Cerebral infarct secondary to traumatic internal carotid artery dissection.

BACKGROUND: Traumatic internal carotid artery dissection (TICAD) is rare and can result in severe neurological disability and even death. No consensus regarding its diagnostic screening and management has been established. AIM: To investigate the clinical presentation, imaging features, diagnostic workup, and treatment of TICAD. METHODS: In this retrospective case series, emergency admissions for TICAD due to closed head injury were analyzed. The demographic, clinical, and radiographic data were retrieved from patient charts and the picture archiving and communication system. RESULTS: Six patients (five males and one female, age range of 43-62 years, mean age of 52.67 years) presented with TICAD. Traffic accidents (4/6) were the most frequent cause of TICAD. The clinical presentation was always related to brain hypoperfusion. Imaging examination revealed dissection of the affected artery and corresponding brain infarction. All the patients were definitively diagnosed with TICAD. One patient was treated conservatively, one patient underwent anticoagulant therapy, two patients were given both antiplatelet and anticoagulant drugs, and two patients underwent decompressive craniectomy. One patient fully recovered, while three patients were disabled at follow-up. Two patients died of refractory brain infarction. CONCLUSION: TICAD can cause catastrophic outcomes and even refractory brain hernia. Early and efficient diagnosis of TICAD is essential for initiating appropriate treatment. The treatment of TICAD is challenging and variable and is based on clinician discretion on a case-by-case basis.

Paraplegia from spinal intramedullary tuberculosis: A case report.

BACKGROUND: Tuberculosis (TB) mostly attacks the lungs, and extrapulmonary TB involving the central nervous system is uncommon; among these cases, spinal intramedullary TB is even more rare. The clinical manifestations of spinal intramedullary TB are similar to those of intramedullary spinal cord tumors. Therefore, it is necessary to make a careful differential diagnosis of spinal intramedullary lesions to achieve the appropriate treatment and favorable prognosis. We report a rare case of a young male patient with paraplegia due to spinal intramedullary TB, which is uncommon and regrettable. CASE SUMMARY: A 23-year-old male presented with fever accompanied by nausea and vomiting lasting for 2 mo and was then diagnosed with tubercular meningitis. After anti-TB treatment, his symptoms were significantly improved. However, 2 mo after the diagnosis of tubercular meningitis, the patient felt numbness below the costal arch level, which lasted for 1 wk, and he paid no attention to this symptom. What followed was paraplegia and urine/fecal incontinence. Magnetic resonance imaging of the thoracic spine showed a ring-enhanced intramedullary cord lesion at T8-T9. Lesion exploration showed enlargement of the spinal cord at T8-T9, and the lesion could be observed by incision. The lesion was adhered to the peripheral tissue and was grayish-white and tough with a poor blood supply and a diameter of approximately 0.8 cm. The lesion was resected completely. The results of pathological examination by both hematoxylin-eosin staining and acid-fast bacilli staining confirmed TB, accompanied by acute and chronic suppurative inflammation and granulation tissue formation. The patient was instructed to continue anti-TB treatment after the operation, but he did not follow the medical advice. Follow-up continued for ten years, the patient had persistent paraplegia, the numbness disappeared and urine/fecal sensation recovered. CONCLUSION: Although TB is a kind of benign disease, some cases progress rapidly. Moreover, spinal intramedullary TB may seriously endanger quality of life and still needs timely diagnosis and proper treatment.

Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin-induced diabetes mellitus.

