Acquired Hemophilia A is an acquired bleeding disorder characterized by reduced FⅧ activity due to the presence of autoantibodies against anticoagulant factor Ⅷ in the circulation. Laboratory tests are typically characterized by prolonged isolated activated partial thromboplastin time (APTT). Clinically, it often manifests as severe bleeding, and 50% of AHA patients can identify the cause. This article reports on a patient with post-traumatic AHA who rapidly improved after antibody removal and bypass replacement therapy, followed by wound healing following surgical intervention. A review of relevant literature is also conducted to enhance clinicians' awareness of AHA, which presents with normal coagulation initially and gradually develops into prolonged APTT accompanied by bleeding manifestations, aiming for early diagnosis and timely treatment.

Acquired Hemophilia A is an acquired bleeding disorder characterized by reduced FⅧ activity due to the presence of autoantibodies against anticoagulant factor Ⅷ in the circulation. Laboratory tests are typically characterized by prolonged isolated activated partial thromboplastin time (APTT). Clinically, it often manifests as severe bleeding, and 50% of AHA patients can identify the cause. This article reports on a patient with post-traumatic AHA who rapidly improved after antibody removal and bypass replacement therapy, followed by wound healing following surgical intervention. A review of relevant literature is also conducted to enhance clinicians' awareness of AHA, which presents with normal coagulation initially and gradually develops into prolonged APTT accompanied by bleeding manifestations, aiming for early diagnosis and timely treatment.

Objective To explore the effect and molecular mechanism of CC chemokine ligand 2 (CCL2) on epithelial-mesenchymal transition in human breast cancer cells.Methods Breast cancer Michigan cancer foundation-7 (MCF-7) cells were treated with 50 ng/ml CCL2.The abilities of invasion were detected by Transwell assay.The expression of epithelial-mesenchymal transition (EMT)-associated markers,E-cadherin and vimentin were detected by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR).The expressions of Snail,protein kinase B (AKT),phosphorylated protein kinase B (p-AKT),phosphorylated glycogen synthase kinase 3β (p-GSK3β3) and GSK3β were detected by Western blot.Snail nuclear localization was detected by immunoflurescence staining.Results We found that CCL2 treatment could induce morphological alteration of MCF-7 cells from epithelial morphology to mesenchymal morphology.CCL2 significantly increased the migration of MCF-7 cells,and increased the expression of mesenchymal maker vimentin and decreased epithelial marker E-cadherin.More important,treatment of CCL2 significantly increased the expression of Snail,and promoted the nuclear localization of Snail.Knockdown of Snail significantly reverse the effects of CCL2 on the EMT in MCF-7 cells.Moreover,treatment of CCL2 significantly increased the phosphorylation levels of p-AKT and p-GSK3β,and AKT inhibitor LY294002 significantly inhibited CCL2-induced Snail and p-GSK3β expression.Conclusion CCL2 might induce EMT in MCF-7 cells,by which mechanism is related to activate AKT/GSK3β Snail pathway.

Objective To observe the effects of Radix Angelica Sinensis ( RAS) on depression be-havior and cytokines,TNF-αand IL-6,in the hippocampus and prefrontal cortex of depression model rats in-duced by chronic unpredictable mild stress ( CUMS) .Methods 32 adult male rats weighting 140-160 g were randomly divided into 4 groups: Control,CUMS,CUMS+fluoxetine and CUMS+RAS groups.CUMS procedure went on 5 consecutive weeks and during the last 3 weeks the rats in CUMS+fluoxetine and CUMS+RAS groups were taken RAS or fluoxetine via intragastric administration.After 5-week CUMS procedure, rats were subjected to sucrose preference test,forced swimming test and open field test.After behavioral tests were finished,all rats were anesthetized with 10%chloral hydrate (350 mg/kg,intraperitoneal injection) and then decapitated.The hippocampus and prefrontal cortex of rats were separated and ELISA was used to detect the expression of TNF-αand IL-6 in these regions.Results Comparing with control rats, rats exposed to CUMS showed decreased sucrose preference ratio((42±15)%),prolonged immobility time ((68.28±16.50) s),decreased crossing numbers (31.25±21.56) and increased TNF-α((206.14±30.53)pg/ml) and IL-6 ((369.51±103.81)pg/ml) expression in hippocampus and TNF-α((199.33±25.67)pg/ml) and IL-6 ((347.74±81.04) pg/ml) expression in prefrontal cortex ( P<0.01).However,RAS treated rats reversed the behavioral changes such as sucrose preference ratio((66±21)%),immobility time ((32.53±10.26)s) and crossing numbers ( 83.00 ±23.25 ) , meanwhile reduced TNF-α( ( 53.42 ±12.43 ) pg/ml ) and IL-6 ((93.84±13.19)pg/ml) expression in hippocampus,TNF-α((57.58±8.33)pg/ml) and IL-6((91.18± 17.37) pg/ml) expression in prefrontal cortex among stress rats ( P<0.01) .Conclusion RAS can amelio-rate CUMS induced depression behaviors of rats through regulating hippocampus and prefrontal cortex cyto-kines ( TNF-α,IL-6) .

