Objective To investigate the expression and significance of p38 mitogen-activated protein kinase (p38MAPK) in hyperoxia-induced lung injury of new-born rats. Methods Totally 160 rats at the age of 12 h were randomly and equally divided into air control group, hyperoxia-induced lung injury group, hyperoxia-induced lung injury+SB203580 group and hyperoxia-induced lung injury + normal saline group. After the injury was inflicted, SB203580 or normal saline at same volume was given intraperitoneally at 5 mg/kg. After the rats were executed at the time points of 12, 24, 72 h and 1 week after the model establishment, the right upper lungs were resected for histopathology, right below lungs for wet weight/dry weight, and left lungs for detecting the expression of p38MAPK by Western blot analysis. Results Hyperoxia-induced lung injury model were established successfully after 72 h by exposure to hyperoxia. No p38MAPK expression was observed in air control group. In hyperoxia-induced lung injury group p38MAPK was detected from 12 h, reached to the peak at 72 h, and decreased 1 week later, and its expression was significantly higher in this group and normal saline group than in SB203580 group. Conclusion p38MAPK is involved in the process of hyperoxia-induced lung injury, and the injury can be relieved by treatment of SB203580.

Ear Diseases ; complications ; Ear, Inner ; Female ; Hearing Loss, Sudden ; etiology ; Hemorrhage ; complications ; Humans ; Middle Aged

Objective To examine the application value of reticulocyte hemoglobin content (CHr)for diagnosing iron deficiency in premenopausal women.Methods The levels of CHr,hemoglobin (Hb), mean cellular volume(MCV),red cell distribution width (RDW) were measured on the ADVIA 120 (Bayer Diagnostics) automated hematology analyzer.Transferrin saturation (TS) and ferritin (SF) were measured on chemistry analyzer.Results CHr in iron deficiency without anemia group were significantly lower than that in the healthy control group (P＜0.01)and significantly higher than that in iron deficiency anemia group(P＜0.01).CHr in anemia of chronic disease group were significantly higher than that in iron deficiency anemia group(P＜0.01).Receiver operator characteristic curve (ROC) analysis in diagnosis of iron dificiency without anemia demonstrated that the area under the curve for CHr,SF,RDW,MCV,Hb were 0.872,0.798,0.721,0.713,0.677,respectively (P＜0.01).So CHr has a better overall sensitivity than SF,Hb,MCV and RDW in the diagnosis of iron deficiency without anemia.ROC also showed that the area under the curve for Hb,RDW,CHr,SF and MCV was 1.000,0.969,0.958,0.953 and 0.926,respectively (P＜0.01) in iron deficiency anemia.Conclusion CHr is the early and sensitive predictor of iron deficiency in premenopausal women,especially for the diagnosis of iron deficiency without anemia.

Objective To obtain the protein interacting with inhibitor of differentiation1′(Id1′). Methods The recombinant bait plasmid pHybLex/Zeo Id1′ was constructed and transformed into yeast strain EGY48/ pSH18 34 to test pHybLex/Zeo Id1′ for non specific activation. Adult human lung cDNA libraries were screened to obtain true positive library plasmid. The true positive library clone was obtained by sequencing and basic local alignment sequence tool (BLAST). Results The recombinant bait vector, named as pHybLex/Zeo Id1′, was confirmed by sequencing. pHybLex/Zeo Id1′ was transformed into yeast strain EGY48/pSH18 34 and the transformants had no autonomously activated reporter genes. One true positive clone, obtained by screening of the adult human lung cDNA libraries, was confirmed to be Fyn by sequencing and BLAST. Conclusion Id1′ can interact with Fyn.

As the neuron-specific actin binding protein,Drebrin ( developmentally regulated brain protein) can affect spiny and synaptic morphology and function by changing the property of cytoskeleton,and modulate synaptic plasticity. Neural excitability regulates expression and activitiy of Drebrin through a variety of signaling molecules,making Drebrin' s function correlated with that of neurons. Under pathological conditions,the abnormal Drebrin affects synaptic plasticity,which leads to different degrees of cognitive dysfunction,and it is closely relates to the progress of cognitive dysfunction. Extensive studies of physiological and pathological functions of Drebrin in overall and molecular ways will not only contribute to a thorough understanding of cognitive dysfunction,but also develop the new target of therapeutics for cognitive dysfunction.

Amino Acid Metabolism, Inborn Errors ; diagnosis ; metabolism ; therapy ; Diagnosis, Differential ; Diet ; Glutarates ; metabolism ; urine ; Humans ; Infant ; Male ; Riboflavin ; therapeutic use ; Treatment Outcome

Objective: To optimize the extraction technology of Chinese medicinal materials in Yanyanling dispersible tablets.Methods: Orthogonal design was used to study the effects of three factors, including the ratio of liquid to materials, extraction time and extraction times on the extraction rate of Chinese medicinal materials and the comprehensive score of gallic acid content and total solid yield was used as the index.Results: The optimum extraction conditions were as follows: the ratio of materials to liquid was 1∶10 (g·ml-1), the extraction time was one hour, and the extraction times was three.Conclusion: Under the optimum conditions, the extraction rate of gallic acid in Chinese medicinal materials in Yanyanling dispersible tablets is 0.058%, and the total solid yield is 21.4%.The optimal process is stable and feasible, which can provide reference for the production of Yanyanling dispersible tablets.

