[Associations between serum GDF15 and glycolipid metabolism disorder in metabolic associated fatty liver patients].

Objective: To investigate relationships between serum growth differentiation factor 15 (GDF15) and glycolipid metabolism in patients with metabolic associated fatty liver disease (MAFLD). Methods: The current investigation was a cross-sectional study. A total of 333 patients from the Fengxian District Central Hospital were recruited into the study after physical examination from February 2020 to February 2021. There were 107 patients with MAFLD and type 2 diabetes mellitus (T2DM), including 54 males and 53 females with a mean age of (57±11) years. There were 65 patients with simple MAFLD only, including 32 men and 33 women with a mean age of (49±5) years. There were 105 patients with T2DM only, including 53 men and 52 women, with a mean age of (56±10) years. A control group of 56 people without MAFLD or diabetes,28 male, 28 female, mean age (48±6) years, was also included in the study. Serum GDF15 was measured via enzyme-linked immunosorbent assays. IBM SPSS 26.0 was used for statistical analysis. Logistic regression was used to evaluate relationships between GDF15 and metabolic abnormalities in MAFLD patients. Results: GDF15 progressively increased in the control [385 (296, 484) ng/L], nonobese MAFLD [388 (319, 435) ng/L], obese MAFLD [426 (354, 527) ng/L], T2DM [664 (483, 900) ng/L], and MAFLD+T2DM groups [770 (560, 1 074) ng/L](H=113.82, P=0.001). There was no significant difference in serum GDF15 between the simple MAFLD [406 (339, 524) ng/L] and control group (U=1 505.50, P=0.132). GDF15 was significantly higher in the MAFLD+T2DM group than in the T2DM-only group (U=4 573.50, P=0.019). In logistic regression analysis increased GDF15 was associated with increased risks of simple MAFLD [odds ratio (OR)=2.202], T2DM (OR=29.656), and MAFLD+T2DM(OR=58.197). In patients with MAFLD, serum GDF15 was higher in the FIB4 index>1.45 group [773 (534, 1 162) ng/L] than in the FIB4 index<1.45 group [527 (389, 787) ng/L] (U=1 709.50, P<0.001). Increased GDF15 was associated with an increased risk of advanced liver fibrosis (OR=2.388). Conclusion: In patients with simple MAFLD, GDF15 level was not significantly higher than in the control group. In the T2DM-only group and the MAFLD+T2DM group GDF15 was significantly higher than in the control group. Increased serum GDF15 was associated with increased risk and severity of MAFLD complicated with abnormal glucose and lipid metabolism. High GDF15 increased the risk of advanced fibrosis in MAFLD patients.

[Read-through circular RNA rt-circ-HS promotes hypoxia inducible factor 1α expression and renal carcinoma cell proliferation, migration and invasiveness].

OBJECTIVE: To identify and characterize read-through RNAs and read-through circular RNAs (rt-circ-HS) derived from transcriptional read-through hypoxia inducible factor 1α (HIF1α) and small nuclear RNA activating complex polypeptide 1 (SNAPC1) the two adjacent genes located on chromosome 14q23, in renal carcinoma cells and renal carcinoma tissues, and to study the effects of rt-circ-HS on biological behavior of renal carcinoma cells and on regulation of HIF1α. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and Sanger sequencing were used to examine expression of read-through RNAs HIF1α-SNAPC1 and rt-circ-HS in different tumor cells. Tissue microarrays of 437 different types of renal cell carcinoma (RCC) were constructed, and chromogenic in situ hybridization (ISH) was used to investigate expression of rt-circ-HS in different RCC types. Small interference RNA (siRNA) and artificial overexpression plasmids were designed to examine the effects of rt-circ-HS on 786-O and A498 renal carcinoma cell proliferation, migration and invasiveness by cell counting kit 8 (CCK8), EdU incorporation and Transwell cell migration and invasion assays. RT-PCR and Western blot were used to exa-mine expression of HIF1α and SNAPC1 RNA and proteins after interference of rt-circ-HS with siRNA, respectively. The binding of rt-circ-HS with microRNA 539 (miR-539), and miR-539 with HIF1α 3' untranslated region (3' UTR), and the effects of these interactions were investigated by dual luciferase reporter gene assays. RESULTS: We discovered a novel 1 144 nt rt-circ-HS, which was derived from read-through RNA HIF1α-SNAPC1 and consisted of HIF1α exon 2-6 and SNAPC1 exon 2-4. Expression of rt-circ-HS was significantly upregulated in 786-O renal carcinoma cells. ISH showed that the overall positive expression rate of rt-circ-HS in RCC tissue samples was 67.5% (295/437), and the expression was different in different types of RCCs. Mechanistically, rt-circ-HS promoted renal carcinoma cell proliferation, migration and invasiveness by functioning as a competitive endogenous inhibitor of miR-539, which we found to be a potent post-transcriptional suppressor of HIF1α, thus promoting expression of HIF1α. CONCLUSION: The novel rt-circ-HS is highly expressed in different types of RCCs and acts as a competitive endogenous inhibitor of miR-539 to promote expression of its parental gene HIF1α and thus the proliferation, migration and invasion of renal cancer cells.

