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Norepinephrine (NE) can raise blood pressure and speed up heart rate. However, because its effect of raising heart rate is less than that of reflex reduction of heart rate caused by the increase of blood pressure, NE causes more heart rate decrease in patients. A case of tachyarrhythmia caused by low dose NE was admitted to department of intensive care unit (ICU) of Shijiazhuang Third Hospital. The heart rate of the patient increased with the elevation of NE application dose. A variety of antiarrhythmic drugs was invalid. The related examination was prescribed to eliminate the cause of arrhythmia caused by the disorder of electrolysis and thyroid function, and found that heart rate decreased as the dose of NE tapered. After NE was stopped, the patient recovered sinus rhythm. During one month of follow-up, the patient's heart rhythm was normal. Therefore, the occurrence of tachyarrhythmia is related to NE.
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Objective@#To explore the spatial-temporal distribution and epidemic characteristics of hemorrhagic fever with renal syndrome (HFRS) in Hebei province from 2005 to 2016.@*Methods@#Records of HFRS cases reported from each county in Hebei during January 2005 to December 2016 were collected from National Notifiable Disease Surveillance System (NNDSS). Global and local spatial association statistics were used to measure the spatial autocorrelation and software GeoDa 1.2.0. Software SaTScan 9.4.1 was used to analyze spatiotemporal clusters. Software ArcGIS 10.2 was used to visualize the yearly scan results.@*Results@#In Hebei province, a total of 8 437 human HFRS cases reported from 170 counties with an annual incidence rate of 0.99/100 000 population during 2005-2016. The peak incidence season was spring. Global spatial autocorrelation analysis on the incidence of HFRS at county-level showed that the value of Moran’s I were all above 0 (P<0.05), indicating that the significant spatial cluster. The result of local indicators on spatial association (LISA) analysis revealed that identified hot spots were mainly in northeastern area, while cold spots were found in some counties of central and southern areas. Spatial-temporal scan detected that the primary cluster of HFRS incidence was mainly distributed in Qinhuangdao city and Tangshan city, including 11 counties (city/district): Beidaihe district, Haigang district, Funing district, Shanhaiguan district, Changli county, Lulong county and Qinglong Manchu autonomous county in Qinhuangdao city, and Qian’an city, Laoting county, Luanzhou city and Luannan county in Tangshan city (RR=39.64, P<0.001), during January-July in 2005.@*Conclusions@#There were significant spatial-temporal cluster of HFRS in Hebei from 2005 to 2016. The cluster areas of HFRS were mainly in northeastern Hebei, it is necessary to strengthen the prevention and control programs of HFRS in these areas.
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Objective@#To explore the clinical implications and prognostic value of TP53 gene mutation and deletion in patients with myelodysplastic syndromes (MDS) .@*Methods@#112-gene targeted sequencing and interphase fluorescence in situ hybridization (FISH) were used to detect TP53 mutation and deletion in 584 patients with newly diagnosed primary MDS who were admitted from October 2009 to December 2017. The association of TP53 mutation and deletion with several clinical features and their prognostic significance were analyzed.@*Results@#Alterations in TP53 were found in 42 (7.2%) cases. Of these, 31 (5.3%) cases showed TP53 mutation only, 8 (1.4%) cases in TP53 deletion only, 3 (0.5%) cases harboring both mutation and deletion. A total of 37 mutations were detected in 34 patients, most of them (94.6%) were located in the DNA binding domain (exon5-8) , the remaining 2 were located in exon 10 and splice site respectively. Patients with TP53 alterations harbored significantly more mutations than whom without alterations (z=-2.418, P=0.016) . The median age of patients with TP53 alterations was higher than their counterparts[60 (21-78) years old vs 52 (14-83) years old, z=-2.188, P=0.029]. TP53 alterations correlated with complex karyotype and International prognostic scoring system intermediate-2/high significantly (P<0.001) . Median overall survival of patients with TP53 alterations was shorter than the others[13 (95%CI 7.57-18.43) months vs not reached, χ2=12.342, P<0.001], while the significance was lost during complex karyotype adjusted analysis in multivariable model.@*Conclusion@#TP53 mutation was more common than deletion in MDS patients. The majority of mutations were located in the DNA binding domain. TP53 alterations were strongly associated with complex karyotype and always coexisted with other gene mutations. TP53 alteration was no longer an independent prognostic factor when complex karyotype were occurred in MDS.
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Objective To reseach the time point of the highest percentage of neural precursor cells derived from adipose stromal cells (ADSCs) in vitro, and to observe the ultrastructure features of neural precursor cells. Methods Used the β-mercaptoethanol to induce ADSCs to differentiate into neural precursor cells and neuron-like cells. The morphology of the uninductedcells and inducted cells were observed with inverted phase contrast microscope. The expression of nestin which was the marker of neural precursor cell in each group was detected using immunofluorescence staining method. The ultrastructural feature of cells which was induced for 3 hours were observed. Results The highest ratio of positive expression of nestin was 3 hours following induction,with the ratio ( 86.25 ± 4.82) %. There were many protuberance on the cell membrane under transmission electron microscopy.There were plenty of organelles in the neural precursor cells. The neural precursor cells had a large size nucleus,large nucleoplasmic index, much extended chromatin,and less condensed chromatin. The nucleus had double-layer nuclear envelope, more nuclear pore on the nuclear envelope. Conclusion The time point of the highest percentage of neural precursor cells derived from ADSCs is 3 hours,and the ultrastructral feature of induced neural precursor cells confirm that cells at this time point are in a state of split active period.
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Objective To induce adult adult adipose-derived stem cells(ADSCs) in vitro to differentiate into neuronal-like cells,and to analyze the features of their cell morphology and ultrastructure. Methods Adipose stromal cells were obtained and amplified in vitro. Then make use of chemical induction to induce them. Observed ADSC and differentiation of cells in morphology and ultrastructure under inverted microscope and transmission electron microscopy. Immunocytochemistry to detection of Nestin, Neuron Specific Endolase( NSE) ,and glial fibrillary acidic protein(GFAP) expression in cells. Used Real-time PCR to detection of Nestin,GFAP gene mRNA expression before and after induction in ADSC. To observe the morphology and ultrastructure of the cells prior to and after induction under microscope and electron microscope. Results The morphology of ADSC was similar to fibroblasts ,and could be amplified stability within 10 passages in vitro. Some of the cells induced display a typical astrocyte-like cells in ultrastructure. Followed neuronal induction,astrocyte-like cells began to stain brightly for CFAP, Nestin. GFAP stained in both the cytoplasm and nuclei of astrocyte-like cells, but Nestin only stained in the cytoplasm. The peak positive expression rate within 14d following neuronal induction. The rate of positive expression cells was( 14.4 ± 3. 6) % for Nestin, (87. 3 ± 5. 3 ) % for GFAP. Then two kinds of protein expression remained the similar rate. The average relative concentration of GFAP and Nestin gene mRNA have significant statistical difference between ADSC and differented cells analyzed by Real-time PCR (P<0.05).The peak concentration of GFAP was within 20 d after induction,and GFAP was within 14 d after induction. Conclusion In the cytoplasm of adult adipose-derived cells possess Nestin genetic material,which is the marker of neural stem cell. The differential astrocyte-like cells have the typical morphology, ultrastructure and GFAP phenotype of mature astrocytes.