Hypoxic-ischemic brain damage (HIBD) is referred to a common type of cerebral damage, which is caused by injury, leading to shallow bleeding in the cortex with intact cerebral pia mater. In recent years, studies show that a various kinds of immune cells and immune cellular factors are involved in the occurrence of HIBD. CC chemokine receptor 2 (CCR2) is a representative of CC chemokine receptor, and is widely distributed in cerebral neuron, astrocyte, and microglial cells, and is the main chemo-tactic factor receptor in brain tissue. CC chemokine ligand 2 (CCL2) is a kind of basophilic protein and the ligand of CCR2, and plays an important role in inflammation. In order to provide evidence for correlational studies in HIBD, this review will introduce the biological characteristics of CCR2 and CCL2, and illustrate the relationship between the immunoreactivity and HIBD.
Animals ; Brain Injuries/pathology* ; Cerebral Cortex/physiopathology* ; Chemokine CCL2/metabolism* ; Chemokines, CC/metabolism* ; Hypoxia-Ischemia, Brain/metabolism* ; Macrophage Inflammatory Proteins/metabolism* ; RNA, Messenger/metabolism* ; Rats ; Rats, Sprague-Dawley ; Receptors, CCR2/metabolism*

italic>Artemisia argyi (A. argyi) is a Chinese herbal medicine in China. The main active components are volatile oils, flavonoids, and other compounds, which have various pharmacological activities. Methoxylated flavonoids are the main active ingredients in A. argyi. Flavonoid O-methyltransferase (FOMT) is a key enzyme in the O-methylation of flavonoids. In order to further understand the function and characteristics of FOMT proteins, this paper carried out the whole genome mining and identification of FOMT genes in A. argyi and performed phylogenetic, chromosomal localization, gene sequence characterization, subcellular localization prediction, protein structure, gene structure analysis, and expression pattern analysis. The results showed that a total of 83 FOMT genes were identified in the genome of A. argyi. The phylogenetic tree shows that FOMT genes are divided into two subgroups, CCoAOMT (caffeoyl CoA O-methyltransferase) subfamily (32 genes) and COMT (caffeic acid O-methyltransferase) subfamily (51 genes). Gene sequence analysis showed that the number of amino acids encoded by FOMT was 70-734 aa, the molecular weight was 25 296.55-34 241.3 Da, and the isoelectric point was 4.51-9.99. Compared with 32 members of the CCoAOMT subfamily, nearly 1/3 of the 51 members of the COMT subfamily were hydrophobic proteins and 2/3 were hydrophilic proteins. Subcellular localization prediction showed that more than 80% of CCoAOMT subfamily members were located in the cytoplasm, and 96% of COMT subfamily members were located in the chloroplast. COMT subfamily members have more motifs than CCoAOMT subfamily members. The N-terminal motifs of COMT subfamily proteins are relatively variable, while the C-terminal motifs are relatively conserved. Expression pattern analysis showed that CCoAOMT subfamily members were mainly expressed in roots, while COMT members were mainly expressed in leaves. Some FOMTs showed the tissue expression specificity by real-time quantitative PCR analysis, especially in leaves. In this study, we identified and analyzed the FOMT gene family in A. argyi, and provided a theoretical basis for further research on the function of FOMTs and the biosynthesis of methylated flavonoids in A. argyi.

Objective To investigate the mRNA and protein expressions of Nav 1.1 and Nav 1.2 in hippocampus following traumatic brain injury ( TBI) in rats.Methods After the lateral fluid percussion model was established in adult male Sprague Dawley rats,the rats were sacrificed at 2,12,24 and 72 hours after percussion and collected ipsilateral hippocampus for detecting mRNA and protein expressions of Nav 1.1 and Nav 1.2 by means of fluorescent quantitation RT-PCR,Western blot and immunofluo rescence staining.Results The mRNA expressions of Nav 1.1 and Nav 1.2 were significantly down-regulated (P<0.01) in hippocampus and reached the lowest level at 2 hours following TBI.The protein expression of Nav 1.1 was significantly down-regulated (P<0.01) but recovered near to level of control group at 72 hours after TBI.While there was no statistical difference on protein expression of Nav 1.2 in hippocampus after TBI compared with control group (P>0.05).Conclusion TBI induces significant down-regulated mRNA and protein expressions of Nav 1.1 in the hippocampus,which may be one of molecular mechanisms for functional alternation of sodium channels and excitotoxic action following TBI.