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Objective To analyze the clinical and imaging characteristics of pediatric neuromyelitis optica spectrum disorders(NMOSD)in children. Methods The clinical data,imaging manifestations and follow - up data of 16 NMOSD patients at Department of Pediatric Neurology,Shandong Provincial Hospital Affiliated to Shandong Univer-sity between July 2013 and September 2017 were respectively analyzed. Results In 16 patients,initial presentations included optica neuritis(ON)in 5 cases,longitudinally extensive transverse myelitis(LETM)in 6 cases,and among them there were 2 cases with acute disseminated encephalomyelitis and 3 cases with both ON and LETM. Eleven cases received aquaporin - 4(AQP4)antibody examination and 4 cases were found seropositive. One case out of 7 detected cases was found AQP4 antibody positive in cerebrospinal fluid. Eleven cases received optica magnetic resonance imaging (MRI),and 8 cases were found abnormal signals in optic nerve and optica chiasma. The spinal cord MRI showed 13 ca-ses with LETM manifestations,and abnormal signals were found in vertebral segments(5 - 13),and among them 1 case had cervical cord,3 cases were thoracic cord and 9 cases were both of the above. Lesions in the cervical cord in 2 cases were extended upward to the medulla. Fifteen cases received brain MRI and all of them had brain lesions,which were mainly involved in the central and subcortical white matter,thalamus,corpus callosum,brainstem,the junction of spinal cord and medulla,cerebellum,and so on. All patients received treatment for acute attacks with high - dose Methylpred-nisolone and/ or gamma globulin and got obvious relief. Two cases with recurrent ON received treatment of Rituximab and their vision became improved. Fifteen patients were followed up,and 2 cases had limb disorders and 4 cases had visual impairment,other patients had no clinical symptoms. Conclusions Pediatric NMOSD has a diverse clinical pre-sentation at the onset disease. Those who are initial diagnosed acute myelitis,ON and acute disseminated encephalomye-litis should be considered the possibility of NMOSD. Antibody to AQP4 testing can assist the diagnosis. The typical ima-ging characters of NMOSD children are abnormal signals in the high expression area of AQP4. Intracranial lesions are more common in children. The acute treatment includes the high - dose Methylprednisolone and gamma globulin. Rituximab can be used for the recurrent patients.
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Amino glycosides, one of the important broad-spectrum antibacterials, treat clinically against various bacterial infections. In the last decade, amino glycoside micro arrays have become one of main technologies for analyzing interactions between antibiotics and therapeutic targets in a high-throughput manner. A series of methods have been developed to immobilize amino glycosides on the functional group-coated glass slides in a micro array format. The amino glycoside micro arrays technology has been widely used for rapid determination of interactions of the amino glycosides with ribosome RNAs [rRNA] and proteins. Several clinically used amino glycosides are mainly exerted by binding to bacterial rRNA, which leads to mistranslation of protein. However, amino glycosides are losing efficacy due to the increased resistance mostly caused by enzymes modification. The micro array-based technology is mainly used in developing novel antibiotics, discovering new RNA targets, and identifying inhibitors of resistance-causing enzymes. This review will focus on the construction of amino glycoside micro arrays, their recent status and applications in biological and biomedical research and some challenges in further research
