Objective Paraneoplastic neurological syndrome is a rare immune-mediated disease induced by underlying tumors， and early identification of special subtypes of paraneoplastic syndrome and specific autoantibodies can guide efficient tumor screening， thereby promoting timely antitumor treatment and prolonging survival time. Methods A retrospective analysis was performed for the diagnosis and treatment of a case of paraneoplastic neurological syndrome with multiple clinical phenotypes and multiple autoantibodies who was admittd to Department of Neurology， Weifang People’s Hospital， and a systmatical review was performed for related articles. Results The patient presented with unsteady gait and mental and behavioral disorders in the early stage and was initially diagnosed with paraneoplastic cerebellar degeneration and paraneoplastic limbic encephalitis with positive anti-SOX-1 and anti-GABABR antibodies. Due to abnormal electrophysiological results and positive P/Q-type VGCC antibodies， the patient was considered to have Lambert-Eaton myasthenic syndrome， and all evidence suggested that the patient had occult small cell lung cancer. Finally thoracoscopic biopsy confirmed that lymph node enlargement on PET-CT was in accordance with the pathological changes of small cell lung cancer. The patient received both antitumor treatment and immunotherapy and had a survival time of 19 months. Conclusion The detection of anti-SOX1 antibodies should promote the screening for small cell lung cancer. In patients with paraneoplastic limbic encephalitis and paraneoplastic neuromuscular syndromes mediated by cell surface antibodies， immunotherapy should be initiated in parallel with antitumor treatment， and such patients tend to have a good prognosis.

OBJECTIVE: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1. METHODS: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability. RESULTS: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( < 0.05) in association with a poorer prognosis of the patients ( < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( < 0.05). CONCLUSIONS miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.
Breast Neoplasms ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Neoplasm Invasiveness ; Neoplasm Metastasis

The purpose of this study was to investigate the anti-injury effect and protective mechanism of hydrogen-enriched water in a rat model of acute liver injury induced by aflatoxin B (AFB). Healthy male Sprague-Dawley (SD) rats were randomly divided into control group, model group (AFB group) and hydrogen-enriched water treatment group (AFB+H group). The rat model of acute liver injury induced by AFB was established by single intragastric administration of AFB (2.0 mg/kg), and then the rats were treated with hydrogen-enriched water intragastrically. HE staining was used to observe the pathological changes of liver tissue. Blood samples were taken from vena cava to measure serum liver function indexes. Live tissue was sampled to detect malondialdehyde (MDA) and reduced glutathione (GSH) contents. Western blot was used to detect phosphorylation levels of MAPK signaling pathway proteins (ERK, JNK and p38 MAPK). The results showed that, compared with the AFB group, the AFB+H group exhibited increased body weights, alleviated acute liver injury, decreased activities of serum glutamic-pyruvic transaminase and glutamic oxaloacetic transaminase, as well as total bilirubin level in the serum. Meanwhile, hydrogen-enriched water decreased MDA content and increased GSH content in liver tissue. AFB-increased phosphorylation levels of ERK, JNK and p38 MAPK in liver tissue were down-regulated significantly by hydrogen-enriched water treatment. These results suggest that hydrogen-enriched water can alleviate liver injury induced by AFB, and its mechanism may be related to the reduction of oxidative stress and the inhibition of MAPK signal transduction pathway activation.
Aflatoxin B1 ; Animals ; Chemical and Drug Induced Liver Injury ; pathology ; prevention & control ; Deuterium Oxide ; therapeutic use ; Liver ; pathology ; MAP Kinase Signaling System ; Male ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley

Objective To observe the inhibit effect of triplex forming oligonucleotide (TFO)(platelet-derived growth factor-B chain, PDGF) on tumor growth and angiogenesis in rats with glioma.Methods 1?10~6 C_6 glioma cells with high-flow microinfusion were seed into right caudate putamens of 18 rats by stereotaxic technique. TFO was injected in situ 1 week after glioma cells inoculation. Treat group Ⅰ and treat group Ⅱ received TFO at dose of 1.5 mg/20 ?l and 3.0 mg/20 ?l, respectively. The same doses were given again at 8, 11 and 14th day after glioma cells inoculation. The control group was treated with 20 ?l normal saline at same time like treat groups. Three weeks after glioma cells inoculation, all the rats were killed. The expressions of, PDGF-B, vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) were detected with microscopic histology.Results The inhibition rate of tumor growth was 66.0% in treat groupⅠand 92.2% in treat group Ⅱ. There was significant difference between the two groups ((P

BACKGROUND: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma. METHODS: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin. RESULTS: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05). CONCLUSIONS Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

OBJECTIVETo study the change of synaptic onset latency and threshold in primary auditory cortex (A1) during the development of SD rat.

METHODSExtracellular recording was used to locate A1, followed by transferred to loose-patch and whole-cell patch in vivo to record the spike activity, synaptic onset latency and threshold responses respectively. Rats were divided into 4 groups according to ages, postnatal 12-15 days, 16-18 days, 19-24 days and adult (> 3 months).

