OBJECTIVE: To research the value of polymorphism of salivary esterase(Set) in paternity and personal identification. METHODS: Phenotype and genotype of human salivary esterase were detected in 114 liquid saliva samples from the Chinese population by disc electrophoresis and fast blue RR staining assay. RESULTS: The frequency of Set type was F 22.81%, FS 50.88%, S2 6.31%. The estimated gene frequency of SetF was 0.4825 and SetS was 0.5175. The PE was 0.1875 and the DP was 0.6199. CONCLUSION Polymorphism of salivary esterase (Set) was practical in paternity and personal identification.
Esterases/genetics* ; Forensic Anthropology/methods* ; Gene Frequency ; Humans ; Paternity ; Polymorphism, Genetic ; Saliva/enzymology*

This study was aimed at the transport across blood-brain barrier (BBB) of polysorbate-80 modified neurotoxin loaded polybutylcyanoacrylate nanoparticle (P-80-NT-NP) and its cytotoxicity. An in vitro model of BBB using rat brain microvascular endothelial cells (rBMECs) was established. The cytotoxicity of P-80-NT-NP was measured by the MTT assays, where neurotoxin (NT), nanoparticle (NP), neurotoxin nanoparticle (NT-NP) as control, and the permeability of P-80-NT-NP was determined by using of Millicell insert coculture with rBMECs and fluorescence spectrophotometry. MTT results showed that NT, NP, NT-NP and P-80-NT-NP were avirulent to rBMECs when the concentration of NT was lower than 200 ng x mL(-1). But the cytotoxicity of NP, NT-NP and P-80-NT-NP would be augmented accordingly as concentration increased (P < 0.01), causing obvious reductions of cell survival rate, with no significant difference between them (P > 0.05). When the concentration of NT was 150 ng x mL(-1), the permeability on rBMECs of P-80-NT-NP and NT-NP were both significantly higher than that of NT (P < 0.01), and the permeability of P-80-NT-NP was greater than that of NT-NP (P < 0.05). In conclusion, polysorbate-80 modified neurotoxin nanoparticles can transport across the BBB, while concentration of NT is greater than 200 ng x mL(-1), P-80-NT-NP has a little cytotoxicity against rBMECs.
Animals ; Biological Transport ; Blood-Brain Barrier ; Brain ; blood supply ; Capillary Permeability ; Cell Survival ; drug effects ; Cells, Cultured ; Drug Carriers ; Electric Impedance ; Enbucrilate ; chemistry ; toxicity ; Endothelial Cells ; cytology ; metabolism ; Female ; Male ; Nanoparticles ; Neurotoxins ; administration & dosage ; pharmacokinetics ; Particle Size ; Polysorbates ; chemistry ; toxicity ; Rats ; Rats, Sprague-Dawley

The purpose of the present study was to determine the effects of recombinant human interleukin-6 (rhIL-6) on the Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons. The control and rhIL-6 treated hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2+10% CO2) for 2 and 4 h and then were reoxygenated for 24 and 72 h. The expression of Bcl-2 and Bax was revealed immunocytochemically using the antiserum against Bcl-2 and Bax. The apoptosis was examined by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis. The results showed that in cultured hippocampal neurons the Bcl-2 expression decreased while Bax expression and the percentage of apoptotic neurons increased after anoxia-reoxygenation compared with those before anoxia. In comparison with the control, after anoxia-reoxygenation the Bcl-2 expression in hippocampal neurons was higher than that in rhIL-6 group; however the Bax expression and the percentage of the apoptosis were decreased in rhIL-6 group. It is suggested that rhIL-6 may play a role in protecting neurons from the damage induced by anoxia-reoxygenation.
Animals ; Apoptosis ; drug effects ; Cell Hypoxia ; drug effects ; physiology ; Cells, Cultured ; Hippocampus ; cytology ; Interleukin-6 ; pharmacology ; Neurons ; drug effects ; physiology ; Proto-Oncogene Proteins ; biosynthesis ; Proto-Oncogene Proteins c-bcl-2 ; biosynthesis ; Rats ; Rats, Wistar ; Recombinant Proteins ; pharmacology ; bcl-2-Associated X Protein

OBJECTIVETo detect the specific mutations in rpoB gene of Mycobacterium tuberculosis by oligonucleotide microarray.

