Objective To investigate whether mesenchymal stem cells can promote the recovery of acute renal tubular damage induced by mercuric chloride and to explore its possible mechanism.Methods Acute renal failure rat model was established by intraperitoneal injection of mercuric chloride.SD rats were randomly divided into three groups which were MSCs injection group, saline infusion group and normal control group.Seven days later,the changes of rat weight,survival,renal function and pathology were observed;PCNA,ED-1 and GFP were detected by immunohistochemistry; The expression of cytokines in kidney and the distribution of GFP plasmid-transfected MSCs in kidney were examined by RT-PCR.Results MSCs infusion ameliorated the decline of rat weight,survival, renal function,and pathological changes.PCNA and ED-1 positive cells in MSCs group were fewer than those in saline group.Expression of growth factors EGF,PDGF,HGF were obviously up- regulated and pre-inflammatory cytokines TNF-?was significantly reduced in MSCs-treated kidneys. GFP-labelled MSCs occurred occasionally in renal interstitium of MSCs-treated rats,but not in renal tubules.Conclusions Bone marrow mesenchymal stem cells can promote the recovery of acute renal tubular epithelial cells damage caused by mercuric chloride.The mechanism may partly depend on regulating the excretion of cytokines in renal microenvironment rather than completely depend on their differentiation to tubular cells.

BACKGROUNDProliferation, cell migration and phenotypic modulation of airway smooth muscle cells (ASMCs) are important features of airway remodelling in asthma. The precise cellular and molecular mechanisms that regulate ASMCs proliferation, migration and phenotypic modulation in the lung remain unknown. Basic fibroblast growth factor (bFGF), a highly specific chemotactic and mitogenic factor for many cell types, appears to be involved in the development of airway remodelling. Our study assessed whether bFGF directly stimulates the proliferation, migration and phenotypic modulation of ASMCs.

METHODSConfluent and growth arrested human ASMCs were treated with human recombinant FGF. Proliferation was measured by BrdU incorporation and cell counting. Migration was examined using Boyden chamber apparatus. Expressions of smooth muscle (sm)-alpha-actin and sm-myosin heavy chain (MHC) isoform 1 were determined by RT-PCR and Western blot analysis.

RESULTSIt was found that hrbFGF (10 ng/ml), when added to ASMCs, induced a significant increase in BrdU uptake and cell number by ASMCs as compared to controls and a significant increase in ASMCs migration with respect to controls. The mRNA and protein expressions of sm-alpha-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls.

CONCLUSIONIt appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells' contractive phenotype decreased.

Actins ; analysis ; genetics ; Bronchi ; cytology ; drug effects ; physiology ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Fibroblast Growth Factor 2 ; pharmacology ; Humans ; Major Histocompatibility Complex ; Myocytes, Smooth Muscle ; drug effects ; Phenotype ; RNA, Messenger ; analysis

OBJECTIVETo analyze factors related to the virulence associated genes of Leptospires.

METHODSTwelve putative virulence associated genes were detected by polymerase chain reaction (PCR) method in 38 reference strains, 81 field strains of Leptospira interrogans isolated from patients or animals, and 12 avirulent strains of Leptospira biflexa.

RESULTSThese putative virulent genes were widely distributed among the strains of Leptospira interrogans, but only few of them were detected in Leptospira biflexa. Gene lipL32 was detected in all strains of Leptospira interrogans. Distribution of gene lipL36 was varied significantly with detected rates from 0 to 90.91%. Gene la1608 had a positive rate of 87.50% for strains of serogroup Icterohaemorrhagiae, but was only detected in few strains of other serogroups with a range from 0 to 25.00%. Rate of detection on gene sphA was 17.65% in Leptospira interrogans, and was absent in serovar hardjo reference strain.

CONCLUSIONResults indicated that these genes might be of importance for the virulence and pathogenicity of Leptospira interrogans, while gene lipL32 might be one of the common antigens. Gene lipL36 might be involved in serogroup specificity with genetic diversity, but gene la1608 was as one of the genes with specificity for serogroup Icterohaemorrhagiae. However, serovar hadjo might hold quite different genetic characteristics when compared with the other serovars of Leptospires.

