Purpose To investigate the clinicopathological and immunohistochemical features of primary renal lymphomas ( PRL) , and to discuss the diagnosis, differential diagnosis, treatment and prognosis of the tumors. Methods Clinical data of 19 patients with PRL from January 2005 to October 2014 were retrospectively analyzed. Result The 19 patients in this study, there were 11 males and 8 females and the age ranged from 37 to 85 years old (averaged 55). Patients were mainly presented with unilateral renal masses, with lumbodynia as the main symptom. 13 patients underwent nephrectomy, 6 patients underwent renal biopsy and 17 patients received CHOP or R-CHOP chemotherapy. All of them were diagnosed as non-Hodgkin’ s lymphoma, with 14 cases of diffuse large B cell lym-phoma (DLBCL) (73. 684%, 14/19), 4 cases of B cell small cell lymphoma (21. 053%, 4/19), and 1 cases of T cell lymphoma (5. 263%, 1/19). Follow-up information was available in 15 patients. 12 were still alive and survived for 1~78 months, while the other 3 were dead with 1 case who died of cerebral infarction, and survived for 3~38 months ( averaged 23 months) . Conclusion PRL is an extranodal lymphoma which is rare in kidney and is often misdiagnosed as renal carcinomas due to its nonspecific clinical manifestations. The diagnosis of PRL can be confirmed by histopathological examination, immunohistochemistry and molecular analy-sis. The majority of the lymphomas are B cell lymphomas and most of them are DLBCL. The recommended treatment is surgery com-bined with chemotherapy and the prognosis is associated with the age, clinicopathological characteristics, tumor types and treatment.

Objective To explore the role of white matter injuries in the schizophrenia induced by the NMDA re-ceptor antagonist. Methods Adult male C57BL/6J mice (8 week old) were equally divided into four groups. One group was sub-chronically treated with saline solution, and the other three groups were intraperitoneally treated with MK-801 at dose of 0.025 mg/mL (M1), 0.050 mg/mL (M2) and 0.100 mg/mL (M3) in a volume 10 ml per kilogram body weight. All ani-mals were tested using Morris water maze at the 9th-15th day and using the Hole Board exploration as well as Rota Rod performance tests on the 16th day. The myelin basic protein (MBP) and the ultrastructure of the myelin sheaths in the cor-pus callosum were then examined using immunohistochemical methods, transmission electron microscope technique and stereological methods. Results The repeated sub-chronic MK-801 treatment did not induce impairment of spatial learning and memory in Morris water maze. The MK-801 treatment at 0.25 mg/kg and 1.00 mg/kg but not at 0.50 mg/kg resulted in less exploration to a new environment. The myelin staining with anti-MBP antibody was less intense in all three schizo-phrenic groups when compared to saline control group (P<0.01). Furthermore, MK-801 treatment caused pathological al-terations of the myelin sheaths including segmental demyelination of myelinated fibers and splitting of myelin sheath lamel- lae in schizophrenic groups. The ratio of the injured myelinated nerve fibers in the corpus callosum of MK-801 treated mice [M3 group, (22.42 ± 4.24)%] was significantly higher when compared to the control mice [(3.84 ± 1.35)%,P<0.01)]. Conclusions The present study demonstrated the white matter damages, mainly low MBP expression and segmental demye-lization in the corpus callosum in the mice sub-chronic treated with MK-801, indicating that the white matter changes might be involved in the schizophrenia induced by NMDA antagonist.

OBJECTIVEIt is known that dementia is a multi-factorial disorder, but the etiological factors other than aging remain to be explored, hence we sought to investigate the risk factors of dementia and Alzheimer's disease (AD).

METHODSWe followed a community-based dementia-free cohort (n = 1301) aged 75 years and over in Stockholm, Sweden. Baseline data were obtained through a structured interview and extensive clinical examination, or by reviewing the inpatient register database. We used the DSM-III-R criteria to define dementia and AD cases.

RESULTSOver six years of a follow-up program,350 subjects were diagnosed as dementia, including 260 Alzheimer cases. Multiple Cox regression analysis suggested that older age,low education (< 8 years), cognitive impairment, functional disability (ADL > or = 1), low diastolic pressure (< 70 mm Hg), diabetes mellitus, coronary heart disease, and APOEepsilon4 allele were significantly or marginally associated with subsequent development of dementia and AD. Dementia was related also to stroke and atrial fibrillation. Antihypertensive drug use was associated with a lower risk of AD and dementia.

CONCLUSIONSOur study revealed that some sociodemographic features, cognitive and physical dysfunctions, vascular disorders, and genetic susceptibility were major risk factors for dementia and AD. Use of antihypertensive drugs might protect against the dementing disorders in a very old population.

