Objective To investigate the ultrastructure and function changes of the thyroid parafollicular cell in ANP rats and to study the possible mechanism of hypocalcemia during ANP.Methods Thirty-two male Wistar rats were randomly divided into 4 groups:sham operation group ( SO group) and ANP 3,6,12 h groups.ANP model was induced by retrograde injection of 5％ sodium taurocholate into the biliopancreatic duct. The serum levels of amylase,lipoidase,calcitonin and Ca2+ were measured.The pathological changes in pancreatic tissue were observed.The ultrastructure changes of thyroid parafollicular cell were observed.ResultsThe serum levels of amylase,lipoidase,calcitonin and Ca2+ were (4025 ±579)U/L,(8272 ± 794) U/L,(383.6 ± 64.5) pg/ml,(2.41 ± 0.12) mmol/L at 6h in ANP group,which were significantly higher than those in SO group [ ( 1063 ± 129 ) U/L,( 55 ± 18 ) U/L,( 143.1 ± 42.2 ) pg/ml,(2.97 ±0.12 ) mmol/L ( P ＜0.05 ) ].Under the electron-microscopy,the nucleus of thyroid parafollicular cells shrinked and mitochondrial proliferation and endoplasmic reticulum fusion appeared.After 6 h,all the organelle reduced and disappeared,and only small amount of secretory granules remained.Conclusions Changes in the structure and function of the thyroid parafollicular cells occur in rats of ANP,and they induce the development of hypocalcemia.

OBJECTIVEThe present study investigated the effects of rapamycin on Aβ1-42-induced deficits in working memory and synaptic plasticity.

METHODSAfter bilateral hippocampal injection of Aβ1-42 and rapamycinin rats, spontaneous alternation in Y-maze and in vivo hippocampal long-term potentiation (LTP) of rats were recorded. All data were analized by two-way repeated measures analysis of variance (ANOVA).

RESULTS(Hippocampal injection of Aβ1-42 alone impaired working memory of rats; (2) Rapamycin did not affect working memory of rats, but alleviated Aβ1-42-induced working memory deficits, compared with Aβ1-42 alone group; (Aβ1-42 remarkably suppressed in vivo hippocampal LTP of fEPSPs in the CA1 region; (4) Pretreatment with rapamycin prevented Aβ1-42-induced suppression of LTP.

CONCLUSIONThese data indicates that rapamycin could protect against Aβ1-42-induced impairments in working memory and synaptic plasticity in rats.

Amyloid beta-Peptides ; adverse effects ; Animals ; Hippocampus ; drug effects ; Long-Term Potentiation ; Maze Learning ; Memory, Short-Term ; drug effects ; Neuronal Plasticity ; drug effects ; Peptide Fragments ; adverse effects ; Rats ; Sirolimus ; pharmacology

OBJECTIVETo analyze the audiological features and genetic background of patients carrying mitochondrial DNA(mtDNA) 1555A>G mutation and factors which may influence the extent of nonsyndromic hearing loss associated with the mutation.

METHODSA literature search was carried out on databases including PubMed, CNKI, Wanfang, and VIP. Combined with author's data, the clinical features of the patients, in particular audiological characteristics, were summarized.

RESULTSA total of 857 effective cases were collected and analyzed. A significantly correlation was identified between history of aminoglycosides exposure and extent of hearing loss, in addition with a negative correlation between the age of onset and extent of hearing-impairment. Drug exposure was corelated with the age of onset but independent to the loss of high-frequency hearing loss. Heteroplasmies had a reverse correlation with the degree of hearing loss. Among the haplotypes of mitochondrial DNA, haplotype D was the most common one, while haplotype B had the highest penetrance.

CONCLUSIONNonsyndromic hearing loss associated with mitochondrial DNA 1555A>G mutation is influenced by factors such as aminoglycosides exposure, age, proportion of mutation, and haplotype of the mitochondrial DNA. Analysis of clinical cases is critical for identifying individuals carrying deafness susceptibility mutations and is the first step for early diagnosis.

