic lesions,pancreatic ductal dilatation,distal pancreatic atrophy,serum CA19-9 level and extrapancreatic organs involvement were analyzed.Results The 16 patients with PL included 8 men and 8 women,the mean age was (46 ± 17)year,and 11.1％ (1/9) patients had elevated CA19-9.The 32 patients with PC included 15 men and 17 women,the mean age was (61 ± 12)year,and 81.3％ patients had elevated CA19-9.There were no significant differences on gender between the two groups,while the mean age of PL patients was younger than that of PC,elevated CA19-9 was less common than that in PC,and the differences were statistically significant (all P＜0.05).There were 12 cases of diffusive large B cell lymphoma,2 cases of B lymphoblastic lymphoma/leukaemia,1 case of follicular lymphoma and 1 case of dysplastic large T cell lymphoma in 16 PL patients.There was no significant difference on the site of pancreatic lesions between the two groups,but long diameter of PL lesions was larger than that of PC [(6.6 ± 3.3) vs (4.3 ± 1.8) cm,P =0.038].Dilated pancreatic duct and distal parenchyma atrophy in PL were less than those in PC (3/16 vs 17/32,1/16 vs 13/32),and SUVmax of PL lesions was significantly higher than that of PC (12.0 ± 5.5 vs 8.6 ± 3.8),indicating that the differences were statistically significant (all P ＜ 0.05).The cut-off value of SUVmax was 9.95,and Youden's index was 0.406 with the sensitivity and specificity of 68.8％ and 71.9％ for differentiating PL from PC.The incidence of extrapancreatic lesions including bone marrow and kidney and spleen infiltration was significantly more frequent in patients with PL than that in patients with PC(56.3％ vs 6.25％,43.8％ vs 3.1％,50.0％ vs 6.3％),while the incidence of liver metastases was significantly lower than that in PC (12.5％ vs 5.0％),indicating that the differences were statistically significant (all P ＜0.01).There were no significant differences on the incidence of other extrapancreatic lesions.Conclusions PL should be considered in relatively younger patients and manifested as a bulky mass with significant FDG uptake and extrapancreatic involvement of bone,kidney and spleen but without distinct pancreatic ductal dilation or distal parenchymal atrophy or liver metastasis.

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.

Objective To study the prevention effects of AduoLa Fuzhenglin(ADL)Oll the brain injury induced by microwave radiation in rats.Methods A total of 140 male Wismr rats were divided randomly into 5 groups,including control group,microwave exposed group,low dosage(0.75 g·kg-1·d-1)group.middle dosage(1.5 g·kg-1·d-1)group and high dosage(3 g·kg-1·d-1)group.Rats in three ADL groups were lavaged with ADL per day for 2 weeks before radiation.After administration,rats were exposed to microwave at 30 mW/cm2 for 15 min.The abilities of learning and memory were detected by Morris water maze,and the contents of amino acids neurotransmitter of hippocampus were detected by HPLC, then the histology and uhrastrncture of hippocampus were observed with light and electron microscope at 6 h,7 and 14 d after exposure.Results The abilities of learning and memory were declined(F=0.000-0.043,P<0.05)from 6 h to 7 d after exposure,and the contents of four kinds of amino acid neurotransmitter in hippocampus were decreased,of which GLU,GLY and GABA were decreased significantly(F=0.000-0.007,P<0.01)at 6h after exposure,then tissue edema,neuronal degeneration,neuron mitoehondria swelling and cavitation,endocytoplasmie rotieulum broaden,synaptic cleft blurred,and perivascular space widen were found in the hippocampus at 6 h and 7 d after exposure.The changes in low dosage group were similar to those of the radiation group.However,in middle and high dosage groups,the abilities of learning and memory were normal to some extent with the significant differences compared to the radiation group from 6 h to 7 d after exposure(F=0.015-0.028.P<0.05).The contents of four kinds of amino acid neurotransmitter were not decreased,especially GLU contents close tO normal level.There were significant differences between middle and high dosage groups and radiation group at 6 h after exposure(F=0.000-0.042,P<0.05).Moreover,no obvious injury in the hippocampus was observed in middle and high dosage groups at 6 h and 7 d after exposure.Conclusions Exposure to 30 mW/cm2 microwave radiation could decrease the abilities of learning and memory,induce amino acid neurotransmitter turbulence,and injure the histology and uhrastructure of hippocampus.ADL at the dosages of 1.5 and 3 g·kg-1·d-1 would have preventive effects on the injury induced by microwave exposure.The concentration of 1.5 g·kg-1 ·d-1 of ADL might be the effective dosage to prevent the brain damage after microwave exposure.