[Mesenchymal chondrosarcoma in central nervous system: a clinicopathological analysis].

Objective: To investigate the clinicopathological features of central nervous system (CNS) mesenchymal chondrosarcoma (MCS). Methods: Nine cases of CNS MCS were collected at the First Affiliated Hospital of Fujian Medical University from September 2010 to September 2020. The clinical,imaging,histopathological and immunohistochemical features were reviewed. NCOA2 gene rearrangement was evaluated by fluorescence in situ hybridization (FISH). Results: There were three male and six female patients, with age range of 1 to 59 years (median 31 years). Six cases were intracranial and three cases were intraspinal, and the tumors showed dural attachment. They were often diagnosed as meningioma basing on preoperative imaging. Microscopically, the tumors showed a characteristic biphasic histologic pattern composed of undifferentiated mesenchymal small cells and well-differentiated hyaline cartilage islands. The small cells area were positive for SOX9 (9/9), CD99 (8/9), and without BRG1 and INI1 deletion. The cartilaginous component expressed SOX9 (9/9) and S-100 protein (8/9). NCOA2 gene break apart signal was identified in five cases (5/5). Eight patients were followed up for 4-124 months. Three patients (3/8) had recurrences within one year and two patients died of the tumor. Conclusions: CNS MCS is an extremely rare malignant neoplasm with a propensity to dural involvement. Preoperative imaging has low diagnostic accuracy. CNS MCS should be differentiated from other CNS small round cell tumors and chondrosarcoma. FISH detection of NCOA2 gene rearrangement will assist the diagnosis of MCS.

[Clinicopathological features of adenocarcinoma of the rete testis].

Objective: To investigate the clinicopathological features, immunophenotype, and differential diagnosis of adenocarcinoma of the rete testis. Methods: Four adenocarcinoma cases of the rete testis diagnosed at West China Hospital, Chengdu, China (3 cases, including 2 consultation cases) and the First Affiliated Hospital of Fujian Medical University, Fuzhou, China (1 case) between January 2009 and December 2017 were included. Their clinical, morphologic and immunohistochemical features were analyzed using histological analysis and immunohistochemical staining. Related literature was reviewed to reveal the characteristics of this tumor. Results: The 4 patients' age range was 26-64 years. The maximum diameters of the tumors were 3.0 and 4.5 cm in 2 cases, respectively. On gross examination, adenocarcinomas of the rete testis appeared as a solid, white to gray or tan to yellow mass that raised at the hilum of the testis. Microscopically, all tumors showed multiple histologic patterns, including corded/trabecular (4/4), glandular, nested, sarcomatoid (3/4), solid (2/4), papillary, cribriform, and slit-like (1/4). Three types of adenocarcinoma cells included cuboidal to columnar (4/4), polygonal (4/4) and spindle-shaped (2/4) with pale eosinophilic and clear cytoplasm. The tumor cell nuclei appeared moderately to markedly atypical and pleomorphic, with a various number of mitoses. Transition from benign to malignant rete epithelium was seen in all cases. Eosinophilic hyaloid globules were found in 1 case. On immunohistochemical study, the tumor cells were diffusely, strongly positive for CKpan (4/4), EMA (4/4), Ber-EP4 (3/3) and CAⅨ(2/2), and focally positive for CK7 (4/4), vimentin (4/4), CD10 (4/4), PAX8 (3/3), PAX2 (3/3). The Ki-67 proliferative index was all>50% (4/4). The prognosis was poor. Two of the 3 patients died within 1 year after the surgical resection. Conclusions: Adenocarcinoma of the rete testis is a rare malignant tumor with several histologic patterns. Transition from benign to malignant rete epithelium is an important diagnostic clue. Detailed clinical history, tumor growth site and immunohistochemistry are helpful for its diagnosis and differential diagnosis.