Aged ; Aged, 80 and over ; Alzheimer Disease ; epidemiology ; prevention & control ; Cohort Studies ; Demography ; Female ; Follow-Up Studies ; Humans ; Linear Models ; Male ; Risk Factors ; Sweden ; epidemiology

Biomedical Research ; China ; epidemiology ; Dementia ; epidemiology ; Humans

OBJECTIVETo investigate the relationship between the changes of the copy numbers of mtDNA in peripheral blood mono-nucle- ar cell(PBMC) and the disordered of antioxidant capacity of hepatocellular carcinoma (HCC) patients.

METHODSThe Ficoll Hypaque method was used to isolate the PBMC from blood specimens. The ND1 gene of the mitochondrial was amplified by real-time PCR; meantime β-actin was served as a quantitative standard marker; the difference of mtDNA copy number in PBMC was compared between HCC and healthy control group. The level of reactive oxygen species (ROS) in PBMC was determined by flow cytometry. The change of total antioxidant capacity (T- AOC) of plasma was detected by the biochemistry examination.

RESULTSThe copy numbers of ND1 gene in PBMC of HCC was 73% that of the healthy control group,which suggested a decrease of the copy numbers of mtDNA in HCC. The levels of ROS of PBMC in HCC was (417. 82 ± 110.62) and (301.82 ± 75.54) in control group, which showed that the levels of ROS of PBMC in HCC were significant higher than that in control group (P < 0.01).Plasma T-AOC in HCC was (1.30 ± 0.85), and (3.20 ± 1.62) in control. The T-AOC of plasma of HCC was significantly lower than in control group (P < 0.01).

CONCLUSIONThere was a certain relationship between the decrease of the copy numbers of mtDNA and the disordered antioxidant capacity in hepatocellular carcinoma, which may be associated with the development of hepatocellular carcinoma.

Actins ; Antioxidants ; metabolism ; Carcinoma, Hepatocellular ; blood ; genetics ; Case-Control Studies ; DNA Copy Number Variations ; DNA, Mitochondrial ; genetics ; Humans ; Leukocytes, Mononuclear ; metabolism ; Liver Neoplasms ; blood ; genetics ; Reactive Oxygen Species ; metabolism

OBJECTIVETo assess the curative effects of different drugs on liver cell damage of rats induced by acute nickel carbonyl poisoning.

METHODSIn present study 220 SD rats were divided into control group (10 rats), carbonyl nickel group (10 rats), 20 mg/kg methylprednisolone group (40 rats), 100 mg/kg DDC group (40 rats), 10 µmol/kg sodium selenite group (40 rats), 0.25 ml shenfuhuiyangtang group (40 rats) and 20 mg/kg methylprednisolone with 100 mg/kg DDC group (40 rats). All rats except for control group inhaled passively 250 mg/m(3) carbonyl nickel for 30 minutes. At 4h and 30h after exposure, the drugs were given intraperitoneally to the rats. On the 3rd and 7th days after exposure, the liver samples were taken from 10 rats each group. The DNA damage of liver cells was detected using comet assay, the ultrastructure changes in liver cells were examined under an electronmicroscope.

RESULTSCompared to carbonyl nickel group, the tail lengths of liver cells in 5 groups administrated at 4 h or 30 h and tested on the 3rd or 7th day after exposure decreased significantly (P < 0.05). Compared to the control group, the tail lengths of liver cells in sodium selenite and shenfuhuiyangtang groups administrated at 4h after exposure or sodium selenite, shenfuhuiyangtang and methylprednisolone with DDC groups administrated at 30h after exposure increased significantly (P < 0.05 or P < 0.01), when tested on the 3rd day after exposure. Except from methylprednisolone sub-group administrated at 4h and tested on the 7th day after exposure, the tail lengths of liver cells in other groups administrated at 4 h or 30 h and tested on the 7th day after exposure increased significantly (P < 0.05). Compared to carbonyl nickel group, the Olive moment of liver cells in 5 groups administrated at 4 h or 30 h tested on the 3rd or 7th day after exposure decreased significantly (P < 0.05 or P < 0.01). Compared to the control group, the Olive moment of liver cells in following groups (selenite and shenfuhuiyangtang groups administrated at 4 h or 30 h and tested on the 3rd or 7th day after exposure, DDC group administrated at 4 h or 30 h and tested on the 7th day after exposure, DDC group administrated at 30h and tested on the 3rd day after exposure, and methylprednisolone with DDC group administrated at 30 h and tested on the 7th day after exposure) increased significantly (P < 0.05 or P < 0.01). As compared with carbonyl nickel group, the ultrastructure observation indicated that the nucleus and other organelles of liver cells in methylprednisolone, DDC and methylprednisolone with DDC groups administrated at 4h and tested on the 3rd day were access to normal levels.

CONCLUSIONThe results of present study showed that methylprednisolone, DDC and methylprednisolone with DDC could improve obviously the repair of rat liver cell damage induced by acute carbonyl nickel poisoning, and the curative effects of early treatment were better than those of later treatment.