To explore a simple and sensitive method to detect minimal residual disease (MRD) in Ph(+)/bcr-abl(+) ALL patients, the bone marrow samples from 84 de novo ALL patients were detected by cytogenetic analysis, nested-PCR and flow cytometry (FCM). Cytogenetic analysis method is used to detect Ph chromosome, nested-PCR and FCM are used to detect bcr/abl mRNA and an abnormal B-cell differentiation pattern in de novo and complete remission (CR) patients, respectively. The results showed that Ph chromosome has not been found in 14 cases of CR; bcr/abl fusion gene was detected in 11 of 14 CR patients by nested-PCR (78.57%) and bcr/abl fusion gene was positive in 5 of 14 in CR patients (35.71%) by FCM. The sensitivity of nested-PCR was 10(-6)-10(-7), and that of FCM was 10(-4)- 10(-5). It is concluded that the cytogenetic analysis is not sensitive for MRD detection, and the sensitivity of nested-PCR is higher than that of FCM in detecting MRD.
Adolescent ; Adult ; Female ; Flow Cytometry ; methods ; Fusion Proteins, bcr-abl ; analysis ; Humans ; Male ; Middle Aged ; Neoplasm, Residual ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; diagnosis ; genetics ; Recurrence ; Reverse Transcriptase Polymerase Chain Reaction ; methods ; Sensitivity and Specificity

Hepatosplenic gammadelta T cell lymphoma represents rare, often aggressive type of malignant peripheral T-cell lymphoma, which is characterized by expressing T-cell-associated markers CD2, CD3 and gammadelta T-cell receptor, and nonactivated cytotoxic cell phenotype (TIA-1+, granzyme B-). The pathological findings of a liver biopsy specimen revealed the diffuse infiltration of lymphocytes in the sinusoids and the aspiration biopsy from spleen revealed the diffuse infiltration of lymphocytes in the red pulp, not shaped to the nodes, often resulted in the misdiagnosis. Recently, by analyzing the immunophenotype and TCR rearrangement from liver, spleen and bone marrow, a case of adult hepatosplenic gammadelta T cell lymphoma was diagnosed. In combination with references, It is belived that immunophenotype and TCR rearrangement are necessary means to diagnosis hepatosplenic gammadelta T cell lymphoma.
Adult ; Antigens, CD20 ; metabolism ; CD2 Antigens ; analysis ; CD3 Complex ; metabolism ; Humans ; Immunohistochemistry ; Ki-1 Antigen ; metabolism ; Liver Neoplasms ; metabolism ; pathology ; Lymphoma, T-Cell ; metabolism ; pathology ; Male ; Receptors, Antigen, T-Cell, gamma-delta ; metabolism ; Splenic Neoplasms ; metabolism ; pathology

The SH2 domain containing inositol 5'-phosphatase (SHIP) was initially described as a 145 kD protein phosphorylated on tyrosines upon growth factor and cytokine stimulation. SHIP is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. To evaluate the role of the SHIP gene in human leukemogenesis, expression and mutation of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 patients with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and sequencing. The RT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 out of 32 AML patients (22%) and one out of 9 ALL patients (12%). Interestingly, two missense mutations that had been observed in one AML patient at diagnosis disappeared after complete remission (CR). In addition, Akt phosphorylation was prolonged and increased following IL-3 stimulation in this patient sample. In conclusion, data of this study demonstrate the mutation of the SHIP gene in acute leukemia for the first time and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP serves as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.
Cell Line ; Humans ; Leukemia, Myeloid, Acute ; genetics ; Mutation ; PTEN Phosphohydrolase ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases ; Phosphoric Monoester Hydrolases ; genetics ; physiology ; Phosphorylation ; Polymorphism, Genetic ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; Protein-Serine-Threonine Kinases ; metabolism ; Proto-Oncogene Proteins ; metabolism ; Proto-Oncogene Proteins c-akt ; Tumor Suppressor Proteins ; physiology

OBJECTIVEThe SH2 domain containing inositol 5'-phosphatase (SHIP) is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. This paper is to evaluate the role of the SHIP gene in human leukemogenesis.