Objective - To investigate the effect of lung flora dysbiosis on the process of pulmonary fibrosis and lung epithelial （ ） Methods - mesenchymal transition EMT in mice with silicosis. Male C57BL/6 mice of specific pathogen free grade were ， ， ， （ ） randomly divided into the blank control group silicosis model group solvent control group vancomycin VM + ampicillin （ ） ， （ ） （ ） ， AMP group metronidazole MNZ + neomycin NEO group and mixed treatment group 12 mice in each group. Except for ， ， the blank control group which was given 20.0 µL of 0.9% NaCl solution the other five groups of mice were dosed with 20.0 µL of silica dust suspension at a mass concentration of 250.0 g/L using a single tracheal drip to establish the silicosis mouse model. ： The intranasal drip method was used to treat silicosis mice in each group as following mice in the solvent control group were - ； ； given double distilled water mice in the VM+AMP group were given VM at a mass concentration of 0.5 g/L and AMP at 1.0 g/L ； mice in the MNZ+NEO group were given MNZ at a mass concentration of 1.0 g/L and NEO at 1.0 g/L mice in the mixed ， treatment group were given the same doses of the four antibiotics mentioned above all in a drip volume of 50.0 µL. Silicosis ， ， mice were treated seven days and half an hour before silica dusting and 7 14 and 21 days after silica dusting. Mouse lungtissue was collected aseptically 28 days after silica dusting. Hematoxylin eosin and Masson trichrome staining methods were - used to observe the pathological changes. Western blotting was used to detect the relative protein expression of α smooth muscle （ - ）， - （ - ） （ ） actin α SMA E cadherin E CAD and vimentin VIM . Immunohistochemistry was used to detect the relative expression of - - E CAD and VIM. Real time fluorescence quantitative polymerase chain reaction was used to detect the expression levels of （Col1a2） Results collagen type Ⅰ alpha 2 mRNA in lung tissues. The histopathological results showed that the alveoli of the ， blank control group were thin and structurally intact with few surrounding infiltrating inflammatory cells and no abnormal ， distribution of collagen fibers. The alveoli of the silicosis model group were structurally disorganized with a large number of ， ， infiltrating inflammatory cells thickened alveolar walls and cellular fibrous nodules with abundant blue collagen deposit. In the ， ， VM+AMP group MNZ+NEO group and the mixed treatment group the inflammation and fibrosis were reduced with diferent degrees in the lung tissues compared to the silicosis model group and the solvent control group. The relative expression levels of - ， Col1a2 α SMA VIM protein and mRNA in lung tissues of mice in the silicosis model group were higher than those in the blank （ P ）， -CAD control group all <0.05 and the relative expression levels of E protein were lower than those in the blank control （P ） - ， Col1a2 group <0.05 . The relative expression levels of α SMA VIM protein and mRNA in lung tissues of mice in the MNZ+ （ P ）， -CAD NEO group and the mixed treatment group were lower all <0.05 and the relative expression levels of E protein were （P ）， Conclusion higher <0.05 when compared with the silicosis model group and the solvent control group. Pulmonary fibrosis ， - was reduced in silicosis mice with interventions in lung flora where anaerobic and gram negative bacteria affected pulmonary fibrosis and dysbiosis of the lung flora affected pulmonary EMT.

Objective To look for the genes of Schistosoma japonicum related to the Schistosoma-resistance of Microtus fortis.Methods The fresh sera of Microtus fortis were used to screen a T7 phage display cDNA library from worms of Schistosoma japonicum established in our lab.The positive clones were sequenced and functionally analysed through bioinformatics.Results The specific phages binding to the sera of Microtus fortis were enriched 857-fold after three rounds of biopanning,and 58 positive clones picked at random were sequenced and 10 ESTs were obtained.BLASTn results showed that 7 ESTs had 99%-100% similarity to the genes of Shistosoma japonicum reported in GenBank and 1 EST had 82% similarity to a zinc finger protein encoden gene from Pan troglodytes.The results of these ESTs function prediction indicated most of them were involved in the regulation of gene expresion of Schistosoma japonicum.Conclusions Several target genes of Schistosoma japonicum related to the Schistosoma-resistance of Microtus fortis are obtained and those would lay foundation to expatiate the native resistance mechnism of Microtus fortis to Schistosoma japonicum.