Bacterial Outer Membrane Proteins ; genetics ; Bacterial Proteins ; genetics ; Carbohydrate Dehydrogenases ; genetics ; Flagellin ; genetics ; Genes, Bacterial ; genetics ; Hemolysin Proteins ; genetics ; Leptospira ; genetics ; pathogenicity ; Lipoproteins ; genetics ; Polymerase Chain Reaction ; Virulence ; genetics ; Virulence Factors ; genetics

OBJECTIVETo probe the effects of long-term oral administration of lanthanum nitrate [La(NO(3))(3)] on morphological change in the liver, aftereffect of deposited La in the liver and their mechanism in rats.

METHODSYoung Wistar rats were divided into two groups, one fed with 0.1, 0.2, 2.0, 10.0 and 20.0 mg/kg of La(NO(3))(3) for six months and the other for the control. Changes in ratio of liver to body weight were observed after exposure to La(NO(3))(3) at varied doses for six months and one month after six-month exposure, as well as morphology of the liver in the rats with routine histochemistry and transmission electron microscopy (TEM) technique. Content of La in the liver was measured with inductively coupled plasma-mass spectrometry (ICP-MS).

RESULTSRatio of liver to body weight was significantly higher in the male rats exposed to 20.0 mg/kg of lanthanum for six months than that in the control group. Ratio of liver to body weight restored to normal in the rats exposed to 20.0 mg/kg of La one month after six-month exposure. Infiltration of inflammatory cells in the portal region of the liver, small amount of fat drops in hepatocytic cytoplasm, increased density of mitochondria stroma, lysosome containing highly-electronic-density bodies and dense granules, normal nucleus and slightly deformed nucleus of hepatocytes could be found in the rats exposed to 20.0 mg/kg. Areas of the liver deposited with glycogen after six-month exposure to 20.0 mg/kg of La accounted for (26.1 +/- 1.5)% and (4.1 +/- 1.4)%, respectively for male and female rats, significantly lower than those in the control group [(31.3 +/- 1.4)% and (39.4 +/- 0.9)%, respectively], with a statistical significance and very statistical significance, respectively. There was a little infiltration of inflammatory cells in the portal region of the liver one month after six-month exposure to 20.0 mg/kg of La, and amount of the dense bodies was lower in the rats exposed to La for six months. Liver contents of La in the rats of all experimental groups were lower one month after six-month exposure than those in the rats exposed for six months.

CONCLUSIONSExposure to a dose of 20.0 mg/kg La(NO(3))(3) for a long term could damage the liver structure to certain extent, but lanthanum deposited in the liver could be eliminated from the body gradually.

Administration, Oral ; Animals ; Female ; Lanthanum ; toxicity ; Liver ; drug effects ; metabolism ; pathology ; Male ; Organ Size ; Rats ; Rats, Wistar

OBJECTIVETo study the clinicopathological features and differential diagnoses of mixed epithelial and stromal tumor of the kidney.

METHODSClinical and pathological characteristics of 4 cases of mixed epithelial and stromal tumor of the kidney were studied.

RESULTSThree patients were female and one was male. All patients presented with flank pain and hematuria. Radiologic studies revealed cystic and solid masses involving the kidney. Grossly the tumors had a solid and cyst appearance. Microscopically, the tumors were composed of a mixture of stromal and epithelial elements. The epithelial elements were variable in cell types including cuboidal, hobnail and columnar cells. One case showed Müllerian and intestinal epithelial differentiations. Stromal elements essentially consisted of spindle cells, with thick-walled blood vessels and bands of smooth muscle cells as distinctive features of the tumor. Immunohistochemical staining revealed that the epithelial components were positive for AE1/AE3, whereas the stromal components were positive for ER, PR, and SMA. All patients underwent nephrectomy and were well without evidence of recurrence.

CONCLUSIONSMixed epithelial and stromal tumor of the kidney is a benign neoplasm with distinct histopathological features. It should be distinguished from many other renal neoplasms. Surgical intervention is a preferred therapy.

Actins ; metabolism ; Adult ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Muscle, Smooth ; metabolism ; Neoplasms, Complex and Mixed ; metabolism ; pathology ; surgery ; Neoplasms, Glandular and Epithelial ; metabolism ; pathology ; surgery ; Nephrectomy ; methods ; Receptors, Estrogen ; metabolism ; Receptors, Progesterone ; metabolism

OBJECTIVETo investigate the mutations of mitochondrial genome in a pedigree with suspected maternally inherited diabetes and deafness and to explore the correlations between the mutations and clinical features.