The diabetes mellitus (DM)-induced reduction of neurogenesis in the hippocampus is consequently accompanied by cognitive decline. The present study set out to define the critical role played by long noncoding RNA H19 (lncRNA H19) in the apoptosis of hippocampal neurons, as well as oxidative stress (OS) in streptozotocin (STZ)-induced DM mice through regulation of insulin-like growth factor 2 (IGF2) methylation. The expression of lncRNA H19 in the hippocampal neurons and surviving neurons were detected. Hippocampal neurons were cultured and transfected with oe-H19, sh-H19, oe-IGF2, or sh-IGF2, followed by detection of the expressions of IGF2 and apoptosis-related genes. Determination of the lipid peroxide and glutathione levels was conducted, while antioxidant enzyme activity was identified. The IGF2 methylation, the binding of lncRNA H19 to DNA methyltransferase, and the binding of lncRNA H19 to IGF2 promoter region were detected. DM mice exhibited high expressions of H19, as well as a decreased hippocampal neurons survival rate. Higher lncRNA H19 expression was found in DM. Upregulated lncRNA H19 significantly increased the expression of Bax and caspase-3 but decreased that of Bcl-2, thus promoting the apoptosis of hippocampal neuron. Besides, upregulation of lncRNA H19 induced OS. LncRNA H19 was observed to bind specifically to the IGF2 gene promoter region and promote IGF2 methylation by enriching DNA methyltransferase, thereby silencing IGF2 expression. Taken together, downregulated lncRNA H19 reduces IGF2 methylation and enhances its expression, thereby suppressing hippocampal neuron apoptosis and OS in STZ-induced (DM) mice.

Effect of Low-Dose Triptolide and Sorafenib Alone and Their Combination on AML Cell Line MV411 and the Pathway of STAT5 / 中国实验血液学杂志

OBJECTIVE@#To investigate the effects of inhibiting proliferation and inducing apoptosis of low-dose triptolide and sorafenib alone or in combination on FLT3-ITD acute myeloid leukemia cell line MV4-11 and STAT5 pathway.@*METHODS@#The MV4-11 cells were treated with low dose triptolide(IC) and sorafenib(IC) alone or in combination for 48 hours. The cell proliferation and inhibition were detected by using CCK-8 kit, the cell apoptosis was detected by flow cytometry, the expression of FLT3,STAT5 in mRNA and protein levels was detected by RT-PCR and Western blot respectively.@*RESULTS@#The treatment of MV4-11 cells with low dose triptolide and sorafenib alone and in combination for 48 hours could inhibit cell proliferation and induce cell apoptosis, moreover the inhibitory rate and apoptotic rate of MV4-11 cells in drug-combination group both were higher than those in single drug group. The mRNA expression and protein expression of FLT3,STAT5 signaling pathway in drug combination group were significantly lower than those in single drug group.@*CONCLUSION@#Low-dose triptolide combined with sorafenib can synergistically inhibit the proliferation and induce the apoptosis of MV4-11 cells, which may be related with the inhibition of FLT3 and STAT5 pathway.

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage.

BACKGROUND/AIMS: Cerebral ischemia is considered to be the most common cause of stroke with high mortality. It occurs as a result of the damage of the hippocampal neurons with lymphocyte function-associated antigen (LFA)-1 being emphasized to play a role in the biological functions of hippocampal neurons. This study was conducted in order to investigate the effects of specific knockdown of LFA-1 expression by lentivirus had on the apoptosis of the hippocampal neurons, simulated by rat models of acute cerebral ischemia after cerebral lymphatic blockage. METHODS: A total of 60 Wistar rats were selected as subjects, among which 50 were used to establish models of the acute cerebral ischemia after cerebral lymphatic blockage, while the remaining 10 rats were treated with the sham operation. The underlying regulatory mechanisms regarding LFA-1 were analyzed with the treatment of si-LFA-1 and LFA-1 vector in the hippocampal CA1 area of brain tissues isolated from the rats with acute cerebral ischemia. The brain water content, electrolyte content, and blood-brain barrier permeability located in ischemic area of rats were measured. TUNEL staining and immunochemistry methods were employed in order to determine the apoptosis rate and positive levels of LFA-1, MMP-9, and Caspase-3. The mRNA and protein levels of related genes were also detected by means of RT-qPCR and western blot assay. RESULTS: The brain water content, Na+ and Ca+ contents, blood-brain barrier permeability, apoptosis rate, positive levels of LFA-1, MMP-9, and Caspase-3 were decreased, and the K+ content was increased in ischemic tissues treated with si-LFA-1. The mRNA and protein levels of LFA-1, MMP-9, Caspase-3, and Bax had all decreased, while the mRNA and protein levels of Bcl-2 were elevated in the hippocampal CA1 area of rat brain tissues treated with si-LFA-1. These situations could be reversed through the up-regulation of LFA-1. CONCLUSION: In conclusion, LFA-1 gene silencing could improve the acute cerebral ischemia after cerebral lymphatic blockage by inhibiting apoptosis of the hippocampal neurons in rats.

