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.

OBJECTIVETo gain an insight into the large intragenic hMSH2 and hMLH1 deletions in Chinese hereditary nonpolyposis colorectal cancer (HNPCC) families.

METHODThe large intragenic hMSH2 and hMLH1 deletions in 17 probands of HNPCC families were detected with multiplex ligation-dependent probe Three large intragenic hMSH2 deletions of examplification (MLPA) and GeneMapper techniques.

RESULTSon 8, exon 1-6, and exon 1-7 were found in three families respectively, and no hMLH1 deletion was found. The deletions accounted for 19% of the total hMSH2 and hMLHI germline pathogenic mutations.

CONCLUSIONSThe incidence of large intragenic mismatch repair (MMR) genes deletions is relatively higher in Chinese families, and hMSH2 deletions may be more common. It is necessary to detect the large intragenic MMR genes deletions in the molecular detection of HNPCC.

Adaptor Proteins, Signal Transducing ; genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis ; genetics ; Female ; Gene Deletion ; Humans ; Male ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; genetics ; Nuclear Proteins ; genetics ; Nucleic Acid Amplification Techniques ; methods ; Pedigree

We investigated the fatty acid profiles of muscle from large yellow croaker (Pseudosciaena crocea R.) of different age. One- and two-year-old fish were cultured in floating net cages and sampled randomly for analysis. Moisture, protein, lipid and ash contents were determined by methods of Association of Analytical Chemist (AOAC) International. Fatty acid profile was determined by gas chromatography. Crude protein, fat, moisture and ash contents showed no significant differences between the two age groups. The contents of total polyunsaturated fatty acids and docosahexaenoic acid (DHA) were significantly higher and eicosapentaenoic acid (EPA) content was significantly lower in the two-year-old large yellow croaker than in the one-year-old (P<0.05). No significant differences were observed in the contents of total saturated fatty acids and monounsaturated fatty acids, or the ratio of n-3/n-6 fatty acids among the large yellow croakers of the two age groups. We conclude that large yellow croakers are good food sources of EPA and DHA.
Age Factors ; Animals ; Fatty Acids ; analysis ; Muscles ; chemistry ; Perciformes ; metabolism

OBJECTIVETo get a better understanding of the mechanisms underlying type 1 diabetes mellitus, the differentially expressed pancreatic proteins from multiple low-dose streptozotocin (MLD-SIZ) mouse and normal mouse were analyzed and compared.

METHODS20 male rats were separated into 2 groups (n=10): model mice treated with MLD-STZ and normal mice,differences of pancreatic proteome among in the two groups of mice, were analyzed by two dimensional polyacryamide gel electrophoresis (2DE). Protein quantification was analyzed and the differentially expressed spots were identified using mass spectrometry and MASCOT database searching.

RESULTSCompared with control group, 23 proteins had changed significantly in the model group, 8 proteins expression were up-regulated, 15 proteins expressions down-regulated significantly. Using MALDI-TOF-MS, 15 proteins with significant change were identified by peptide fingerprinting map and the results were searched in MASCOT database. The function analyzed showed that proteins with change were associated with metabolic, anti-oxidant, structural, catalytic enzymes and chaperone, et al.

CONCLUSIONType 1 diabetes is probably exerted via multi-target and multi-path mechanism. The proteins with significant change are newly target for type 1 diabetes early diagnosis and treatment.

Animals ; Diabetes Mellitus, Experimental ; physiopathology ; Diabetes Mellitus, Type 1 ; chemically induced ; metabolism ; physiopathology ; Male ; Mice ; Pancreas ; metabolism ; Proteins ; metabolism ; Proteomics ; methods ; Streptozocin

Objective To enhance the diagnosis of cerebral infarction of the hematopathy patient by analyzing its causes and MRI manifestations.Methods Totally 36 hematopathy patients with cerebral infarction from April 2010 to November 2015 had their data discussed retrospectively on involved vessel,anatomic distribution and MRI manifestations.Results Of the 36 patients,12 ones had only an artery involved in and 24 ones had multi arteries affected,31 ones had multi cerebral infarction foci and 5 ones had single focus.The foci had high or slighdy high signals in T2WI and very high signals in DWI,and there were no enhancement or only gyrus-like enhancement around the foci found by enhanced scan.Conchusion MRI gains advantages over CT when used to diagnose and find the hematopaty patient with cerebral infarction,when it has to be differentiated with cerebral early infection and parenchymal infiltration.It's suggested that the hematopathy patient has to undergo MRI examination in case central nervous system symptoms especially cerebral infarction occur.