METHODSFour wild-type and 8 mutant probes were used to detect rifampin resistant strains. Target DNA of M. tuberculosis was amplified by PCR, hybridized and scanned. Direct sequencing was performed to verify the results of oligonucleotide microarray.

RESULTSOf the 102 rifampin-resistant strains 98 (96.1%) had mutations in the rpoB genes.

CONCLUSIONOligonucleotide microarray with mutation-specific probes is a reliable and useful tool for the rapid and accurate diagnosis of rifampin resistance in M. tuberculosis isolates.

Antibiotics, Antitubercular ; pharmacology ; Bacterial Proteins ; genetics ; metabolism ; DNA-Directed RNA Polymerases ; Drug Resistance, Bacterial ; genetics ; Gene Expression Regulation, Bacterial ; Mutation ; Mycobacterium tuberculosis ; drug effects ; genetics ; metabolism ; Oligonucleotide Array Sequence Analysis ; Rifampin ; pharmacology

OBJECTIVETo investigate the protective action of Epimedium against chemotherapy-induced damage to rat epididymides.

METHODSFifty 60-day-old male rats were divided into a control, a model and a treatment group. Procarbazine was injected into the abdominal cavity of the model rats at the dose of 30 mg/(kg x d). In addition to procarbazine, Epimedium was given intragastrically to the treatment group. The changes in the ultrastructure of the epididymis were observed after 10 and 20 days.

RESULTSElectron microscopy showed that the chemotherapy-induced damages to the epididymal epithelia mainly included cell swelling, local cavitation of mitochondria, tumor-like change in nucleoli, agglutination of marginal translocation of heterochromatin and cell apoptosis. The damage to the epithelial ultrastructure was slight in the treatment group as compared with the model rats. Chemotherapy significantly affected sperm concentration, sperm viability and sialic acid (SA), which were (15.59 +/- 4.01) x 10(6)/ml, (76.71 +/- 10.11)% and (19.38 +/- 9.34) g/mg prot in the model group in comparison with (10.63 +/- 3.82) x 10(6)/ml (P < 0.01), (60.03 +/- 7.54)% (P < 0.01) and (13.62 +/- 7.81) g/g prot (P < 0.05) in the control. Epimedium significantly increased sperm viability in the treatment group (60.03 +/- 7.54)% as compared with the model rats (69.90 +/- 12.58)% (P < 0.05).

CONCLUSIONEpimedium can lessen chemotherapy-induced damage to the epididymis and protect the reproductive function of rats.

Animals ; Antineoplastic Agents ; toxicity ; Drugs, Chinese Herbal ; pharmacology ; Epididymis ; drug effects ; physiopathology ; ultrastructure ; Epimedium ; chemistry ; Infertility, Male ; chemically induced ; physiopathology ; prevention & control ; Male ; Microscopy, Electron, Transmission ; Phytotherapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents.

METHODSAfter hypoxic preconditioning and acute anoxia the I(Na), I(K) were measured in cultured hypothalamic cells by patch-clamp whole cell recording technique.

RESULTSThe amplification of Na+ currents did not been significantly changed, but the amplification of K+ currents was in hypoxic preconditioning neurons; acute anoxia lead to the inhibition of Na+, K+ currents in the two groups, while Na+, K+ currents in non-preconditioned control group were inhibited severity than hypoxic preconditioning group.

CONCLUSIONIt is presumed enhanced anoxia tolerance induced by hypoxic preconditioning may be related to the opening of K+ channels.

Animals ; Cell Hypoxia ; Cells, Cultured ; Hypothalamus ; cytology ; physiopathology ; Neurons ; physiology ; Oxygen ; physiology ; Patch-Clamp Techniques ; Potassium ; physiology ; Rats ; Rats, Wistar ; Sodium ; physiology

AIMTo study the effects of hypoxic preconditioning on anoxic tolerance and Jun expression in cultured rat hippocampal neurons after anoxia/reoxygenation.

METHODS12 day cultured hippocampal neurons in control and hypoxic preconditioning group were exposed to anoxic environment (0.90L/L N2 + 0.10 L/L CO2) for 4 h, and then reoxygenated for either 24 h or 72 h. The neurons were immunocytochemically stained using the antiserum against Jun. The number of survival neurons and the percentage of Jun expressing neurons were investigated.