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage.

BACKGROUND/AIMS: Acute cerebral ischemia is a manifestation of cerebral vascular insufficiency and has a high mortality. However, the therapy for acute cerebral ischemia is still limited. This study aimed to investigate the effect of microRNA-381 (miR-381) on the repair of nerve injury in rats with acute cerebral ischemia after cerebral lymphatic blockage (CLB) by targeting leucine-rich repeat C4 protein (LRRC4) through the Stromal cell-derived factor-1/CXC chemokine receptor-4 signaling pathway. METHODS: Rat models of CLB and middle cerebral artery occlusion (MCAO) were established, and 56 Wistar rats were divided into sham, MCAO, CLB + MCAO, CLB + MCAO + miR-381 inhibitor, CLB + MCAO + miR-381 mimic, CLB + MCAO + AMD3100 and CLB + MCAO + miR-381 mimic + AMD3100 groups. Modified neurological severity score (mNSS was used to determine nerve injury, TTC staining to measure infarction volume, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry to evaluate cell apoptosis, immunofluorescence to measure BrdU-positive cell number, enzyme-linked immunosorbent assay (ELISA) to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-10 (IL-10), nerve growth factor (NGF) and neurite outgrowth inhibitor -A (Nogo-A), Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting to evaluate expression of miR-381, LRRC4, SDF-1, CXCR4, pERK, Slit2 and vascular endothelial growth factor (VEGF). RESULTS: LRRC4 was a target gene of miR-381. Compared with the results in the CLB + MCAO group, mNSS, infarction volume, apoptosis rate and TNF-α, IL-1ß, IL-6 and Nogo-A contents as well as LRRC4 expression in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups were increased (those in the CLB + MCAO + AMD3100 group > those in the CLB + MCAO + miR-381 mimic + AMD3100 group), while BrdU-positive cell number, contents of NGF and IL-10, and expression of SDF-1, CXCR4, pERK, Slit2 and VEGF in brain tissues were decreased (those in the CLB + MCAO + AMD3100 group < those in the CLB + MCAO + miR-381 mimic + AMD3100 group). The results in the CLB + MCAO + mimic group were opposite of those in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups. CONCLUSION: Taken together, we concluded that up-regulation of miR-381 promoted nerve injury repair in acute cerebral ischemia rats after CLB by negatively regulating LRRC4 through activating the SDF-1/CXCR4 signaling pathway.

Effects of microRNA-21 on Nerve Cell Regeneration and Neural Function Recovery in Diabetes Mellitus Combined with Cerebral Infarction Rats by Targeting PDCD4.

We aimed to determine the effect and mechanism of microRNA-21 (miR-21) on nerve cell regeneration and nerve functional recovery in diabetes mellitus combined with cerebral infarction (DM + CI) rats by targeting PDCD4. A total of 125 male Wistar rats were selected for DM + CI rat model construction and assigned into the blank, miR-21 mimics, mimics control, miR-21 inhibitor, inhibitor control, miR-21 inhibitor + si-PDCD4 and si-PDCD4 groups. And, 20 healthy rats were selected for the normal group. Triphenylterazolium chloride (TTC) staining and HE staining were used for determination of the area of CI and pathological changes, respectively. Behaviors of rats in the eight groups were determined by forelimb placement test and balance beam walking test. Immunohistochemical staining, double immunofluorescence staining assay, Western blotting, and qRT-PCR were used to detect expressions of miR-21, PDCD4, HNA, Nestin, NeuN, ß-III-Tub, PTEN, FasL, and GFAP. DNA laddering and TUNEL staining was used for cell apoptosis. TTC and HE staining confirmed that 87.5% rats were induced into CI + DM models successfully. Results of forelimb placement test and balance beam walking test showed that miR-21 mimics, and si-PCDC4 improved the nerve defect of model rats. Comparing with the blank group at the same time, rats in the miR-21 inhibitor group displayed significant decrease in the forelimb placement test score, significant increase in the balance beam walking test score, and exacerbation of nerve defect, while rats in the miR-21 mimics and si-PCDC4 groups displayed significant increase in forelimb placement test score and significant decrease in the balance beam walking test score and improvement of nerve defect situation. The HNA, Nestin, and PDCD4 expressions were decreased and the NeuN, ß-III-Tub, and GFAP expressions were increased in the miR-21 mimics and si-PDCD4 groups comparing with the blank group. The results of miR-21 inhibitor group were on the contrary. In comparison to the blank group, the miR-21 mimics group and the si-PDCD4 had lower miR-21 expressions and higher expressions of PDCD4, PTEN, and FasL, while the miR-21 inhibitor group was in the opposite trend. The results of qRT-PCR were the same with Western blotting. The expressions of fluorescence in other groups were higher than the normal group; compared with the blank group, the miR-21 mimics group and the si-PDCD4 group had lower fluorescence expression and DNA ladder. However, the fluorescence expressions and DNA ladder of miR-21 inhibitor group increased markedly in contrast with the blank group. Comparing with the blank group, BrdU+/DEX+ fluorescence intensity significantly enhanced in the miR-21 mimics and si-PDCD4 groups and significantly reduced in the miR-21 inhibitor group. And, comparing with the blank group, in the miR-21 mimics group, the signal strength of luciferase carrying the wild-type PDCD4 was reduced by 25%. The present studies demonstrated that miR-21 could promote the nerve cell regeneration, suppress apoptosis of nerve cells in DM + CI rats and improves the nerve defect situation of DM + CI rats by inhibiting PDCD4.

