OBJECTIVE: To investigate the effect of bromocriptine on the expression of Pit-1 in prolactinoma rats. METHODS: Firstly, to prepare prolactinoma model in rats. Adult Wistar rats were divided into two groups at random. The rats in control group were subscutaneously implanted with a blank implant. Rats in 17β-estradiol group were implanted with 17β-estradiol-containing implants. Secondly, rates in 17β-estradiol group were divided into two groups at random: model group and bromocriptine group. Water was administrated to rats in model group. Bromocriptine (0.225 mg · kg-1 · d-1) were orally administrated to rats in bromocriptine group, the rats in control group were orally administrated with water. After four weeks of treatment, all the animals were executed. Each pituitary gland was weighed. Serum prolactin (PRL) levels were measured by RIA method. Pit-1 mRNA levels in pituitaiy tissue were measured by RT-PCR method. RESULTS: The weights of pituitary gland and PRL levels in 17β-estradiol group were individually higher than those in control group (P<0.001). The expression levels of Pit-1 mRNA in bromocriptine group was obviously lower than that in model group (P≤0.001). CONCLUSION: Bromocriptine has potential preventive effect to estrogen-induced rat prolactinoma. The decrease of Pit-1 mRNA level may be involved in the mechanism of anti-prolactinoma effect of bromocriptine.

Adolescent ; Adult ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Child ; Cytarabine ; administration & dosage ; Daunorubicin ; administration & dosage ; adverse effects ; Female ; Humans ; Leukemia, Myeloid, Acute ; drug therapy ; Male ; Middle Aged ; Mitoxantrone ; administration & dosage ; adverse effects ; Young Adult

Cardiomyopathies ; diagnosis ; etiology ; Child ; Humans

Objective To study the life quality of 2 - 3 years old survivors in Neonatal Intensive Care Unit (NICU). Methods Severe neonates were randomly assigned to intervention group (group 1,30 cases) and non- intervention group (group 2,30 cases) depending on the early intervention applied or not,as well as 30 healthy newborns as normal controls. The physical,neurological conditions and intelligence test were taken regularly. To investigate the psychological state, actions, temperament and family conditions when they were2-3 years old.Results Mental development index(MDI) and physical development index(PDI) in early interventional group were significant higher than those in group 2(P

OBJECTIVETo observe the changes of the mechanical pain threshold in the rat model of autoimmune prostatitis, explore the mechanism of autoimmune prostatitis pain and offer some animal experimental evidence for the drug therapy of the condition.

METHODSTwenty male Wistar rats weighing 180 - 220 g were divided into a model and a control group. The autoimmune prostatitis model was established by subcutaneous injection of an extract of male rat prostate glands (RPG) at 60 mg/ml in Freund's complete adjuvant (FCA) and pertussis-diphtheria-tetanus vaccine at 0 and 30 days, respectively. Mechanical tactile hyperalgesia was measured once a week using Von Frey Filaments from the beginning of the study. At 8 weeks after modeling, the rats were sacrificed and the prostate tissues harvested for observation of histomorphological changes by HE staining.

RESULTSHE staining revealed different degrees of benign prostatitis in the model rats. Compared with the controls, the mechanical pain threshold in the model rats was significantly decreased with the increased time of modeling, from (65.52 +/- 6.27) g at 0 week to (23.67 +/- 4.09) g at 8 weeks (P < 0.01). Statistically significant differences were found in the variation trend at different time points between the two groups (P < 0.01).

CONCLUSIONAutoimmune prostatitis models were successfully established in rats and hyperalgesia was induced after modeling.

Animals ; Autoimmune Diseases ; physiopathology ; Disease Models, Animal ; Male ; Pain Threshold ; physiology ; Prostatitis ; immunology ; physiopathology ; Rats ; Rats, Wistar

Adrenal Hyperplasia, Congenital ; complications ; metabolism ; Body Height ; Growth Disorders ; etiology ; Humans ; Risk Factors ; Steroid 21-Hydroxylase ; metabolism

Animals ; Cell Culture Techniques ; Cells, Cultured ; Male ; Neural Stem Cells ; cytology ; Neurons ; cytology ; Olfactory Mucosa ; cytology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the detrimental effects of ouabain on cochlear spiral ganglion neurons (SGCs) in vivo and in vitro.

METHODSSeventy-five male SD rats were randomly divided into 5 groups. In addition to the normal control group, rats in other 4 groups received 0.01, 0.02, 0.05 mmol/L of Ouabain or saline through cochlear scala tympani drilling. Seven days after surgery, the hearing threshold was measured by distortion product otoacoustic emissions (DPOAE) and auditory brainstem response (ABR) in rats. In the in vitro study, SGNs were isolated from SD rats (E14) and treated with 1 × 10(-8) mmol/L of Ouabain. The damaged of SGCs were detected after ouabain treatment using immunohistochemistry, transmission electron microscope and scanning electron microscope in vitro.

RESULTSAfter administration of Ouabain, DPOAE did not change significantly. No significant difference in the amplitude of DPOAE could be observed among all the groups (P > 0.05). Compared with saline and normal control, ABR threshold was significantly increased in the Ouabain treated groups (P < 0.05), which correlated with the concentration of Ouabain. Electron microscopy showed that after treated with Ouabain, SGCs presented degenerative changes, including collapse of organelle structures, the karyotheca dissolved, myelin sheath disintegrating. Ouabain could damage type I SGCs but not type II SGNs.