METHODSGenomic DNA was isolated from blood leucocytes of each member of the pedigree. The mitochondrial genome was amplified with 24-pair primers that could cover the entire mitochondrial DNA. Direct sequencing of PCR products was used to identify any mitochondrial DNA mutations.

RESULTSFamily members on the maternal side all harbored the tRNALeu(UUR) A3243G mutation. The paternal side family members did not have the mutation. The age-of-onset of diabetes of the 4 maternal side family members was 15, 41, 44, and 65 years old, and their corresponding heteroplasmy level of the mutation was 34.5%, 14.9%, 14.6%, and 5.9%, respectively. The age-of-onset of diabetes and heteroplasmy level of A3243G mutation were negatively correlated with a correlation coefficient of -0.980 (P = 0.02). Meanwhile, patient with high heteroplasmy level of A3243G mutation had relatively low severity of disease. Moreover, 6 reported polymorphisms and 2 new variants were found.

CONCLUSIONSThe main cause of diabetes in this pedigree is the tRNALeu(UUR) A3243G mutation. However, other gene variants may contribute to its pathogenicity. The heteroplasmy level of the tRNALeu(UUR) A3243G mutation is positively associated with earlier age-of-onset and increasing severity of diabetes.

Adolescent ; Adult ; Age of Onset ; Aged ; Asian Continental Ancestry Group ; genetics ; China ; Diabetes Mellitus, Type 1 ; diagnosis ; genetics ; Female ; Hearing Loss ; genetics ; Humans ; Middle Aged ; Mitochondria ; genetics ; Pedigree ; Point Mutation ; genetics ; Polymorphism, Single Nucleotide ; genetics ; RNA, Transfer ; genetics ; RNA, Transfer, Leu ; genetics ; Young Adult

To observe the expression of cyclin D1, hTERT, and telomerase activity in MNC, HL-60, HL-60A and to explore their effects on leukemogenesis and drug-resistance, normal human peripheral blood mononuclear cells, HL-60 cells sensitive to adriamycin and HL-60A cells resistant to adriamycin were investigated. The cell cycle was analyzed by flow cytometry, and the apoptosis was analyzed by Annexin V-FITC(+) PI staining. Expressions of cyclin D1 and hTERT were determined by real-time PCR and Western blot. Telomerase activity was detected by TRAP-ELISA. The results indicated that the percentage of MNC, HL-60 and HL-60A in S phase was (10.21 + 2.11)%, (44.93 + 3.00)%, and (51.38 + 1.10)% respectively; the percentage of apoptosis cells was (16.14 + 2.13)%, (7.53 + 0.92)%, (4.15 + 0.96)% respectively; the expression of mRNA and protein for cyclin D1 and hTERT increased; the telomerase activities of HL-60 and HL-60A were higher (p = 0.000), whereas the difference between HL-60 and HL-60A was no statistically significant (p = 0.232); positive correlation between cyclin D1, hTERT and telomerase activity had been found (p < 0.01). It is concluded that the cells of S phase increased while the apoptotic cells decreased in HL-60 and HL-60A, especially in HL-60A, which may be due to the up-regulation of cyclin D1, hTERT and telomerase activity.
Cell Cycle ; Cyclin D1 ; metabolism ; HL-60 Cells ; Humans ; Leukemia ; metabolism ; Telomerase ; metabolism

OBJECTIVETo explore the relationship between heavy metals exposure and neurobehavioral function impairment in welders.

METHODSThe metals exposure in 82 welders and 51 operators were investigated with blood Pb, Cd and Mn via AAS, and the nervous impairment was evaluated with neurobehavioral core test battery (NCTB).

RESULTSPb [(115.49 +/- 79.22) microg/L] and Cd [(3.67 +/- 3.19) microg/L] in welders were significantly higher than operators [(69.32 +/- 50.79) and (0.83 +/- 0.76) microg/L respectively] (P < 0.05). Welders had worse standard scores of NCTB 13 items such as depression-dejection than non-welders (P < 0.05). Significant difference of confusion-bewilderment and forward digit span in welders only existed in different groups of Pb and Mn, respectively. A dose-effect relationship was found between forward digit span and serum Mn level in welders. General linear regression analysis indicated that Pb exposure, Mn exposure and alcohol consume had negative relation with the loss of nervous system function.