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Aminoglycosides are broad-spectrum antibacterials to treat bacterial infections, especially gram-negative bacteria infections. However, aminoglycosides are losing efficacy because of the increase in antibiotic resistance and their inherent toxicity, attracting more interests in developing new aminoglycosides. Several clinically used aminoglycosides are mainly exerted by inhibition of protein synthesis through binding to bacterial rRNA. The bacterial ribosome RNA is the most currently exploited RNA drug target. Identification of new compounds that target RNAs is indispensable to fight with the growing threat that bacteria pose to human safety. In this work, we used carbohydrate microarrays to probe interactions of low molecular weight ligands with RNAs and proteins. Carbohydrate microarrays, comprising hundreds to thousands of different glycan structures on surfaces in a spatially discrete pattern, are sensitive and versatile tools to study the interactions between biological macromolecules. Herein, aminoglycosides have been immobilized onto the modified glass microscope slides and their interactions with RNAs and proteins are then measured through the labeled fluorescence. The results displayed that microarray can be used to detect the binding of aminoglycosides with three types of target molecules, including the small RNA oligonucleotide mimics of aminoglycoside binding sites in the ribosome (rRNA A-site mimics), the large group I ribozyme RNA (approximately 400 nucleotide) and certain proteins (toxicity-causing enzymes, such as DNA polymerase and phospholipase C). For rRNA A-site mimics, the fluorescence intensities of 16S rRNA is stronger than that of 18S rRNA, illustrating that as a screen technique, the microarray method can not only determine the binding affinity to RNA but also detect the specific binding to bacterial rRNA mimic. The ability to screen group I ribozyme RNA can be helpful to the discovery of new RNA therapeutic targets. Binding of immobilized aminoglycosides to toxicity-causing proteins (DNA polymerase and phospholipase C) is a new method to study of aminoglycoside toxicity. These studies lay the foundation for rapid identification of new RNA-binding ligands with strong and specific binding affinity for their desired targets.
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Objective To evaluate the plasma levels of D‐dimer in lung cancer and pulmonary tuberculosis (PTB) patients and their clinical significances .Methods The plasma of 130 patients with lung cancer ,126 patients with PTB and 50 healthy controls were collected .All the patients were enrolled in Beijing Affiliated to Chest Hospital Capital Medical University ,from July 2014 to October 2014 .Full‐automatic analyzer was used to examine the level of plasma D‐dimer .Results The levels of plasma D‐dimer in patients with lung cancer were significantly higher than patients with PTB and healthy controls (Z=2 .704 ,P<0 .01);The levels of plasma D‐dimer in patients with PTB were significantly higher than healthy controls (Z=2 .54 ,P<0 .05);The levels of plasma D‐dimer were significantly higher in stages Ⅲ and Ⅳ than stages Ⅰ and Ⅱ(Z=2 .195 ,P<0 .05);The positive rate in patients with lung cancer was significantly higher than patients with PTB (χ2 =10 .525 ,P<0 .01) .Conclusion Activation of coagulation and fi‐brinolysis exist in lung cancer and PTB patients ,the level of plasma D‐dimer is related to the clinical stage of lung cancer .
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Objective To investigate the changes of the pulmonary surfactant protein-D (SP-D) in serum and cerebrospi-nal lfuid in children with viral encephalitis (VE). Methods The levels of SP-D in serum and cerebrospinal lfuid were detected by a double-antibody sandwich enzyme-linked immunosorbent assay and compared in thirty children with VE in acute and con-valescent phases and in 12 children without VE. Results The levels of SP-D in serum and cerebrospinal lfuid between groups of VE acute phase and convalescent phase and no VE were statistically signiifcant (F=103.58,118.15, all P<0.01). The levels of SP-D in serum and cerebrospinal lfuid in children with VE in acute phase and in convalescent phase were signiifcantly lower than children without VE (P<0.01). The levels of SP-D in serum and cerebrospinal lfuid in children with VE in convalescent phase were all signiifcantly higher than those in acute phase (P<0.01). In children with VE, the level of SP-D in cerebrospinal lfuid was weakly correlated negatively with the count of nucleated cells. Conclusions SP-D might be involved in the pathogenesis in VE. The detection of SP-D in serum and cerebrospinal lfuid has a certain value for diagnosis of VE.