CONCLUSIONSOuabain can damage SGCs, either in the in vivo or in vitro conditions.

Animals ; Cells, Cultured ; Cochlea ; cytology ; drug effects ; Male ; Ouabain ; toxicity ; Rats ; Rats, Sprague-Dawley ; Spiral Ganglion ; drug effects

OBJECTIVETo report the results of clinical characteristics, enzyme activity determination and mutation analysis of GLB1 gene in a Chinese patient with mucopolysaccharidosis (MPS) type IVB (Morquio B disease).

METHODA 14-year-old Chinese boy with MPS type IVB was firstly diagnosed by blood leucocytes galactosamine-6-sulfate sulfatase (GALNS) and β-galactosidase (GLB1) determination, who was characterized by short stature, multiplex skeletal abnormalities, difficulty in walking. PCR-sequencing analysis was applied to detect the mutations in GLB1 of the patient.

RESULTThe patient was characterized by dwarfism, pectus carinatum, kyphosis, normal intelligence, and no neurologic damage of spasms, linguistic capacity and so on. The patient had normal GALNS enzyme activity and very low GLB1 enzyme activity [5.03 nmol/(h·mg) vs. normal value 118 - 413 nmol/(h·mg) ] in leukocytes. A compound heterozygous missense mutations c.442C > T(p.R148C)/c.1454A > G(p.Y485C) in GLB1 gene were detected in this patient. The mutation p.Y485C is a novel variant. With the method of gene analysis of new variant, the mutation p.Y485C was considered to be a pathogenic mutation.

CONCLUSIONThe MPS IVB patient showed severe multiple skeletal deformities, normal intelligence, no neurologic damage and very low GLB1 enzyme activity, who carries compound heterozygous mutations p.R148C/p.Y485C. The mutation p.Y485C in GLB1 gene may be a novel pathologic mutation of MPS type IVB.

Adolescent ; Amino Acid Sequence ; Asian Continental Ancestry Group ; genetics ; Chondroitinsulfatases ; genetics ; metabolism ; DNA Mutational Analysis ; Humans ; Joints ; pathology ; Male ; Molecular Sequence Data ; Mucopolysaccharidosis IV ; enzymology ; genetics ; pathology ; Mutation, Missense ; Pedigree ; Polymerase Chain Reaction ; Radiography ; Spine ; diagnostic imaging ; pathology ; beta-Galactosidase ; genetics ; metabolism

OBJECTIVETo explore the effect of ITF2357, a novel histone deacetylase (HDAC) inhibitor, on the growth, differentiation and apoptosis of acute myeloid leukemic (AML) cells and its mechanism.

METHODSAML cell lines kasumi-1 cells as a model for AML1-ETO positive, and THP1 cells for AML1-ETO negative, the leukemic cells proliferation was analyzed by MTT assay, expression of myeloid-specific differentiation antigen and cell cycle by flow cytometry, cell apoptosis by annexin V staining and flow cytometry. AML1-ETO, acetyl-histone, and caspase protein was analyzed by Western blot.

RESULTS0.5 µmol/L ITF2357 treatment significantly inhibited kasumi-1 cells proliferation, with the 48 h half inhibitory concentration (IC(50)) of 0.1 µmol/L. The initial inhibitory concentration of THP1 cell line was 5 µmol/L. ITF 2357 induced apoptosis of kasumi-1 cells in a time- and dose-dependent manner. A dose-dependent increase in early apoptosis occurred at 24 hours treatment and in late apoptosis at 48 hours treatment by ITF2357. Early apoptosis cells increased from (1.44 ± 1.52)% to (24.51 ± 5.79)%. Late apoptosis cells increased from (2.37 ± 2.8)% to (63.66 ± 1.56)%. ITF2357 induced AML1-ETO degradation by caspase-dependent pathway. 0.25 µmol/L ITF2357 induced a time- and dose-dependent increase in expression of myeloid cell surface protein CD13 and CD15. 5 µmol/L ITF2357 blocked the cells at G(0)/G(1) phase, G(0)/G(1) cells increased from (39.69 ± 6.56)% to (79.2 ± 6.51)% and s-phase cells declined from (60.12 ± 3.29)% to (18.97 ± 6.62)%. Kasumi-1 cells incubated with 0.5 µmol/L of ITF2357, AML1-ETO protein began to decrease at 24 hours and could hardly be detected at 96 hours. ITF2357 induced AML1/ETO degradation through a caspase-dependent mechanism. At the same time, acetylated H3 and H4 increased.

CONCLUSIONLow-dose HDAC inhibitor ITF2357 can effectively inhibit the AML cells proliferation, especially for AML1-ETO positive AML cells. It inhibits Kasumi-1 cells proliferation degradation of AML1-ETO protein expression, blocks the cells at G(0)/G(1) phase, and induces apoptosis and differentiation of the cells.

Acetylation ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Histone Deacetylase Inhibitors ; pharmacology ; Histones ; metabolism ; Humans ; Hydroxamic Acids ; pharmacology ; Oncogene Proteins, Fusion ; metabolism