Objective To observe effect of environmental enrichment on the learning and memory ability and the expressions of hypoxia inducible factor 1α (HIF-1a) and vascular endothelial growth factor (VEGF) in rats with chronic cerebral hypoperfusion.Methods A total of 40 rats were randomly divided into 3 groups: bilateral vascular occlusion (2VO) of the common carotid arteries group (n=14, 2VO group), 2VO + enriched environment (EE) group (n=14, 2VO+EE group) and sham group (n=12, SHAM group).Morris water maze, novel object recognition test, real-time reverse transcription-polymerase chain reaction (real-time RT-PCR), immunohistochemistry methods and Western blotting were used to detect changes in learning and memory ability of rats and HIF-1α and VEGF expression levels in hippocampus.Results Morris water maze showed that the escape latency was longer in the 2VO group than in the SHAM group at 3, 4 and 5 day during the training (all P＜0.05), while the 2VO+EE group spent significantly less time in finding the platform as compared with the 2VO group at 4 and 5 day (both P＜0.05).The time for space exploration in target quadrant was less in 2VO group than in SHAM group (P＜0.05), while it was longer in 2VO +EE group than in 2VO group (P＜0.05).Novel object recognition test showed that the 2VO operation impaired the priority index (PI) of time spending at exploring the novel object (P＜0.05), and environmental enrichment could improve the PI in 2VO group (P＜0.05).The real-time RT-PCR and Western blotting showed that the HIF-1α mRNA expression was higher in 2VO group than in SHAM group (P＜0.05).The VEGF mRNA and protein expressions were higher in 2VO+EE group than in 2VO group (both P＜0.05).The expression of HIF-1α in hippocampal CA1 area was higher in 2VO group than in SHAM group (P＜0.05).Conclusions Environmental enrichment can alleviate the damages of spatial and non-spatial learning and memory ability which are caused by chronic cerebral hypoperfusion.And HIF-1α and its downstream gene VEGF may be involved in the restoration of cognitive function by enriched environment.

Objective To investigate the effects of hippocampal neurogenesis in spatial learning and memory,especially in spatial long-term memory.Methods Totally 24 wistar rats were randomly divided into two groups:normal control group (NC group,n =12) and irradiation group (IRR group,n =12).We use low-dose irradiation at subgranular zone to inhibit adult hippocampal neurogenesis and new neurons were investigated by 5-Bromo-2-deoxyUridine/neuron specific nuclear protein double-labeling.Four weeks after irradiation,Morris water maze,including navigation test and space exploration assay,was used to detect spatial leaming and memory.Then,in the day 8 and day 15 after the navigation test,space exploration assay was repeated to detect spatial long-term memory.The expression levels of postsynaptic density protein 95 and synaptophysin were evaluated using western blot and real-time quantitative PCR.Results Hippocampal neurogenesis was inhibited by low dose irradiation(2.80 ± 0.44 vs 23.50 ± 1.12,t =20.21,P ＜ 0.01).After the inhibition,the escape latency did not change,while the time spent in target quadrant was significantly declined in the day 2((14.76 ±.2.04) s vs (20.47 ± 1.29) s),day 8((11.95 ± 1.34) s vs (19.52±1.43) s)and day 15((11.79 ±1.35) s vs (21.58 ±1.07) s) after the navigation test (t=2.45,P＜0.05; t =3.76,P＜0.01; t =5.39,P＜0.01).The postsynaptic density protein 95 and synaptophysin expressions were significantly decreased in IRR group.As to the RNA levels,there was also a significant difference between the two groups.Conclusion Hippocampal neurogenesis in the dentate gyrus plays an important role for the formation of spatial long-term memory.

Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.
Animals ; Brain Ischemia ; metabolism ; Disease Models, Animal ; Granulocyte Colony-Stimulating Factor ; metabolism ; Hyperlipidemias ; metabolism ; Male ; Neuroprotective Agents ; metabolism ; Rats ; Rats, Sprague-Dawley

Objective To investigate the risk factors for nosocomial bacteremia and decrease the prevalence of nosocomial bacteremia.Methods We collected the data of bacteremia patients in our hospital from January,2006 to December,2009.According to the criterion of nosocomial infection,the patients were divided into nosocomial bacteremia group (83) and community-onset bacteremia group (119).The influence of a series of variables on the development on both types of bacteremia was analyzed by Student＇s t test and x2 test.The risk factors were performed using multivariate logistic regression.Results Compared to that of community-onset bacteremia group,the proportion of malignancy (21/83 vs 12/119,x2 =8.2846,P ＜ 0.01 ),venous catheter ( 28/83 vs 3/119,x2 =36.67,P ＜ 0.01 ),diabetes ( 37/83 vs 0/119,x2 =68.226,P ＜0.05),surgical operation(37/83 vs 0/119,x2 =68.226,P ＜0.01),previous antibiotics(78/83 vs 10/119,x2 =173.5657,P ＜ 0.01 ) in nosocomial bacteremia group were higher.Multivariable logistic regression analysis showed that only 4 factors were significantly and independently responsible for nosocomial bacteremia,They were malignancy ( P ＜ 0.05,OR =3.186),diabetes ( P ＜0.001,OR =4.821 ),venous catheter( P ＜ 0.05,OR =2.135),previous antibiotics ( P ＜ 0.05,OR =2.135 ).The bacteria in nosocomial bacteremia group showed more ability to resist to antibiotics.Conclusions We should pay more attention to the patients with diabetes or malignancy or venous catheter or previous treated with antibiotics.These patients have more chances to develop to nosocomial bacteremia and infect by the drug-resistant bacteria.

Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.

Objective To obtain the specific human scFv basic fibroblast growth factor(bFGF)using phage antibody library technology. Methods The library was panned with human recombinant bFGF for 4 rounds. The antigen binding activities of random clones were tested by ELISA in order to select specific antibodies, which were then examined by DNA sequence analysis. Results The positive clone selected from the 104 random clones was able to bind bFGF specifically, while not able to bind other growth factors,such as aFGF, VEGF(vascular endothelial growth factor). By competition ELISA assay we found one clone 44 could inhibit bFGF binding to FGFR1. Conclusion Seven specific human phage antibody against bFGF was obtained by phage display technique, one clone could inhibit bFGF binding to its high affinity receptor FGFR1.