Long non-coding RNA H19 induces hippocampal neuronal apoptosis via Wnt signaling in a streptozotocin-induced rat model of diabetes mellitus.

Defects in hippocampal synaptic plasticity and disorders of memory and learning are the central nervous system complications of diabetes mellitus (DM). Here, we used a streptozotocin-induced rat DM model to investigate the effects of long non-coding RNA H19 (lncRNA H19) on learning and memory and apoptosis of hippocampal neurons, and the involvement of the Wnt signaling. Our data demonstrate that lncRNA H19 is highly expressed in rats with DM. Over-expression of lncRNA H19 increased positioning navigation latency in DM rats and decreased duration of space exploration. lncRNA H19 over-expression also increased hippocampal neuronal apoptosis and expression of Wnt3, ß-catenin, TCF-1, Bax, caspase-8 and caspase-3. By contrast, expression of GSK-3ß and Bcl-2 was suppressed in DM rats over-expressing lncRNA H19. These results suggest that lncRNA H19 induces hippocampal neuronal apoptosis via Wnt signaling, and that inhibition of lncRNA H19 may serve as a promising novel target for the treatment of cognitive decline in patients with DM.

Suppression of Basic Fibroblast Growth Factor Expression by Antisense Oligonucleotides Inhibits Neural Stem Cell Proliferation and Differentiation in Rat models With Focal Cerebral Infarction.

This study is designed to investigate the role of basic fibroblast growth factor (bFGF) antisense oligonucleotide (ASODN) on the proliferation and differentiation of neural stem cells (NSCs) in rat models with focal cerebral infarction (CI). Seventy-five Sprague-Dawlay (SD) rats were randomly divided into the control, sham, middle cerebral artery occlusion (MCAO), MCAO + nonsense oligonucleotide (NODN), and MCAO + ASODN groups. Proliferation and differentiation of NSCs were detected by bromodeoxyuridine (BrdU) and immunofluorescence staining, respectively. ELISA was performed to detect the expressions of endogenous factors that include insulin-like growth factor 1 (IGF-1), glial cell line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), transforming growth factor-α1 (TGF-α1), bFGF, and nerve growth factor (NGF). Results show significant neurological deficits and focal CI in the MCAO and MCAO + NODN groups. An obvious increase of NSC proliferation, reactive proliferation of astrocytes in CI areas, differentiation of newly proliferated NSCs into mature neuronal cells, and expressions of endogenous growth factors exhibited in the MCAO, MCAO + NODN and MCAO + ASODN groups. Compared to the MCAO and MACO + NODN groups, the MCAO + ASODN group showed a significant decrease NSC proliferation and differentiation in CI areas as well as decrease expressions of endogenous growth factors. These findings may offer insight to help us understand more as to how bFGF ASODN can effectively suppress the proliferation and differentiation of NSCs. These findings are expected to help contribute to research for new targets in the treatment of focal CI. J. Cell. Biochem. 118: 3875-3882, 2017. © 2017 Wiley Periodicals, Inc.

Effects of the TLR4 signaling pathway on apoptosis of neuronal cells in diabetes mellitus complicated with cerebral infarction in a rat model.

This study aims to explore the effects of the TLR4 signaling pathway on the apoptosis of neuronal cells in rats with diabetes mellitus complicated with cerebral infarction (DMCI). A DMCI model was established with 40 Sprague Dawley rats, which were assigned into blank, sham, DM + middle cerebral artery occlusion (MCAO) and DM + MCAO + TAK242 groups. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. A TUNEL assay was applied for detecting cell apoptosis, and Western blotting was used for detecting the expression of TLR4, TNF-α, IL-1ß and apoptosis-related proteins. Compared with the blank and sham groups, there was an increase in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1ß and TLR4 proteins and MDA content and a decrease in SOD activity in the DM + MCAO and DM + MCAO + TAK242 groups. Compared with those in the DM + MCAO group, rats in the DM + MCAO + TAK242 group exhibited an increase in SOD activity and a decrease in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1ß and TLR4 proteins and MDA content. Inhibition of the TLR4 signaling pathway reduces neuronal cell apoptosis and nerve injury to protect the brain.

Overexpression of lncRNA ANRIL up-regulates VEGF expression and promotes angiogenesis of diabetes mellitus combined with cerebral infarction by activating NF-κB signaling pathway in a rat model.

OBJECTIVE: This study aimed to explore the effects of lncRNA ANRIL on vascular endothelial growth factor (VEGF) and angiogenesis in diabetes mellitus (DM) combined with cerebral infarction (CI) through NF-κB signaling pathway. METHODS: Adult male Wistar rats were randomly divided into control group and DM + CI group, and the DM + CI group were subdivided into Vector, shANRIL, PDTC, pcDNA-ANRIL, and pcDNA-ANRIL + PDTC groups. VEGF and FMS-like tyrosine kinase (FLT-1) expressions were measured by immunohistochemistry and endothelium dependent microvessel density (MVD) was detected by differentiation 31 (CD31) and para-amiuosalicylic acid (PAS) double staining. The qRT-PCR was applied to measure mRNA expressions of VEGF, FLT-1, Kinase insert domain protein receptor (FLK-1) and NF-κB, and Western blotting was conducted to detected expressions of VEGF, NF-κB and p-IκB/IκB. RESULTS: Compared with the control group, protein expressions of VEGF, NF-κB, p-IκB/IκB, expression of ANRIL, and mRNA expressions of VEGF, FLT-1 and NF-κB were increased in the DM + CI group. Compared with the Vector group, protein expressions of VEGF, NF-κB, p-IκB/IκB, expression of ANRIL, mRNA expressions of VEGF, FLT-1 and NF-κB, and endothelium dependent MVD were increased in the pcDNA-ANRIL group, while decreased in the shANRIL group and PDTC group. Compared with the pcDNA-ANRIL group, protein expressions of VEGF, NF-κB, p-IκB/IκB, expression of ANRIL, mRNA expressions of VEGF, FLT-1 and NF-κB, and endothelium dependent MVD were decreased in the pcDNA-ANRIL + PDTC group. CONCLUSION: Overexpressed lncRNA ANRIL upregulates VEGF and promotes angiogenesis by activating NF-κB signaling pathway in DM + CI rats. .

Application of the chick embryo chorioallantoic membrane in neurosurgery disease.

The chick embryo chorioallantoic membrane (CAM) is a highly vascularized extraembryonic membrane. Because of its ease of accessibility, extensive vascularization and immunodeficient environment, the CAM has been broadly used in the oncology, biology, pharmacy, and tissue regeneration research. The present review summarizes the application of the CAM in neurosurgery disease research. We focused on the use of the CAM as an assay for the research of glioma, vascular anomalies, Moyamoya Disease, and the blood-brain barrier.

Research progress on vertebrobasilar dolichoectasia.

