SALL4 gene is closely related to body malformations related diseases, embryonic stem cell development, and hematopoietic malignancies. SALL4 can activate hematopoietic stem cell through Wnt signaling pathways, and promote continued proliferation of leukemia stem cells, leading to leukemia. In-depth study of SALL4 gene and its protein function will help clarify the pathogenesis of leukemia, providing a new target for the treatment of leukemia.

OBJECTIVE: To investigate the clinical feature,diagnostic and therapeutic methods of ultimobranchial fistula and cyst of thyroid. METHOD: Four cases of ultimobranchial fistula and cyst of thyroid in our hospital were reported and the relevant literatures were reviewed. RESULT: The branchial fistula and cyst of four cases were adhered to thyroid,with unclear anatomical landmarks, the function of recurrent laryngeal nerve were bad before the operation in two cases. The nerve of four cases were retained, the function of thyriod and parathyroid gland were normal and no recurrence were found. CONCLUSION Ultimobranchial fistula and cyst of thyroid is rare and is easier to be misdiagnosed and wrong treated. Surgical excision is effective for it and recurrent laryngeal nerve should be protected when performing the operation.
Cysts ; Diagnostic Errors ; Fistula ; Humans ; Parathyroid Glands ; Recurrent Laryngeal Nerve ; Thyroid Diseases ; pathology ; surgery

ObjectiveTo evaluate the long-term outcomes of carotid endarterectomy versus carotid artery stenting for carotid stenosis.MethodsPubMed, EMBASE, and the Cochrane databases were retrieved.The randomized controlled trials of comparing CEA with CAS in patients with carotid artery stenosis were enrolled.The data such as the research basic characteristics and the long-term outcomes including stroke or death combined endpoints, any stroke or any death were extracted.The Stata software was used to conduct statistical analysis.ResultsA total of 7 randomized controlled trials and 8 210 patients were included.The median follow-up time was 2-7.4 years.The overall quality of the included studies was high and the risk of bias was low.The meta-analysis showed that the risks of the combined endpoint of stroke or death (hazard risk [HR] 1.21, 95% confidence interval [CI] 1.04-1.39), any stroke (HR 1.32, 95% CI 1.15-1.51) and ipsilateral stroke (HR 1.26, 95% CI 1.02-1.55) in the CAS group were significantly higher than those in the CEA group;the risks of death (HR 1.06, 95% CI 0.95-1.18), disabling stroke (HR 1.23, 95% CI 0.95-1.60), non-ipsilateral stroke (HR 1.12,95% CI 0.81-1.55) and restenosis (HR 1.18,95% CI 0.91-1.52) were not significantly different between between the CAS group and the CEA group.Conclusions CAS and CEA are associated with similar risks of long-term death, disabling stroke, non-ipsilateral stroke and restenosis.The risks of long-term combined endpoint of stroke or death, any stroke and ipsilateral stroke significantly higher with CAS.These results suggest that CEA remains the treatment of choice for carotid stenosis.

OBJECTIVETo explore the mechanism of matrine (Mat) induced human erythroleukemia TF-1 cell apoptosis and its effect on SALL4 expression.

METHODDifferent concentrations of the Mat (0.5, 1.0, 1.5, 2.0 g x L(-1) ) were cultured in vitro in TF-1 cells at different time (24, 48, 72 h). Cell proliferation was assayed by MTT. Cell cycle was determined by flow cytometry (FCM). Cell apoptosis was detected by Annexin V and PI double staining method. SALL4 mRNA expression was detected by reverse transcription RT-PCR (RTT-PCR).

RESULTAdministrated with Mat (0.5-2.0 g x L(-1)) after 24, 48, 72 h, the proliferation of TF-1 cells were inhibited (P < 0.01) , and in dose- and time-dependent manner. Half inhibitory concentration (IC50 ) was 1.0 g L(-1) at 48 h. After 48 h that the Mat acted on TF-1 cells, the proportion of G0/G1 phase cells increased while compared with the control group, and S phase cells decreased (P < 0.01). Apoptosis were 8.6% , 11.21%, 15.26% , 17.63%, which showed statistically significant difference (P < 0.01) compared with the control group (5.05%). RT-PCR results showed the ratio between SALL4 mRNA expression and beta-actin (internal reference) expression significantly decreased (P < 0.01) with Mat dose increased.

CONCLUSIONIn a certain range of concentration and time, Mat can inhibit TFT-1 cells proliferation. The mechanism is to make the cells G0/G1 phase blocked, to inhibit SALL4 gene expression and induce cell apoptosis.

Alkaloids ; pharmacology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Gene Expression ; drug effects ; Humans ; Leukemia, Erythroblastic, Acute ; drug therapy ; genetics ; metabolism ; physiopathology ; Quinolizines ; pharmacology ; Transcription Factors ; genetics ; metabolism

Objective To investigate the effect ofdiammonium glycyrrhizinate on neurovascular units in rats after cerebral ischemia reperfusion (IR) injury.Methods Two hundred and forty health SD rats were randomly assigned into normal control group (n=30),sham-operated group (n=30),IR group (n=90) and diammonium glycyrrhizinate group (DG,n=90).The rats in the IR group and DG group were divided into 2,6 and 12 h subgroups after modeling,respectively (n=30).The rats in the IR group and DG group were induced middle cerebral artery occlusion (MCAO) models,and after the models were successfully established,9.11 mL DG sodium chloride injection was given to DG group,while equal saline to normal group,sham-operated group and IR group via the tail vein.The brain tissues of each group were harvested 2,6 and 12 h,resperctively,after modeling.The infraction rate was measured by TTC staining;immunohistochemistry was employed to detect the expresions of Claudin-5 and vessel endothelium (VE)-Cadherin;Western blotting was used to detect the protein expression levels of Rac-1 and Claudin-5.Results The DG group had signficantly lower infarction rate than IR group 2,6 and 12 h after modeling (P＜0.05).The Claudin-5 expression rates in the 6 h and 12 h DG subgroups were signficantly higher than those in the 6 h and 12 h IR subgroups (P＜0.05).The VE-Cadherin expression rates in the DG group were significantly higher than that in IR group at 2,6 and 12 h after modeling (P＜0.05).Samely,the Claudin-5 relative quantity in DG group was significantly higher than that in IR group at 2,6 and 12 h after modeling (P＜0.05).The Rac-1 quantity in DG group was only statistically higher than IR group at 2 h after modeling (P＜0.05).Conclusion The DG can upregulate the Rac-1,VE-Cadherin and Claduin-5 expressions in neurovascutar units,and partly protect neurovascular units after cere bral acute IR injury.

ObjectiveTo explore the mechanism of Jiebiao Qingli decoction （JQD） in treating pneumonia caused by influenza A virus （IAV） infection. MethodsA total of 132 Balb/c mice were randomly assigned into normal control （NC）， model control （IAV）， oseltamivir （OSV， 37.5 mg·kg^-1）， and high-， medium-， low-dose JQD （H-， M-， and L-JQD： 6.05， 3.02， and 1.51 g·kg^-1， respectively） groups. The NC group was treated with normal saline nasal drops， and the other groups were intranasally inoculated with A/Brisbane/02/2018 （H1N1） ［pdm09-like virus （H1N1）］ for the modeling of IAV infection. Two hours post-modeling， the NC and IAV groups were administrated with normal saline by gavage， while other groups received corresponding drugs for 7 d. The body mass， survival status， and deaths of mice were recorded daily during the administration of the drugs. On days 3 and 7， the lung index was measured for mice in each group. Pathological changes in the lung tissue were observed via hematoxylin-eosin staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was conducted to measure the viral load （IAV-M） and the mRNA levels of Toll-like receptor 7 （TLR7）， p38 mitogen-activated protein kinase （p38 MAPK）， and nuclear factor-kappa B （NF-κB） in the lung tissue. Western blot was employed to measure the protein levels of p38 MAPK and NF-κB. Enzyme-linked immunosorbent assay was used to quantify serum levels of interleukin-2 （IL-2）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. ResultsCompared with the NC group， the IAV group showed reduced survival quality and survival days （P<0.01）， lung congestion， inflammatory cell infiltration， elevated lung index （P<0.01）， increased viral load （P<0.01）， upregulated TLR7， p38 MAPK， and NF-κB levels （P<0.05， P<0.01）， decreased IL-2 level （P<0.01）， and elevated IL-6 and TNF-α levels （P<0.01）. Compared with the IAV group， H-JQD prolonged survival days （P<0.05）. All JQD groups alleviated pathological changes in the lung tissue and reduced the lung index （P<0.01）. M-JQD and H-JQD decreased the viral load （P<0.01）. H-JQD downregulated the mRNA levels of TLR7， p38 MAPK， and NF-κB （P<0.05， P<0.01） and the protein levels of p38 MAPK and NF-κB （P<0.01）， increased the serum IL-2 level （P<0.01）， and lowered the IL-6 and TNF-α levels （P<0.05， P<0.01）. M-JQD downregulated the mRNA level of NF-κB （P<0.01） and the protein level of p38 MAPK （P<0.05）， elevated the IL-2 level （P<0.01）， and lowered the TNF-α level （P<0.01）. ConclusionM- and H-JQD can prevent and control IAV infection-induced pneumonia dose-dependently by inhibiting the TLR7/MAPK/NF-κB signaling pathway， increasing IL-2， and reducing excessive secretion of IL-6 and TNF-α.

ObjectiveTo explore the mechanism of Jiebiao Qingli decoction （JQD） in treating pneumonia caused by influenza A virus （IAV） infection. MethodsA total of 132 Balb/c mice were randomly assigned into normal control （NC）， model control （IAV）， oseltamivir （OSV， 37.5 mg·kg^-1）， and high-， medium-， low-dose JQD （H-， M-， and L-JQD： 6.05， 3.02， and 1.51 g·kg^-1， respectively） groups. The NC group was treated with normal saline nasal drops， and the other groups were intranasally inoculated with A/Brisbane/02/2018 （H1N1） ［pdm09-like virus （H1N1）］ for the modeling of IAV infection. Two hours post-modeling， the NC and IAV groups were administrated with normal saline by gavage， while other groups received corresponding drugs for 7 d. The body mass， survival status， and deaths of mice were recorded daily during the administration of the drugs. On days 3 and 7， the lung index was measured for mice in each group. Pathological changes in the lung tissue were observed via hematoxylin-eosin staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was conducted to measure the viral load （IAV-M） and the mRNA levels of Toll-like receptor 7 （TLR7）， p38 mitogen-activated protein kinase （p38 MAPK）， and nuclear factor-kappa B （NF-κB） in the lung tissue. Western blot was employed to measure the protein levels of p38 MAPK and NF-κB. Enzyme-linked immunosorbent assay was used to quantify serum levels of interleukin-2 （IL-2）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. ResultsCompared with the NC group， the IAV group showed reduced survival quality and survival days （P<0.01）， lung congestion， inflammatory cell infiltration， elevated lung index （P<0.01）， increased viral load （P<0.01）， upregulated TLR7， p38 MAPK， and NF-κB levels （P<0.05， P<0.01）， decreased IL-2 level （P<0.01）， and elevated IL-6 and TNF-α levels （P<0.01）. Compared with the IAV group， H-JQD prolonged survival days （P<0.05）. All JQD groups alleviated pathological changes in the lung tissue and reduced the lung index （P<0.01）. M-JQD and H-JQD decreased the viral load （P<0.01）. H-JQD downregulated the mRNA levels of TLR7， p38 MAPK， and NF-κB （P<0.05， P<0.01） and the protein levels of p38 MAPK and NF-κB （P<0.01）， increased the serum IL-2 level （P<0.01）， and lowered the IL-6 and TNF-α levels （P<0.05， P<0.01）. M-JQD downregulated the mRNA level of NF-κB （P<0.01） and the protein level of p38 MAPK （P<0.05）， elevated the IL-2 level （P<0.01）， and lowered the TNF-α level （P<0.01）. ConclusionM- and H-JQD can prevent and control IAV infection-induced pneumonia dose-dependently by inhibiting the TLR7/MAPK/NF-κB signaling pathway， increasing IL-2， and reducing excessive secretion of IL-6 and TNF-α.