[Epithelioid glioblastoma with BRAF V600E mutation: a clinicopathological and molecular study].

Objective: To investigate the clinicopathological and molecular characteristics of the epithelioid glioblastoma (eGBM) with BRAF V600E mutation. Methods: Sixteen cases of eGBM with BRAF V600E mutation diagnosed at the West China Hospital of Sichuan University, China from 2012 to 2019 were collected. Their clinicopathological and molecular characteristics were analyzed. Results: The range of patients' age was from 7 to 61 years (median 31.5 years). There were 4 males and 12 females, with a male to female ratio of 1∶3. Eleven cases were newly diagnosed eGBM and five cases had a previous history of astrocytomas. Most of the tumors were located in the cerebral hemisphere, often in the frontal lobe, with an average diameter of 4.6 cm (2.0-8.0 cm). The tumors were composed of relatively uniform, closely packed epithelioid cells, some showing discohesion, with distinct cell membrane, eosinophilic cytoplasm, eccentric nuclei, distinct nucleoli and mitotic activity. Palisaded/coagulative necrosis was seen in all cases. Glomerular microvascular proliferation was seen in most of the cases, while mono-or multi-nucleated tumor giant cells were seen in some cases. Focal sarcomatoid area was seen in 2 cases, and focal pleomorphic xanthoastrocytoma (PXA)-like area was seen in 3 cases. Immunohistochemistry showed variable positivity for GFAP, Olig2 and p53. The median Ki-67 index was 30% (10%-50%). Only one case lost ATRX protein expression. Sanger sequencing identified the BRAF V600E mutation in all sixteen patients. Five cases also had mutations in the TERT gene promoter. No IDH1 (R132) or IDH2 (R172) mutation was detected. Surgical resection of the tumors was performed for all patients, and 3 patients also received adjuvant radiotherapy and chemotherapy. Follow-up data were available for 15 patients, with a follow-up time of 1-89 months (median 10 months). Among the 15 patients, 7 patients died of disease and another 5 patients had recurrences. The overall survival time of the patients under 35 years of age was significantly longer than that of the patients aged 35 years or older (P=0.014), but their progression-free survival was not statistically different (P=0.232). Conclusions: eGBM with BRAF V600E mutation is more commonly detected in young women than other the populations (i.e. elderly or male). The epithelioid morphology should include rhabdoid meningioma, anaplastic PXA, atypical teratoid/rhabdoid tumor, metastatic tumors, and melanoma in its differential diagnosis. PXA-like area is observed in some eGBM cases, suggesting a relationship of these two types of tumor. eGBM is a high-grade malignant tumor and most of the cases show recurrences or deaths in a short-period time. The younger patients have a relatively better prognosis than the older ones.

[Sporadic meningioangiomatosis: a clinicopathological analysis].

Objective: To analyze the clinicopathological characteristics, diagnosis and prognosis of meningioangiomatosis (MA), and to investige the possible origion of spindle cells. Methods: Seventeen cases of MA were collected at Xuanwu Hospital of Capital Medical University and the First Affiliated Hospital of Fujian Medical University, from June 2012 to March 2020. The clinical manifestations, radiologic, histopathologic, immunohistochemical features and patients' outcome were analyzed. The presumed origin of spindle cells was evaluated by immunohistochemical staining. Results: Of the 17 patients, 9 were males and 8 were females. The age ranged from 3 to 56 years old. Thirteen patients presented with seizure as the initial symptom. The lesions were solitary and located in the cerebral cortex. Histopathologically, there were proliferation of small blood vessels and perivascular spindle cells in the cerebral cortex. The spindle cells had no obvious atypia, mitoses and necrosis. Four cases were combined with transitional meningioma. Immunohistochemically, the proliferative perivascular spindle cells were positive for vimentin in all cases, and focally positive for EMA and SSTR2. Ki-67 proliferation index was low. Neurofibrillary tangles were demonstrated by AT8. All 17 patients received surgical treatment and were followed up for one to 93 months. None had seizure attacks or tumor recurrence. Conclusions: MA is a rare slow-growing intracranial lesion, and the perivascular spindle cells could be derived from meningothelial cells, and MA is often associated with degeneration of the cerebral cortex and meningioma. The patients have good prognosis after surgical treatment.

[Effect of endoplasmic reticulum stress induced by all-trans retinoic acid on apoptosis of FLT3-ITD mutated leukemia cells by activating autophagy in FLT3-ITD mutated protein].

Objective: Endoplasmic reticulum stress(ERS)was used as the research emphasis to further investigate the mechanisms of apoptosis of FLT3-ITD-mutated leukemia cells and decreased expression of FLT3-ITD mutated protein induced by all-trans retinoic acid(ATRA). Methods: FLT3-ITD-mutated leukemia cell lines(MV4-11 and MOLM13)were treated with ATRA. Flow cytometry was conducted to assess cell apoptosis. Real-time fluorescent quantitative PCR(RT-qPCR)and Western blot were used to detect the expression of ERS-related and autophagy-related genes and protein, respectively. Results: A low-dose ATRA further increased FLT3-ITD cells and ERS levels. ATRA acted on the ERS-related PERK/eif2ɑ signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression. After the treatment with ATRA, FLT3-ITD protein in FLT3-ITD cells was decreased. Of the two main ERS-related protein degradation pathways, ER-associated degradation(ERAD)and ER-activated autophagy(ERAA), the expression of ERAD-related protein ATF6 in FLT3-ITD cells was not significantly changed on ATRA, whereas the expression of ERAA-related proteins Atg7 and Atg5 were significantly increased. Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2ɑ signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. These results provide preliminary evidence on the use of ATRA in the treatment of refractory leukemia with FLT3-ITD.

[Regulatory relationship between lncRNA KCNQ1OT1 and miR-146a-3p in preeclampsia].

Objective: To observe the changes of the expression level of long non-coding RNA (lncRNA) KCNQ1OT1 and microRNA (miR)-146a-3p in placenta tissues of preeclampsia (PE) patients, as well as their effect and mechanism on the biological functions of trophoblast cells. Methods: A total of 45 cases of hospitalized PE patients in Hainan General Hospital from July 2017 to July 2018 were selected as the PE group, 55 normal pregnant women during the same period were chosed as the control group. The expression level of KCNQ1OT1 mRNA and miR-146a-3p in the placenta tissues between two groups were detected by using quantitative real time (qRT)-PCR. Pearson's test was furtherly analyzed the correlation between them. Human trophoblast cell line (HTR8/SVneo) were randomly divided into control and lipopolysaccharide (LPS) groups, and then LPS group were divide into four sub-groups,included LPS group, short hairpin RNA (sh)-KCNQ1OT1 (after silencing the expression of KCNQ1OT1), miR-146a-3p inhibitor and sh-KCNQ1OT1+miR-146a-3p inhibitor. The targeting relationship between KCNQ1OT1 and miR-146a-3p were predicted by bioinformatics software and confirmed by luciferase assay. The cell proliferation and invasion capacities were respectively detected by cell counting kit-8 (CCK-8) and transwell assay. The expression level of KCNQ1OT1 mRNA and miR-146a-3p were detected by qRT-PCR and the protein expression level of CXC chemokine ligand 12 （CXCL12） and CXC chemokine receptor type 4 (CXCR4) were tested by western blot. Results: (1) The mRNA expression level of KCNQ1OT1 in the placenta of PE group was lower than that of control group (0.23±0.03 vs 0.51±0.04, P<0.05), and the miR-146a-3p expression level was higher than that of the control group (0.49±0.03 vs 0.31±0.03, P<0.05), there were statistical significant differences between the two groups. (2) Luciferase assay showed that there was a targeting relationship between KCNQ1OT1 and mir-146a-3p. Compared with the control group, the mRNA expression level of KCNQ1OT1 in the LPS group were significantly decreased (0.91±0.03 vs 0.35±0.03, P<0.05), and the expression level of miR-146a-3p were significantly increased (0.22±0.03 vs 0.63±0.04, P<0.05). The cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 significantly reduced in the LPS group compared with control group (all P<0.05). The mRNA expression level of KCNQ1OT1 (0.23±0.03) in the sh-KCNQ1OT1 group were further decreased, the expression of miR-146a-3p (0.85±0.03) were further increased, and the cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 were all further reduced compared with control group，there were significant difference between two groups (all P<0.05). Comparing the miR-146a-3p inhibitor group, and sh-KCNQ1OT1+miR-146a-3p inhibitor group with the sh-KCNQ1OT1 group, respectively, the expression level of KCNQ1OT1 mRNA (0.78±0.04 vs 0.50±0.03) increased, and the expression level of miR-146a-3p (0.42±0.03 vs 0.46±0.03) decreased, the cell proliferation, invasion and migration capacities and the protein expression of CXCL12 and CXCR4 were all increased ,there were statistically significant differences (all P<0.05). Conclusion: KCNQ1OT1 could target the regulation of miR-146a-3p through CXCL12/CXCR4 pathway in the proliferation, invasion an migration of HTR8/SVneo cells, which may be involved in the pathogenesis of PE.

[Comparison of intraocular pressure reduction in eyes with different intraocular tamponades after pars plana vitrectomy by 20% mannitol].

Objective: To investigate the efficacy of 20% mannitol in reducing intraocular pressure (IOP) in eyes with different intraocular tamponades after pars plana vitrectomy (PPV). Methods: Retrospective case-control study. Sixty-eight patients were administered with 20% mannitol and IOP was noted at regular intervals after simple PPV with ocular hypertension, including 24 males (26 eyes) and 44 females (46 eyes), aged (45.6±19.3) years. These cases were divided into three groups according to different tamponades: silicon-oil tamponade, 23 eyes; gas tamponade, 30 eyes; balanced salt solution (BSS), 19 eyes. The data were analyzed using the t test, variance and q test. Results: There was a significant decrease in IOP in all patients after using 20% mannitol. The IOP in the group of silicon-oil decreased from (33.25±2.56) mmHg (1 mmHg=0.133 kPa) to (23.21±1.85) mmHg, with a maximum decrease of 30.10%; the reduction in the group of C(3)F(8) was from (33.25±2.84) mmHg to (12.15±1.12) mmHg, with a maximum decrease of 33.44%. The IOP of the two groups dropped to a minimum both at 75 minutes. In the group of BSS, the IOP decreased from (32.95±2.33) mmHg to (17.50±1.35) mmHg, and the maximum extent of the decrease was 45.82% at 45 minutes. The difference in the IOP among the three groups at 20 min, 30 min, 45 min and 60 min was statistically significant (F=34.02, 112.68, 122.07, 34.83, all P=0.00). There were significant differences between the BSS group and the silicone-oil group (q=6.44, 13.04, 15.00, 17.11, all P=0.00), and between the BSS group and the C(3)F(8) group (q=7.68, 12.56, 12.93, 13.61, all P=0.00). Conclusion: In eyes with different intraocular tamponades, 20% mannitol was useful for short-term IOP reduction after vitrectomy, especially in those with BSS within one hour. But after 75 minutes, there was no statistically significant difference between groups. (Chin J Ophthalmol, 2019, 55:289-293).

[Application of da Vinci robot's bilateral axillo-breast approach in thyroid surgery of obese patients].

Objective:To discuss the effect of obesity on the operation of thyroid gland surgery and surgical results.Method:The clinical data of 446 patients who underwent robot thyroid surgery through bilateral axillo-breast approach (BABA) from the General Hospital of Jinan Military region from February 2014 to November 2017 were analyzed retrospectively, and the patients were divided into BMI<25 kg/m²; group, BMI 25-30 kg/m²; group and BMI>30 kg/m²; group according to body mass index (BMI). The operative complications were compared between the three groups of benign and malignant patients, such as operation time, postoperative lead flow, postoperative hospitalization time, tumor size (malignant), lymph node metastasis (malignant), cosmetic satisfaction score, laryngeal nerve injury and parathyroid function decrease. Statistical methods using Variance analysis and χ² test to compare the differences between the two groups of indicators, difference is statistically significant (P<0.05).Result:The difference of operation time, postoperative average hospitalization time and postoperative drainage fluid volume in 3 groups was not statistically significant（P>0.05）. ①Intraoperative and postoperative pathological results were benign: BMI<25 kg/m²; group 69 cases, BMI 25-30 kg/m²; group 48 cases, BMI>30 kg/m²; group 8 cases, temporary recurrent laryngeal nerve injury were 1 case, 0 case and 0 case respectively, temporary parathyroid function decrease 3 cases, 2 cases and 1 case. ②Intraoperative and postoperative pathological results were malignant:BMI<25 kg/m²; group 180 cases, BMI 25-30 kg/m²; group 119 cases,BMI>30 kg/m²; group 22 cases, temporary recurrent laryngeal nerve injury were 2 cases,1 case and 0 case respectively, temporary parathyroid dysfunction in 64 cases,29 cases and 5 cases respectively.③1 patient in BMI<25 kg/m²; group had lymphatic leakage after operation, 1 patient in BMI 25-30 kg/m²; group had subcutaneous tunnel hemorrhage, and 1 patient had lymphatic leakage during operation.Conclusion:For overweight or obese patients, the da Vinci robot thyroid operation is reliable, does not increase the risk of surgical complications, but also has a good cosmetic effect.

[BABA of da Vinci robot thyroid surgery in the standard treatment of thyroid cancer surgery].

Thyroid cancer is the most common malignant tumor in endocrine surgery. Surgery is the first choice for most patients with thyroid cancer. Da Vinci robot system as the auxiliary system is the most advanced endoscopic surgery, largely to fill the cavity mirror device cannot bend, complex operation and so on insufficiency, has now become an important way of surgical treatment of thyroid cancer, and its curative effect, high safety, but because of the economic cost is higher, is currently not widespread popularity.

SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway.

OBJECTIVE: To investigate whether SENP3 protects H9C2 cells from apoptosis triggered by H/R through the signal transducer and activator of transcription 3 (STAT3) pathway. MATERIALS AND METHODS: Male C57BL mice were cultured and mouse models of myocardial I/RI were established. At the same time, cardiomyoblast H9C2 cell line of rat embryo was cultured. Reactive oxygen species (ROS) level was detected during H/R using 2',7'-dichlorofluorescein diacetate (DCFH) kit. Apoptotic cells were checked by flow cytometry. The expressions of p-JAK2, JAK2, STAT3, p-STAT3, cleaved-caspase3 (c-caspase3), and Bcl/Bax were detected using Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: We revealed that SENP3 rose in mice of I/R group and in H9C2 cells following H/R with an increase in p-STAT3. Furthermore, increased expression of SENP3 was found to be dependent on the generation of ROS, as the SENP3 accumulation was inhibited by antioxidant (NAC). Inhibition of SENP3 suppressed the p-STAT3 expression, but promoted cell apoptosis, c-caspase3 expression, and Bcl/Bax ratio. Besides, SENP3 overexpression alleviated the cell apoptosis, which was abrogated by AG490. CONCLUSIONS: SENP3 could protect H9C2 against H/R through enhancing JAK2/STAT3 pathway.

Ambipolar ferromagnetism by electrostatic doping of a manganite.

Complex-oxide materials exhibit physical properties that involve the interplay of charge and spin degrees of freedom. However, an ambipolar oxide that is able to exhibit both electron-doped and hole-doped ferromagnetism in the same material has proved elusive. Here we report ambipolar ferromagnetism in LaMnO3, with electron-hole asymmetry of the ferromagnetic order. Starting from an undoped atomically thin LaMnO3 film, we electrostatically dope the material with electrons or holes according to the polarity of a voltage applied across an ionic liquid gate. Magnetotransport characterization reveals that an increase of either electron-doping or hole-doping induced ferromagnetic order in this antiferromagnetic compound, and leads to an insulator-to-metal transition with colossal magnetoresistance showing electron-hole asymmetry. These findings are supported by density functional theory calculations, showing that strengthening of the inter-plane ferromagnetic exchange interaction is the origin of the ambipolar ferromagnetism. The result raises the prospect of exploiting ambipolar magnetic functionality in strongly correlated electron systems.