OBJECTIVEIt was revealed that t(8; 21) (q22; q22) was one of the most common chromosomal aberrations in acute non-lymphoid leukemia. The translocation was found to be involved in the AML1 gene on the chromosome 21 and the ETO gene on the chromosome 8, and resulted in the formation of AML1/ETO fusion gene on the derivative chromosome 8. The fusion gene was a transcription factor and played a direct role in the leukemogenesis. The translocation was mainly observed in M(2), accidentally in M(4) and M(1) and rarely in MDS. Here we studied the main clinical data in children with acute non-lymphoid leukemia (ANLL) carrying the AML1/ETO fusion gene. In addition, we discussed the significance of the detection of AML1/ETO fusion gene in the diagnosis and prognosis of children with ANLL.

METHODSThe authors investigated 29 patients in our hospital from December 2000 to March 2002. The patients were divided into two groups. Group A included 21 patients, 14 males and 7 females. They were 3.6 to 14 years old and the median was 9. Group B included 8 patients, 6 males and 2 females. They were 0.8 to 14 years old and the median was 6. Diagnosis was made according to FAB and MIC criteria and the expression of AML1/ETO fusion gene was detected with nested RT-PCR. The patients were treated according to DA, DAE or BFM regimen, respectively. The main clinical indexes including age, Hb, white blood count, platelet, blasts in PBC and BM, and time of arrival at complete remission (CR), were compared statistically between the two groups with t test of independent samples.

RESULTSAll the 21 patients in group A were found carrying AML1/ETO, and 17 patients (81%) were classified as M(2), the other 4 cases were of M(2) developed from MDS-RAEB-T, M(4Eo), M(5) and eosinophil leukemia, respectively. Eighteen out of 20 patients whose effects could be assessed reached CR, and the CR ratio was 90%. Two patients in group B were of AML-M(1), 3 M(2), 1 M(3), 1 M(4), and 1 M(5), respectively. None of them was found carrying AML1/ETO. Seven cases reached CR and the ratio was 87.5%. There was no significant difference between the two groups in the above clinical indices.

CONCLUSIONSBetween the two groups of patients there was no significant difference in the above clinical indices. RT-PCR for the detection of AML1/ETO in children with ANLL was quick, convenient and sensitive, and could be regarded as a useful method for the diagnosis and prognosis of ANLL.

Adolescent ; Child ; Child, Preschool ; Core Binding Factor Alpha 2 Subunit ; Female ; Humans ; Leukemia, Myeloid, Acute ; classification ; drug therapy ; genetics ; Male ; Oncogene Proteins, Fusion ; genetics ; Prognosis ; RNA, Neoplasm ; genetics ; metabolism ; RUNX1 Translocation Partner 1 Protein ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors ; genetics

BACKGROUNDGenetic mechanisms contribute to blood pressure regulation. This study investigated whether glutathione peroxidase (GPx-3) tag single nucleotide polymorphisms (SNPs) are associated with hypertension in the rural areas of Fuxin county, Liaoning province, China.

METHODSIndigenous Fuxin Han people participated, 523 unrelated hypertensives and 547 controls were recruited. All tag SNPs of GPx-3 gene were selected. We estimated SNP allele frequency in DNA pools with pyrosequencing.

RESULTSBefore Bonferroni correction, C allele frequency for rs8177417 was significantly higher in hypertensives than those in controls (23.4% vs. 19.3%, P = 0.014); T allele frequency for rs3828599 was significantly lower in hypertensives than those in controls (35.6% vs. 40.8%, P = 0.009). However, when a Bonferroni correction for multiple testing was applied, only the polymorphisms rs3828599 of GPx-3 gene was associated with hypertension (P = 0.045, OR: 0.833, 95%CI: 0.695 - 0.998).

CONCLUSIONThe polymorphism of rs3828599 of GPx-3 gene might be associated with hypertension in rural Han Chinese from Fuxin, Liaoning.

Aged ; Female ; Gene Frequency ; genetics ; Genetic Predisposition to Disease ; genetics ; Glutathione Peroxidase ; genetics ; Humans ; Hypertension ; genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; genetics

OBJECTIVETo evaluate the clinical significance of prostate-specific antigen (PSA) screening in early detection of prostate cancer in Chinese men.

METHODSPSA screening was performed in 8562 asymptomatic men who had been enrolled for health checkup and all were > or = 50 years old. Prostate biopsy was recommended for those with a serum PSA level > or = 4.0 ng/ml. The pathological and clinical features of the patients with prostate cancer detected by the PSA screening were compared with that of 82 clinically diagnosed prostate cancer patients during the same period.