Animals ; Chemical and Drug Induced Liver Injury ; drug therapy ; pathology ; DNA Damage ; Drugs, Chinese Herbal ; therapeutic use ; Hepatocytes ; pathology ; Male ; Methylprednisolone ; therapeutic use ; Organometallic Compounds ; poisoning ; Rats ; Rats, Sprague-Dawley ; Sodium Selenite ; therapeutic use ; Zalcitabine ; therapeutic use

Objective To observe DNA damage and morphological changes of lung cells in rats with acute carbonyl nickel poisoning. Methods SD rats were exposed to 20, 135 and 250 mg/m3 carbonyl nickel for 30 min by inhalation. On the third day and 7th day after exposure, DNA damage of lung cells were examined by single cell gel electrophoresis (SCGE) and the pathological changes in lung tissues and the changes of microstructure in lung cells were observed. Results The DNA damage of the rat lung cells were obviously found in all exposure groups at different exposure times and there was the most obvious DNA damage at 72 hour after exposure to nickel carbonyl but the damage appeared later than chlorine exposure group. The inflammatory infiltration and hyperplasia in lung tissue, bronchiolar damage and the bronchial mucosa defulvium appeared in the rats exposed to carbonyl nickel. The results of microstructure examination indicated that the organelles of type I pneumocytes was swellen, the body of type Ⅱ pneumocytes was emptied. The cytoplasm empty bubbles increased, the mitochondria was swellen, and alveolar mediastinum inside the collagen fiber in alveolar mediastinum increased. Conclusion The acute carbonyl nickel exposure could induce the injury of lung tissues and cells with dose-effect relationship and time-effect relationship.

Objective： The current study was designed to investigate the relationship between cyclin A expression in non-small cell lung carcinoma (NSCLC) and the proliferative activity and the prognosis. Methods： Cyclin A expression in 60 non-small cell lung carcinoma specimens was detected by immunohistochemical method. DNA content was measured by flow cytometry. Results： Twenty-nine cases (48.3％ ) showed cyclin A expression. The median S-phase fraction of the cyclin A-positive 14.4± 3.9％ was higher than that of the cyclin A-negative 9.4± 3.5％ . The overall survival was significantly lower in patients with cyclin A expression than in those without cyclin A expression. Conclusion： Cyclin A expression contributed to the high proliferative activity in non-small cell lung carcinoma cells. Cyclin A might be a prognostic marker of non-small cell lung carcinoma.

Objective To observe DNA damage and morphological changes of lung cells in rats with acute carbonyl nickel poisoning. Methods SD rats were exposed to 20, 135 and 250 mg/m3 carbonyl nickel for 30 min by inhalation. On the third day and 7th day after exposure, DNA damage of lung cells were examined by single cell gel electrophoresis (SCGE) and the pathological changes in lung tissues and the changes of microstructure in lung cells were observed. Results The DNA damage of the rat lung cells were obviously found in all exposure groups at different exposure times and there was the most obvious DNA damage at 72 hour after exposure to nickel carbonyl but the damage appeared later than chlorine exposure group. The inflammatory infiltration and hyperplasia in lung tissue, bronchiolar damage and the bronchial mucosa defulvium appeared in the rats exposed to carbonyl nickel. The results of microstructure examination indicated that the organelles of type I pneumocytes was swellen, the body of type Ⅱ pneumocytes was emptied. The cytoplasm empty bubbles increased, the mitochondria was swellen, and alveolar mediastinum inside the collagen fiber in alveolar mediastinum increased. Conclusion The acute carbonyl nickel exposure could induce the injury of lung tissues and cells with dose-effect relationship and time-effect relationship.

OBJECTIVETo evaluate the prevalence of TET2 gene mutation in acute myeloid leukemia (AML) patients, and analyze their clinical characteristics and prognosis.

METHODSPolymerase chain reaction (PCR) and direct sequencing were used to sequence exon 3 to 11 of TET2 gene.

RESULTSAmong 96 AML patients, TET2 gene mutation was detected in 13 (13.54%) patients (95%CI 6.70% - 20.38%). The median age was 54 years in mutated group and 41 years in unmutated group (P = 0.010). Mutated and unmutated patients did not significantly differ in gender, white blood cells (WBC) count at diagnosis, platelet count, PB and BM blast percentage and chromosome karyotype, excepting for hemoglobin level 84 (70 - 108) g/L in mutated group versus 70 (55 - 87) g/L in unmutated group (P = 0.032). TET2 gene mutation had no significant correlation with C-KIT, FLT3, JAK2V617F mutations, but did with NPM1 mutation. TET2 mutated patients had lower CR1 rate and 2-year overall survival than unmutated in non-M(3) patients (P < 0.05).

CONCLUSIONSTET2 gene mutation is more prevalent in older AML patients and has a certain correlation with clinical characteristics and outcome. It may be a molecular marker for poor prognosis in AML.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; DNA Mutational Analysis ; DNA-Binding Proteins ; genetics ; Exons ; Female ; Humans ; Karyotype ; Leukemia, Myeloid, Acute ; genetics ; Male ; Middle Aged ; Proto-Oncogene Proteins ; genetics ; Young Adult