Long noncoding RNA RUSC1-AS-N indicates poor prognosis and increases cell viability in hepatocellular carcinoma.

OBJECTIVE: This study aimed at exploring the expression and prognostic values of a novel long noncoding RNA RUSC1-AS-N in hepatocellular carcinoma (HCC), and to investigate the biological roles of RUSC1-AS-N in HCC cells. PATIENTS AND METHODS: RUSC1-AS-N expression in public available microarray data was analyzed. The expression of RUSC1-AS-N in our cohort containing 66 HCC tissues and paired adjacent non-cancerous hepatic tissues was measured by qRT-PCR. The correlation between RUSC1-AS-N expression and clinicopathological characteristics was evaluated by Pearson χ2-test. The prognostic value of RUSC1-AS-N was analyzed by Kaplan-Meier survival analysis. The biological roles of RUSC1-AS-N on HCC cell viability were evaluated by Glo cell viability assays and Ethynyl deoxyuridine incorporation assays. The effects of RUSC1-AS-N on HCC cell cycle were evaluated by fluorescence-activated cell sorting (FACS) analyses of propidium-iodide (PI) stained cells. The effects of RUSC1-AS-N on HCC cell apoptosis were evaluated by TdT-mediated dUTP nick end-labeling (TUNEL) assays. RESULTS: RUSC1-AS-N is upregulated in HCC tissues and associated with poor prognosis of HCC patients from GSE54238 and GSE40144. In our cohort, we further confirmed the upregulation of RUSC1-AS-N in HCC tissues. High expression of RUSC1-AS-N associates with large tumor size, vein invasion, encapsulation incompletion, advanced BCLC stage, and poor recurrence-free survival and overall survival. Functional assays revealed that RUSC1-AS-N knockdown markedly decreases cell viability, induces cell-cycle arrest and apoptosis of HCC cells. CONCLUSIONS: RUSC1-AS-N is upregulated and acts as an oncogene in HCC. RUSC1-AS-N may be a promising prognostic biomarker and therapeutic target for HCC.

[Job burnout and related influencing factors in community medical staff in Nanchong, China].

Objective: To investigate job burnout and related influencing factors in community medical staff in Nanchong, China. Methods: From June to July, 2015, cluster random sampling was performed to select 181 medical staff members in Nanchong Community Health Service Center as study subjects. The Chinese Maslach Burnout Inventory (CMBI) was used to measure the level of job burnout. Results: The overall detection rate of job burnout in community medical staff in Nanchong was 95.0%, and among these staff members with job burnout, 119 (65.7%) had mild job burnout, 44 (24.3%) had moderate job burnout, and 9 (5.0%) had severe job burnout. There were significant differences in the scores of emotional exhaustion and reduced sense of personal accomplishmentbetween the medical staff members with different ages (F=5.820 and 3.180, both P<0.05) . There was a significant difference in the score of emotional exhaustion between the medical staff members with different working years (F=2.909, P<0.05) . There was also a significant difference in the score of reduced sense of personal accomplishment between the medical staff members with different types of work (F=5.797, P<0.05) , and the nurses had the lowest score. Conclusion: The medical staff members in Nanchong have a high incidence rate of job burnout, with the feature of reduced sense of personal accomplishment. An old age, long working years, and nursing occupation are major risk factors for job burnout.

SCC-112 gene is involved in tumor progression and promotes the cell proliferation in G2/M phase.