CONCLUSIONThe nervous impairment in welders is attributed to occupational exposure to Pb and Mn, concomitantly.

Adult ; Air Pollutants, Occupational ; adverse effects ; Central Nervous System Diseases ; chemically induced ; physiopathology ; Cross-Sectional Studies ; Female ; Humans ; Male ; Metals, Heavy ; adverse effects ; Neuropsychological Tests ; Occupational Exposure ; adverse effects ; Welding ; Young Adult

OBJECTIVETo explore the effects of chloride channels on the regulation of platelet cytoplasmic free calcium concentration ([Ca2+]i) and platelet aggregation (PAG).

METHODSFreshly separated platelets were activated by thrombin. Chloride channel blockers DIDS or NFA and calcium channel blockers SK&F96365 or nifedipine were added to study the effects on platelet [Ca2+]i and PAG by a single reagent or the combination of reagents and find out the interactions among DIDS, NFA, SK&F96365 and nifedipine.

RESULTSBoth DIDS and NFA could inhibit the thrombin (1 U/ml) induced PAG in a dose-dependent manner, whereas had little effect on resting [Ca2+]i. As compared with the control group, DIDS, SK&F96365 and Nifedipine could significantly reduce the PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05). The combination of DIDS and SK&F96365 had greater effects in reducing the PAG, Ca2+ release and Ca2+ influx than either reagent alone (P < 0.05). The combination of DIDS and nifedipine also had greater effect than each alone in reducing Ca2+ release (P < 0.05). The combination of NFA and SK&F96365 weakened each other's effect on Ca2+ release (P < 0.05), while NFA and nifedipine weakened each other's effects on PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05).

CONCLUSIONDIDS and NFA have no effect on the resting [Ca2+]i and the leak calcium influx of platelet. DIDS can inhibit the Ca2+ release, Ca2+ influx and PAG of platelet induced by thrombin, while NFA can only inhibit the Ca2+ release. The chloride channel and calcium channel blockers have interactions in affecting resting [Ca2+]i and PAG of platelet. The opening of chloride channel can influence the cellular calcium movement of platelet.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid ; pharmacology ; Adult ; Blood Platelets ; cytology ; drug effects ; metabolism ; Calcium ; metabolism ; Calcium Channel Blockers ; pharmacology ; Cells, Cultured ; Chloride Channels ; antagonists & inhibitors ; physiology ; Cytoplasm ; drug effects ; metabolism ; Drug Interactions ; Humans ; Imidazoles ; pharmacology ; Nifedipine ; pharmacology ; Niflumic Acid ; pharmacology ; Platelet Aggregation ; drug effects ; Thrombin ; pharmacology

OBJECTIVETo clone the entire coding sequence and analyze the function of P2X7 receptor of J6-1 human leukemia cells.

METHODSThe entire coding sequence of P2X7 receptor was amplified by RT-PCR and then inserted into pTARGET plasmid to construct an eukaryotic expressing plasmid followed by DNA sequencing. HEK293 cells stably expressing P2X7 receptor were obtained after transfection and screening, and confirmed by RT-PCR and Western blotting. The bleb formation upon agonist stimulation was observed under phase contrast microscope.

RESULTSThe entire coding sequence of P2X7 receptor of J6-1 cells was successfully cloned. DNA sequencing analysis revealed a substitution of G559, for A559, causing a substitution of Glu187 for Gln187. The P2X7 receptor derived from J6-1 cells could be functionally expressed in HEK293 cells, in which bleb formation could be detected upon stimulation.

CONCLUSIONSThe entire coding sequence of P2X7 receptors was successfully cloned from J6-1 leukemia cells. Other unknown mechanism may contribute to the dysfunction of P2X7 receptor in these cells.

Cell Line, Tumor ; Cloning, Molecular ; DNA, Complementary ; genetics ; Gene Expression ; Humans ; Leukemia ; genetics ; metabolism ; Receptors, Purinergic P2 ; genetics ; physiology ; Receptors, Purinergic P2X7 ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection