Objective To study image findings of nonossifying fibroma.Methods The pathological and image findings fo 22 cases of nonossifying fibromas proved by operation were analysed.There were 12 cases of male and 10 cases female,with age ranging from 10 to 35 years(mean age 17 years).X-ray plain films were obtained in all 22 cases,CT images in 7 cases,and MRI in 2 cases.Results The tumors were located in long bone in 19 cases,in which 14 cases were located in metaphyses,2 cases in diaphyses and 2 cases in bone end,and 4 cases in irregular bone,which was seen in clavicle,rib,illum and maxilla respectively.The tumor maximum diamneter ranged from 2 to 6.5 cm,with mean diameter of 3.2 cm,and the ratio of longitudinal to transverse diameter was 2.51.The tumors were round,oral or mild lobular in 17 cases.The tumors were showed sclerotic borders in 20 cases,and no sclerotic border in 2 cases(clavicle and rib).Septum was demonstrated in 19 cases.Bone expasion was showed in one case.Conclusion If a tumor is located in cortex or marrow of long or irregular bone which is showed a welldefined lytic lesion with sclerotic rim,the diagnosis of nonossifying fibroma will be considered.

OBJECTIVETo study the effect of protein tyrosine phosphatase non-receptor type 12 (PTPN12) in regulating cardiac HERG channel currents.

METHODSThe plasmids pcDNA3.1-PTPN12-RFP and herg mutant constructed by PCR technique were transfected into HEK293 cells via Lipofectamine 2000, and the cells stably expressing PTPN12 selected with G418 were identified by Western blotting with anti-PTPN12 antibody. HERG channel current in cells expressing HERG alone (HEK293/HERG cells), cells overexpressing PTPN12 (HEK293/HERG cells transfected with pCDNA3.1-PTPN12-RFP), PAO-treated cells (PTPN12/HERG cells treated with PAO), and herg mutant cells (HEK293/HERGY327A-Y700A-Y845A cells transfected with pcDNA3.1-PTPN12-RFP) were recorded by patch-clamp technique.

RESULTSThe plasmids pcDNA3.1-PTPN12-RFP and herg mutant were successfully constructed, and the stable expressing cell lines were established. Red fluorescence was obversed in HEK293/HERG cells transfected with pcDNA3.1-PTPN12-RFP, and the protein expression of PTPN12 was detected. Overexpression of PTPN12 significantly decreased HERG current density in HEK293/HERG cells, and this change was significantly weakened in the inhibitor group and herg mutant group.

CONCLUSIONPTPN12 negatively regulates cardiac HERG channel cerrent possibly by decreasing the phosphorylation level of HERG tyrosine residues. This finding provides further insight into the regulatory mechanism of HERG channel and the pathogenesis of long QT syndrome.

Ether-A-Go-Go Potassium Channels ; physiology ; HEK293 Cells ; Heart ; Humans ; Long QT Syndrome ; Patch-Clamp Techniques ; Protein Tyrosine Phosphatase, Non-Receptor Type 12 ; physiology ; Transfection

Objective:To analyze the influencing factors, prevention and treatment strategy of short-term poor prognosis of continuous lumbar cistern external drainage after aneurysms subarachnoid hemorrhage (aSAH).Methods:Used retrospective research method, the clinical data of 300 patients with aSAH combined with continuous lumbar cistern external drainage treated in Sanya Central Hospital (Hainan Third People′s Hospital) from March 2019 to March 2021 were selected as the training set. In addition, the clinical data of 144 patients with aSAH with continuous lumbar cistern external drainage treated in Sanya Central Hospital (Hainan Third People′s Hospital) from March 2017 to May 2019 were selected as the verification set. According to the results of postoperative follow-up, the patients in the training set were divided into two groups: good prognosis group ( n=208) and poor prognosis group ( n=92). The demographic characteristics, past history, Hunt-Hess grade, modified Fisher grade, location of responsible aneurysm, postoperative complications, bone flap decompression and lumbar cistern drainage were compared between the two groups. The independent risk factors for prognosis of aSAH patients undergoing continuous lumbar cistern external drainage were screened by Cox proportional hazard regression model, and these factors were included and XGboost model was established. The prediction model was validated internally and externally in the training set and verification set: AUROC(C-index) was used to verify the model differentiation; GiViTI calibration band and Hosmer-Lemeshow test were used to verify the model calibration; DCA curve was used to verify the clinical validity of the model. Results:Hunt-Hess grade, modified Fisher grade, drainage duration, average daily drainage volume, shunt-dependent hydrocephalus, aneurysm rebleeding, cerebral vasospasm and delayed cerebral ischemia were independent risk factors for poor prognosis in patients with aSAH who underwent continuous lumbar cistern external drainage( P<0.05). The XGboost model was successfully established by incorporating the above independent risk factors, and the internal and external verification of the XGboost model was carried out in the training set and verification set, respectively, the area under the curve of receiver operating characteristic was 0.882(95% CI: 0.820-0.955) and 0.878(95% CI: 0.774-0.928) respectively, and the model differentiation was good; the 80%-90% confidence interval of the GiViTI calibration curve did not cross the 45° angle bisector ( P>0.05). In the Hosmer-Lemeshow goodness-of-fit test, the P value were 0.581 and 0.716, respectively. The threshold probability value in the DCA curve was 30.4%. The clinical net benefit rate of the training set and verification set were 31% and 34%, respectively, indicating that the prediction model was clinically effective. Conclusions:The independent risk factors for poor prognosis of aSAH patients undergoing continuous lumbar cistern drainage are Hunt-Hess grade, modified Fisher grade, cerebral vasospasm, delayed cerebral ischemia and shunt-dependent hydrocephalus. The XGboost model constructed in this study can effectively predict the prognosis of patients with aSAH undergoing continuous lumbar cistern drainage, and provide reference for the formulation of follow-up treatment plans.

Objective To study the effect of protein tyrosine phosphatase non-receptor type 12 (PTPN12) in regulating cardiac HERG channel currents. Methods The plasmids pcDNA3.1-PTPN12-RFP and herg mutant constructed by PCR technique were transfected into HEK293 cells via Lipofectamine 2000, and the cells stably expressing PTPN12 selected with G418 were identified by Western blotting with anti-PTPN12 antibody. HERG channel current in cells expressing HERG alone (HEK293/HERG cells), cells overexpressing PTPN12 (HEK293/HERG cells transfected with pCDNA3.1-PTPN12-RFP), PAO-treated cells (PTPN12/HERG cells treated with PAO), and herg mutant cells (HEK293/HERGY327A-Y700A-Y845A cells transfected with pcDNA3.1-PTPN12-RFP) were recorded by patch-clamp technique. Results The plasmids pcDNA3.1-PTPN12-RFP and herg mutant were successfully constructed, and the stable expressing cell lines were established. Red fluorescence was obversed in HEK293/HERG cells transfected with pcDNA3.1- PTPN12- RFP, and the protein expression of PTPN12 was detected. Overexpression of PTPN12 significantly decreased HERG current density in HEK293/HERG cells, and this change was significantly weakened in the inhibitor group and herg mutant group. Conclusion PTPN12 negatively regulates cardiac HERG channel cerrent possibly by decreasing the phosphorylation level of HERG tyrosine residues. This finding provides further insight into the regulatory mechanism of HERG channel and the pathogenesis of long QT syndrome.

Objective To study the effect of protein tyrosine phosphatase non-receptor type 12 (PTPN12) in regulating cardiac HERG channel currents. Methods The plasmids pcDNA3.1-PTPN12-RFP and herg mutant constructed by PCR technique were transfected into HEK293 cells via Lipofectamine 2000, and the cells stably expressing PTPN12 selected with G418 were identified by Western blotting with anti-PTPN12 antibody. HERG channel current in cells expressing HERG alone (HEK293/HERG cells), cells overexpressing PTPN12 (HEK293/HERG cells transfected with pCDNA3.1-PTPN12-RFP), PAO-treated cells (PTPN12/HERG cells treated with PAO), and herg mutant cells (HEK293/HERGY327A-Y700A-Y845A cells transfected with pcDNA3.1-PTPN12-RFP) were recorded by patch-clamp technique. Results The plasmids pcDNA3.1-PTPN12-RFP and herg mutant were successfully constructed, and the stable expressing cell lines were established. Red fluorescence was obversed in HEK293/HERG cells transfected with pcDNA3.1- PTPN12- RFP, and the protein expression of PTPN12 was detected. Overexpression of PTPN12 significantly decreased HERG current density in HEK293/HERG cells, and this change was significantly weakened in the inhibitor group and herg mutant group. Conclusion PTPN12 negatively regulates cardiac HERG channel cerrent possibly by decreasing the phosphorylation level of HERG tyrosine residues. This finding provides further insight into the regulatory mechanism of HERG channel and the pathogenesis of long QT syndrome.