RESULTSThe percentage of Jun expressing neurons induced by anoxia in hypoxic-preconditioning group was significantly less than that in control group. The number of survival neurons was more in the hypoxic-preconditioning group than that in control group after anoxic reoxygenation.

CONCLUSIONHypoxic-preconditioning can induce the development of anoxic-tolerance in cultured hippocampal neurons. The decrease in Jun expressing neurons in hippocampus may be an adaptive reaction to acute anoxia.

Animals ; Animals, Newborn ; Cell Hypoxia ; Cells, Cultured ; Genes, jun ; Hippocampus ; metabolism ; Neurons ; metabolism ; Oxygen ; metabolism ; Rats ; Rats, Wistar

The aim of this study was to investigate the effect of proteasome inhibitor bortezomib on the expression of ERK, JNK, and P38 in daunorubicin (DNR)-resistant K562 cells and its mechanism. MTT method was used to determine the drug-resistant K562 cells and the cellular toxicity of bortezomib; Western blot was used to detect the expression of protein ERK, JNK and P38 in K562 cells after treatment with 100 nmol/L DNR alone or combined with 1 nmol/L and 10 nmol/L bortezomib for 36 hours. Flow cytometry assay was used to detect the apoptosis rate in each group cells. The results indicated that the expression of ERK and P38 were significantly suppressed (p < 0.05) and the expression of JNK was significantly enhanced (p < 0.05) in the cells treated by DNR combined with bortezomib. It is concluded that bortezomib can decrease the expressions of protein ERK and P38 and enhance the expression of JNK, the bortezomib reverses the cellular drug-resistance and promote cell apoptosis through MAPK pathway.
Antineoplastic Agents ; administration & dosage ; pharmacology ; Boronic Acids ; administration & dosage ; pharmacology ; Bortezomib ; Drug Resistance, Neoplasm ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; K562 Cells ; Protease Inhibitors ; administration & dosage ; pharmacology ; Pyrazines ; administration & dosage ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; metabolism

AIMTo study effect of CoCl2 pretreatment on the voltage-gated Na+ and K+ currents of the rat hippocampal neurons after acute hypoxia.

METHODSPrimarily cultured hippocampal neurons were divided into CoCl2 pretreated and non-pretreated groups. Patch clamp whole cell recording technique was used to examine Na+ and K+ currents of the hippocampal neurons.

RESULTSAfter acute hypoxia, I(Na) and I(K) of the hippocampal neurons were significantly decreased and the threshold of I(Na) was right-shifted. Pretreatment of the neurons with CoCl2 inhibited the reduction of I(Na) and I(K).

CONCLUSIONCcCl2 pretreatment alleviates the acute hypoxia-induced changes of I(Na) and I(K), which may be one of the mechanisms for the protective effect of CoCl2 on neurons.

Animals ; Animals, Newborn ; Cell Hypoxia ; Cobalt ; pharmacology ; Hippocampus ; cytology ; physiopathology ; Neurons ; drug effects ; Patch-Clamp Techniques ; Potassium Channels ; metabolism ; Rats ; Rats, Wistar ; Sodium Channels ; metabolism

AIMTo establish the model of oxygen-glucose deprivation in vitro rat hippocampal neurons.

METHODSThe hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5-4 h and then cultured with original medium in normoxia for 24 h. Auto-biochemical analyzer determined LDH activity. The change of neuronal morphology and neuron survival were observed by converted contrast microscope and assessed by photography analysis system. Neuron apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method.

RESULTSThe neurons swelled, LDH release increased and neuron survival decreased after gradually oxygen-glucose deprivation. The percentage of apoptosis increased obviously 24 h after recovering the supply of oxygen and glucose.

CONCLUSIONThe model of oxygen-glucose deprivation in vitro rat hippocampal neurons is established successfully by using the modified ACSF (artificial cerebral spinal fluid) with serum and glucose free.

Animals ; Animals, Newborn ; Cell Hypoxia ; Cells, Cultured ; Glucose ; deficiency ; Hippocampus ; cytology ; Neurons ; cytology ; Oxygen ; physiology ; Rats ; Rats, Wistar