PURPOSE: SCC-112 is a novel cell cycle-related gene and differentially expressed in cancers. Suggesting the complex role of SCC-112 might be existent in cell proliferation and tumor development. The relative research on SCC-112 has been few so far. This study is attempted to explore the role of SCC-112 in tumorigenesis. EXPERIMENTAL DESIGN: RT-PCR and western blot were performed on seven tumor-normal paired tissues and nine cell lines. Immunohistochemistry was carried out for analyzing the expression of SCC-112 in nasopharyngeal tissues. 293T and three nasopharyngeal cell lines were transfected with expression vector (pCMV-SPORT6-SCC-112) or its siRNA. Cell proliferation was examined by MTT and clone formation experiments. Immunoprecipitation determined the interacted protein of SCC-112, and FACS detected cell cycle parameter on cells treated with synchronized reagent. RESULTS: SCC-112 ( approximately 150 kDa) is up-regulated in tumor tissue as compared to the corresponding normal tissue and was detected in the tested cell lines. Overexpression of SCC-112 ( approximately 150 kDa) in 293T and three nasopharyngeal cell lines promoted cell proliferation and clone formation while downregulation of SCC-112 ( approximately 150 kDa) in these cells resulted in the opposite. Moreover, SCC-112 was found to interact with p63 and overexpression of SCC-112 up-regulated p63 expression. SCC-112 expression level positively correlated with cells in G2/M phase. CONCLUSIONS: These findings suggest that SCC-112 improve cell proliferation and contributes to tumorigenesis by interacting with p63 and promoting cell cycling. SCC-112 might be an alternative target in tumor biomarking and mechanistic investigation.

Zinc diphosphonates templated by organic amines: syntheses and characterizations of [NH3(CH2)2NH3]Zn(hedpH2)2*2H2O and [NH3(CH2)nNH3(CH2)nNH3]Zn2(hedpH)2*2H2O (n=4,5,6) (hedp=1-hydroxyethylidenediphophonate).

Four new zinc diphosphonate compounds with formulas [NH(3)(CH(2))(2)NH(3)]Zn(hedpH(2))(2).2H(2)O, 1, [NH(3)(CH(2))(n)()NH(3)]Zn(2)(hedpH)(2).2H(2)O, (n = 4, 2; n = 5, 3; n = 6, 4) (hedp = 1-hydroxyethylidenediphosphonate) have been synthesized under hydrothermal conditions at 110 degrees C and in the presence of alkylenediamines NH(2)(CH(2))(n)()NH(2) (n = 2, 4, 5, 6). Crystallographic data for 1: monoclinic, space group C2/c, a = 24.7422(15), b = 5.2889(2), c = 16.0338(2) A, beta = 117.903(1) degrees, V = 1856.17(18) A(3), Z = 4; 2: monoclinic, space group P2(1)/n, a = 5.4970(3), b = 12.1041(6), c = 16.2814(12) A, beta = 98.619(5) degrees, V = 1071.07(11) A(3), Z = 2; 3: monoclinic, space group P2(1)/n, a = 5.5251(2), b = 12.5968(3), c = 16.1705(5) A, beta = 99.182(1) degrees, V = 1111.02(6) A(3), Z = 2; 4: triclinic, space group P-1, a = 5.4785(2), b = 14.1940(5), c = 16.0682(6) A, alpha = 81.982(2) degrees, beta = 89.435(2) degrees, gamma = 79.679(2) degrees, V = 1217.11(8) A(3), Z = 2. In compound 1, two of the phosphonate oxygens are protonated. The metal ions are bridged by the hedpH(2)(2-) groups through three of the remaining four phosphonate oxygens, forming a one-dimensional infinite chain. The protonated ethylenediamines locate between the chains in the lattice. In compounds 2-4, only one phosphonate oxygen is protonated. Compounds 2 and 3 have a similar three-dimensional open-network structure composed of [Zn(2)(hedpH)(2)](n) double chains with strong hydrogen bonding interactions between them, thus generating channels along the [100] direction. The protonated diamines and water molecules reside in the channels. Compound 4 contains two types of [Zn(2)(hedpH)(2)](n) double chains which are held together by strong hydrogen bonds, forming a two-dimensional network. The interlayer spaces are occupied by the [NH(3)(CH(2))(6)NH(3)](2+) cations and water molecules. The significant difference between structures 2-4 is also featured by the coordination geometries of the zinc atoms. The geometries of those in 2 can be described as distorted octahedral, and those in 3 as distorted square pyramidal. In 4, two independent zinc atoms are found, each with a distorted octahedral and a tetrahedral geometry, respectively.