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Objective To detect specific polymorphisms in Toll-interleukin 1 receptor domain containing adaptor protein(TIRAP) coding region for Chinese Han population, and verify whether they are associated with susceptibility to tuberculosis. Methods Search TIRAP polymorphisms by sequencing in small sample; detect single nucleotide polymorphism(SNP) by ligase detection reaction technique in large sample; analyze whether polymorphisms are related to tuberculosis by statistic methods. Results Four polymorphisms were present in the TIRAP coding region. 394A had higher frequencies in the tuberculosis(TB)group than the control. But allelic and genotypic analysis showed that there were no significant difference in statistic between TB patients and controls(P>0.05). The SNP G164A mutation related with TB patient's condition. Comparing to controls, retreatment patients' allelic frequencies had significant difference in statistic(P<0.05), sputum positive patients and lung cavitation patients had lower 164A frequencies. Conclusion TIRAP coding region polymorphisms may be risk factors for TB occurrence and development in Chinese Han population.
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Objective To investigate whether the signaling pathway of PI3K-AKT is involved in Ang II-induced apoptosis in rat renal tubular epithelial cells (NRK-52E).Methods Cultured cells were incubated in media containing either buffer (control) or different concentrations of Ang II (10-9 to 10-6 mol/L) for 24 h. Cells were stained by Annexin V-F1TC/PI Kit and apoptosis was evaluated by flow cytometer. Western blotting was performed to assess the levels of PI3K, total- and phosphor-AKT. Results Ang II induced tubular epithelial cell apoplosis in a dose dependent manner. Ang II significantly inhibited the phosphorylation of AKT. The level of AKT phosphorylation was negatively correlated with apoptosis in Ang II-stimulated cells(r=-0.90 ,P
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Objective To investigate the renoprotective effect of irbesartan on tubulointerstitial fibrosis in rats with adriamycin-induced nephropathy and its possible mechanism. Methods Rats received twice-intravenous injections of adriamycin(ADR) after the right kidney was removed. Those rats were randomly assigned to irbesartan treatment group and nephropathy group. Treatment group received 50 mg? kg-1 ? d-1 irbesartan for 4 weeks. Rats with sham operation served as normal control. Proteinuria and serum creatinine of were measured after 4 weeks. Renal histopathological changes were evaluated as well. Immunohistochemistry was used to examine the protein expression of TGF-?1, MMP-9 and TIMP-1. The mRNA levels of MMP-9 and TIMP-1 were detected by in situ hybridization. Results Proteinuria of treatment group decreased significantly as compared to nephropathy group. TGF-?1, TIMP-1 and MMP-9 were significantly lower than that of nephropathy group in tubulointerstitium and consistently associated with tubular degeneration and interstitial fibrosis progressed. Conclusion Irbesartan has a renoprotective effect on tubulointerstitial fibrosis by modulating the ECM degradation.
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Objective To develop a rat model of type 2 diabetes, and to investigate the effect of AT1 receptor antagonist-irbesartan on activation of renal NF-?B in type 2 diabetic rat. Methods The rats of model groups were intraperitoneally given low-dose streptozotocin (STZ, 30 mg/kg) after having the sucrose-and fat-enriched diets(20% sucrose, 10% pig fat, 2. 5% cholesterol) for one month. Immuohistochemistry and computer image-pattern analysis system were used to analyze activation of NF-?B and expression of monocyte/macrophage (ED-1) in renal tissues. Results (1) Insulin resistance was induced by feeding diets enriched in sucrose and fat, and hyperglycemia was induced with a dose of STZ that did not cause diabetes in chow-fed rats. After 6 weeks, rats of model group presented itself early changes of diabetic nephropathy (DN). (2) Compared to normal group, the activation of NF-?B and expression of ED-1 increased in glomeruli of experimental type 2 diabetic rat. Irbesartan inhibited significantly the activation of NF-?B, ameliorated monocyte/macrophage infiltration, partly improved the renal function and matrix accumulation. Conclusions (1) A rat model of type 2 diabetes mellitus is developed successfully by combination of dietary-induced insulin resistance and low-dose STZ-induced hyperglycemia. (2) Renal NF-?B activation is greatly increased in experimental type 2 diabetic rat. The protection of irbesartan against kidney is associated, at least in part, with down-regulating NF-?B activation and monocyte/macrophage recruitment in renal tissue.