RESULTS1. The onset latency of local field potential in A1 of adult rats[(10-20)ms] was shorter than young rats[(20-30)ms]. 2. During development, the onset latency of spikes of a single neuron in response to white noise pulses decreased. And the latency in young rats P12-15 [(40.15 ± 2.67) ms] and P16-18 [(33.86 ± 4.61) ms] were longer than in adults [(22.93 ± 2.94) ms] (ANOVA-test, t = 4.330 and 1.995, P = 0.00 and 0.04) . However, the onset latencies of P19-24 [(24.80 ± 3.63) ms] and adult had no significant difference (P > 0.05). 3.Synaptic onset latencies of both excitation and inhibition were significantly longer in P12-15[ (38.94 ± 1.90) ms, (35.26 ± 2.40) ms] and P16-18[ (32.68 ± 2.52) ms, (30.24 ± 2.18) ms] than in adults [(19.4 ± 1.06) ms, (18.91 ± 0.77) ms] excitation (t = 6.255 and 4.662, P < 0.01) inhibition (t = 8.918 and 4.820, P < 0.01) showed significant difference. Whereas the onset latencies of P19-24[ (23.67 ± 2.46) ms, (21.43 ± 1.80) ms] and adults displayed no prominent difference(P > 0.01). Meanwhile, the difference between the onset latencies of excitation and inhibition became narrower during development[ (3.15 ± 1.02) ms, (2.01 ± 0.73) ms, (1.79 ± 0.85) ms, (0.39 ± 0.48) ms]. P12-15 had notably difference in comparison to adults (t = 1.739, P < 0.01). 4. The thresholds of synaptic response were notably higher in P12-15 (40.0 ± 1.6) dB and P16-18 (41.3 ± 11.6) dB when compared with adults (30.9 ± 0.6) dB (t = 5.284 and 5.867, P < 0.01) . While that of P19-24 (35.0 ± 32.7) dB showed no distinct difference (P > 0.01).

CONCLUSIONSingle neuron spiking activity, synaptic onset latency and threshold evoked by sound stimulus gradually mature during the development in rat A1.

Acoustic Stimulation ; Animals ; Auditory Cortex ; physiology ; Neurons ; physiology ; Rats ; Rats, Sprague-Dawley

ObjectiveTo investigate the effect of finasteride on the microvascular density (MVD) and the expression of the vascular endothelial growth factor (VEGF) in the seminal vesicle of rats.

METHODSForty male SD rats were randomly and equally divided into groups A, B, C and D, those in groups A and B fed with normal saline as the control and those in C and D with finasteride at 40 mg per kg of the body weight per day, A and C for 14 days and B and D for 28 days. Then the seminal vesicles of the animals were harvested for HE staining, measurement of MVD, determination of the expressions of CD34 and VEGF by immunohistochemistry, and observation of histomorphological changes in the seminal vesicle.

RESULTSThe expressions of CD34 in groups C and D were decreased by 6.7% and 15.8% as compared with those in A and B (P<0.01), and that in group D decreased by 9.3% in comparison with that in C (P<0.01). The expression indexes of VEGF in groups C and D were decreased by 6.9% and 14.1% as compared with those in A and B (P<0.01), and that in group D decreased by 9.0% in comparison with that in C (P<0.01).

CONCLUSIONSFinasteride can inhibit the expression of VEGF in the seminal vesicle tissue of the rat and hence suppress the angiogenesis of microvessels of the seminal vesicle.

Angiogenesis Inhibitors ; pharmacology ; Animals ; Antigens, CD34 ; metabolism ; Finasteride ; pharmacology ; Immunohistochemistry ; Male ; Neovascularization, Physiologic ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Seminal Vesicles ; blood supply ; drug effects ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

Objective To investigate the expression patterns of fibroblast growth factor 23 (FGF23) in osteoblast and its responses to calcium, phosphate, exogenous PTH and 1,25(OH)_2D~3. Methods The primary rat calvarial osteoblasts were cultured in MEM medium which containing 10% FBS, then were harvested when cells were in half-confluence, confluence, osteoid deposition and osteoid mineralization stages respectively. The procedure was monitored under microscopy. Total RNA was extracted from cells according to the Trizol procedure. FGF23 mRNA levels were determined by Real-time PCR. Further, the confluent osteoblasts were treated with 3.2 mmol/L CaCl_2, 4.4 mmol/L β-glycerophosphate, 10~(-9) mol/L rhPTH(1-34) and 10~(-8) mol/L 1,25(OH)_2D_3 respectively for 3 days, and same volume of the medium was added as the control. The gene expressions were determined by Real-time PCR. Results FGF23 expression was transiently up-regulated at cell confluent stage and down-regulated after that. The FGF23 mRNA levels were 7.5-fold higher in confluent cells compared with that in half-confluent cells (P<0.001). The markedlly stimulating effect (about 16 times) on FGF23 expression was stimulated by exogenous 1,25(OH)_2D_3 treatment while no significant effect was found on FGF23 mRNA levels by CaCl_2,β-glycerophosphate, and rhPTH(1-34) treatments when compared with the control. Conclusions The FGF23 expression in osteoblast is developmental stage-related and its powerful stimulator is 1,25(OH)_2D.

Objective To investigate the differentiation of dendritic cells from monocytes of the peripheral blood in patients with psoriasis. Methods Flow cytometry was used to analyze the phenotype of monocyte derived dendritic cells (MoDC). The capacity of MoDC to stimulate the proliferation of T lymphocytes was evaluated by allogeneic mixed lymphocyte reaction. Results Monocytes in the peripheral blood of patients with psoriasis could differentiate into dendritic cells. Expression of CD40, CD80, CD86 and HLA-DR by MoDC was significantly increased in patients with psoriasis compared with that in normal controls (P