RESULTSOf the 8562 asymptomatic men, 719 had PSA levels > or = 4.0 ng/ml and biopsy was performed in 295 of them. Fifty-eight prostate cancers were detected. The biopsy rate was 41.0% and positive detection rate was 19.7%. The overall age distribution in the screening group and the clinical groups was not significantly different (P = 0.176). However, 41.4% (24/58) of the patients in screening group were > 75 years old, and significantly more than that in the clinical group (25.6%, P = 0.0491). The proportion of the patients with PSA levels > or = 20 ng/ml in the screening group was significantly less than that in the patients of the clinical group (44.8% vs. 75.6%, P = 0.0002). Whether in the patients whose age was > 75 years old (P < 0.05) or < or = 75 years old (P = 0.0002), the patients in the screening group had significantly lower Gleason scores < 7 (60.3% vs. 34.1%, P = 0.002), more T1 or T2 tumor (87.9% vs. 26.8%, P < 0.0001) and more chance to receive radical prostatectomy (50.0% vs. 18.3%, P < 0.0001) than the patients in the clinical group did. However, the distributions of PSA levels at diagnosis and biopsy Gleason scores were not significantly different between the above mentioned two groups (P > 0.05).

CONCLUSIONProstate-specific antigen (PSA) screening is useful for early detection of prostate cancer in Chinese men aged > or = 50 years. The patients detected by PSA screening usually show a lower PSA level, Gleason scores and early clinical stage disease, and have more chance for radical prostatectomy than the clinically diagnosed patients.

Aged ; Aged, 80 and over ; Biopsy ; Early Detection of Cancer ; methods ; Humans ; Male ; Middle Aged ; Neoplasm Staging ; Prostate-Specific Antigen ; blood ; Prostatic Neoplasms ; blood ; diagnosis ; pathology

OBJECTIVETo explore multi-drug resistance (MDR) of bladder cancer for the intravesical instillation.

METHODSUsing immunohistochemical staining, in 44-case human bladder cancer cells, the expressions of P-glycoprotein (P-gp), glutathione S-transferase (GST-pi) and topoisomerase (TOPO-II), were detected to find out the resistance to drugs.

RESULTSP-gp had a higher expression in 54.5% cases. GST-pi had no or a lower expression in 65.9% cases. TOPO-II had a higher expression in 29.5% but a lower expression in 65.9% cases.

CONCLUSIONDetecting the factors of MDR in bladder cancer cells could help to choose drugs for intravesical chemotherapy.

ATP-Binding Cassette, Sub-Family B, Member 1 ; analysis ; Administration, Intravesical ; Adult ; Aged ; DNA Topoisomerases, Type II ; analysis ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; Glutathione Transferase ; analysis ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Urinary Bladder Neoplasms ; drug therapy ; metabolism

OBJECTIVETo ascertain whether connexin 26 (Cx26) gene was a nuclear modifier gene in an extensive family with matrilineal nonsyndromic deafness associated with A1555G mutation in Huaiyin, China.

METHODSFollowing PCR-restriction fragment length polymorphism (PCR-RFLP) with ApaI restriction enzyme, Cx26 genes from 26 cases, with A1555G mitochondrial mutations in this family, and 62 controls (including 2 patrilineal relatives, 10 spouse controls and 50 unrelated controls), were sequenced.

RESULTSCompared with the reference sequence of Cx26 gene, totally four kinds of nucleotide changes,79G -->A, 109G-->A, 341G-->A and 235delC, were detected in a heterozygous form. However, the former three were previously reported polymorphisms, and only the 235delC was a previously described recessive mutation associated with most autosomal nonsyndromic sensorineural hearing loss in Japan and China. Further study showed that the heterozygous 235delC mutation existed in both one individual with mild hearing loss and two individuals with normal hearing. Clinical characterization showed that 235delC mutation did not seem to modify the deafness phenotype due to the A1555G mutation. Moreover, this 235delC mutation was deduced to derive from a married-in control. Finally, there were no co-segregation between the phenotypes of hearing loss and the genotypes for Cx26 genes based on the four kinds of nucleotide changes.

CONCLUSIONSThe heterozygous 235delC mutation of the Cx26 gene may not modulate the severity of hearing loss associated with A1555G mutation and Cx26 gene is unlikely to be a modifier gene for hearing loss due to A1555G mitochondrial mutation in this Chinese family.

Adolescent ; Adult ; Case-Control Studies ; Child ; Child, Preschool ; China ; epidemiology ; Connexin 26 ; Connexins ; genetics ; Deafness ; epidemiology ; ethnology ; genetics ; Female ; Genotype ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Mutation ; Pedigree ; Phenotype ; Polymorphism, Restriction Fragment Length ; Sequence Analysis ; Young Adult