METHODSExpression of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and DNA sequencing.

RESULTSRT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 (22%) of 32 AML patients and one (12%) of 9 ALL patients. Interestingly, two missense mutations that had been observed in a AML patient at diagnosis disappeared after complete remission (CR). In addition, in vitro Akt phosphorylation was prolonged and increased following IL-3 stimulation of this patient's cells.

CONCLUSIONOur data demonstrate for the first time the mutation of SHIP gene in acute leukemia and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP may serve as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.

Blotting, Western ; Cell Line, Tumor ; DNA Mutational Analysis ; HL-60 Cells ; Humans ; Inositol Polyphosphate 5-Phosphatases ; Interleukin-3 ; pharmacology ; K562 Cells ; Leukemia, Myeloid, Acute ; genetics ; metabolism ; Mutation ; Oncogene Protein v-akt ; metabolism ; Phosphoric Monoester Hydrolases ; genetics ; metabolism ; Phosphorylation ; drug effects ; Polymorphism, Single-Stranded Conformational ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; U937 Cells

The aim was to construct a prokaryotic expression plasmid encoding the fusion gene of single-chain variable fragment and monocyte chemotactic protein-3 (MCP-3). The cDNAs of immunoglobulin (Ig) VH and Ig VL were amplified by RT-PCR and assembled into the single-chain variable fragment (scFv) by recombinant PCR method. The cDNAs of Ig VH and Ig VL were connected by a (Gly4Ser)3 linker. Then, the fragments of scFv and MCP-3 were connected with a NDAQAPKS spacer, using recombinant PCR method again. The results indicated that the fusion gene of scFv-MCP-3 were constructed correctly and cloned into the prokaryotic expression plasmid successfully identified by sequencing and restriction endonucleases examination. Finally, the fusion protein was expressed in E coli DH5alpha under induction by arabinose. And the fusion protein was 65 kD and account for 30% of the total protein of the bacteria. In conclusion, a prokaryotic plasmid, encoding the fusion gene of single-chain variable fragment with MCP-3 and expressing idiotype protein vaccination against B cell lymphoma, was constructed correctly.
Amino Acid Sequence ; Animals ; Cancer Vaccines ; biosynthesis ; genetics ; immunology ; Chemokine CCL7 ; biosynthesis ; genetics ; immunology ; Genetic Vectors ; Humans ; Immunoglobulin Idiotypes ; immunology ; Immunoglobulin Variable Region ; biosynthesis ; genetics ; immunology ; Lymphoma, B-Cell ; immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Plasmids ; genetics ; Prokaryotic Cells ; metabolism ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; immunology ; Vaccines, DNA ; biosynthesis ; genetics ; immunology

The hematopoietic cell phosphatase (HCP or SHP-1), the SH2 domain contain protein tyrosine phosphatase, is a crucial negative regulator in the process of hematopoietic cell development, proliferation and receptor-mediated mitogenic signaling pathways, and its mutation is responsible for the over-expansion and inappropriate activation of myelomonocytic population in motheaten mice. The aim of the study was to evaluate the role of the HCP gene in leukemogenesis. Bone marrow and/or peripheral blood from 32 acute myeloid leukemia (AML) patients, 9 acute lymphocytic leukemia (ALL) patients, 8 leukemia cell lines and 50 normal controls were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) based on single strand conformation polymorphism (SSCP) and sequencing. RT-PCR showed that all samples expressed HCP gene, only one missense mutation at codon 225 (AAC to AGC, Asn to Ser) within N-terminal SH2 domain was found in an ALL patient. In addition, four polymorphic base substitutions were detected in codon 69, 85, 86 and 266, respectively. In conclusion, mutation of HCP gene is an infrequent genetic aberration which may only play a role in pathogenesis of a small part of leukemia, however, its significance needs to be further clarified.
Acute Disease ; Cell Line, Tumor ; Humans ; Intracellular Signaling Peptides and Proteins ; Leukemia ; enzymology ; genetics ; Mutation ; Polymorphism, Single-Stranded Conformational ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases ; genetics