An efficient protocol for plant regeneration from protoplasts of the methionine resistant variant of Astragalus melilotoides was established. The friable calli induced from internode segments of variant plants were used for protoplast preparation. The protoplasts were isolated through enzyme digestion. Calli were formed after sustained divisions of protoplasts. High frequency of shoot differentiation was obtained from the protocalli on differentiated medium. The effects of different media, culturing methods and plating densities on protoplast divisions and plant regeneration were studied. The results show that agarose-beads culture method, KM8p medium supplemented with 1.0 mg/L 2,4-D, 0.5mg/L 6BA, 0.3 mol/L mannitol, 2% (W/V) sucrose and 500 mg/L casein hydrolysate at a plating density of 3 x 10(5)/mL are the appropriate conditions for protoplast division of the methionine resistant cell line. The division frequency is over 38%. The protoplast-regenerated plants still preserve resistance to methionine and ethionine.This research builds up the foundation for the resistant cell line as a parent of somatic hybridization.
Astragalus Plant ; growth & development ; physiology ; Culture Media ; Culture Techniques ; methods ; Drug Resistance ; Methionine ; pharmacology ; Protoplasts ; cytology ; Regeneration

Objective To re-evaluate the immunogenicity of meningococcal serogroups A and C polysaccharide vaccine among a healthy population of age 5 to 59.Methods Pre and post-vaccination ser-um samples were collected from the subjects involved in a randomized , controlled clinical trial conducted in 2005 at Hechi, Guangxi, China.Enzyme-linked immunosorbent assay (ELISA) was performed for the quan-titative detection of specific anti-capsule IgG antibody against meningococcal serogroups A and C in serum samples.Serum bactericidal assay ( SBA) was used to measure the bactericidal antibody activity against se-rougroups A and C bacterial strains .Results Geometric mean concentrations (GMCs) of specific anti-cap-sule IgG antibody were 23.66 μg/ml and 78.83 μg/ml for serogroup A (P<0.05), and 1.23 μg/ml and 51.25 μg/ml for serogroup C (P<0.05) in serum samples of pre and post-vaccination, respectively.Be-fore immunization , 99% of serum samples ( 97/98 ) showed serogroup A-specific IgG concentration ≥2μg/ml, which reached up to 100%(98/98) after vaccination (P>0.05).The percentage of serum sam-ples with serogroup C-specific IgG concentration ≥2 μg/ml rose from 20%to 99% after vaccination ( P<0.05).The ratio of positive serum samples with at least four times of increases in concentration of specific IgG against serogroup A and serogroup C after vaccine immunization were 34% and 100%, respectively . The rSBA geometric mean titers ( GMTs) for serogroups A and C in serum sample of post-vaccination were respectively elevated from 1164 to 5530 (P<0.05), and from 4 to 6225 (P<0.05).The percentage of se-rum samples with rSBA GMTs≥128 increased from 91% to 99% for serogroup A (P>0.05), and from 14%to 96%for serogroup C (P<0.05) after vaccination.The rSBA GMTs with at least four times of in-creases after vaccination were detected respectively in 53% and 100% of serogroups A and C vaccinated subjects.Pearson correlation coefficient between IgG concentration and rSBA GMTs was r=0.15 (pre) and r=0.23 (post) for serogroup A, and r=-0.14 (pre) and r=0.58 (post) for serogroup C (P<0.05). Conclusion This study has demonstrated an efficient and sustained immunogenicity with meningococcal sero -groups A and C polysaccharide vaccine as evidenced by the data from standardized assays of ELISA and SBA .

Hepatic encephalopathy is a common metabolic neuropsychiatric syndrome in the development of end-stage liver disease. Since the concept of intestinal-liver-brain axis was proposed, the relationship between the pathogenesis of hepatic encephalopathy and the gut microbiota has been a hot research topic. In recent years, studies have confirmed that gut microbiota is involved in and affects various pathological processes of hepatic encephalopathy. This article combines the latest research progress at home and abroad to elaborate on the research status of regulating gut microbiota and thus interfering with the pathological process of hepatic encephalopathy, hoping to provide new ideas and methods for the intervention of hepatic encephalopathy based on the regulation of gut microbiota.