Vertebrobasilar dolichoectasia (VBD) is a rare disease characterized by significant expansion, elongation, and tortuosity of the vertebrobasilar arteries. Current data regarding VBD are very limited. Here we systematically review VBD incidence, etiology, characteristics, clinical manifestations, treatment strategies, and prognosis. The exact incidence rate of VBD remains unclear, but is estimated to be 1.3% of the population. The occurrence of VBD is thought to be due to the cooperation of multiple factors, including congenital factors, infections and immune status, and degenerative diseases. The VBD clinical manifestations are complex with ischemic stroke as the most common, followed by progressive compression of cranial nerves and the brain stem, cerebral hemorrhage, and hydrocephalus. Treatment of VBD remains difficult. Currently, there are no precise and effective treatments, and available treatments mainly target the complications of VBD. With the development of stent technology, however, it may become an effective treatment for VBD.

Apoptosis-inducing effect of tetrandrine and imatinib on K562/G01 cells and its related mechanism / 中国实验血液学杂志

This study was purposed to explore the apoptosis-inducing effect of tetrandrine (Tet) and imatinib (IM) alone or both combined on K562/G01 cells and their mechanism. MTT assay was used to detect the inhibitory effect of drugs on cell growth, flow cytometry was used to detect the cell cycle and apoptosis rate. The expression of caspase-3/BCL-2 mRNA was determined by real time-PCR, and the expression of caspase-3/BCL-2 protein was assayed by Western blot. The results showed that after being treated by 1.0 µmol/L IM or 1.5 µmol/L Tet alone and combination of these two drugs for 48 h, the inhibitory rate was (22.74 ± 0.05)%, (20.34 ± 0.57)% and (44.28 ± 0.60)%, respectively, suggesting that inhibitory effect of two drug combination was more obvious. The arrest of cell cycle at G1/S phase could be observed after Tet treatment. Early apoptosis rate was (7.81 ± 0.16) %, (14.10 ± 0.28) % respectively after being treated by combination of 1.5 µmol/L and 3.0 µmol/L Tet with 1.0 µmol/L IM. After being treated with Tet alone, FQ-PCR and Western blot showed that the expressions of caspase-3 mRNA and caspase-3 protein were up-regulated, the expressions of BCL-2 mRNA and protein were down-regulated, the effect of both drug combination was more significant. It is concluded that IM or Tet alone can induce apoptosis of K562/G01. Combination of IM with Tet shows obvious synergistic effect, mechanism of which may associate with up-regulation of caspase-3 mRNA and protein expressions, and down-regulation of BCL-2 mRNA and protein expressions.

[Experimental investigation of the chemical effect of direct current arc plasma igniter].

To study the chemical effect of direct current arc plasma igniter, the emission spectrum of plasma jet was measured, and the active particles produced by the interaction of plasma jet with atmospheric air were analyzed. The NO and CO volume fractions were measured quantificationally by smoke analyzer at the 8cm downstream the plasma igniter exit, and the changing law between arc current and NO, CO volume fractions was obtained. The results show that the plasma jet interacting with atmospheric air produced active particles (H, O, N), charged particles (O2 +, N2+), and excited particles (N2 (A3), N2 (B3), N2 (C3), N2 (a1), O2 (a1), O2 (b1)). The NO and CO volume fractions increased with rising of are current and feedstock argon flow rate.

Triptolide inhibits proliferation and induces apoptosis of imatinib resistant K562/G01 cells / 中国实验血液学杂志

This study was aimed to explore the inhibitory effect of triptolide on proliferation and inducing apoptosis effect of K562/G01 cells and their possible mechanism. MTT assay was used to detect the effect of imatinib or triptolide alone and their combination on K562/G01 proliferation; the cell cycle, apoptosis rate, P-gp protein expression were detected by flow cytometry (FCM); the expression of P-gp was assessed by Western blot; the BCR/ABL gene expression was assayed by real time quantitative PCR. The results showed that triptolide could enhance the effect of imatinib on proliferation inhibition and apoptosis of K562/G01, arrested the cell cycle in G1 phase, down-regulated the expression of BCR/ABL gene and P-gp protein. It is concluded that triptolide induces K562/G01 cell proliferation inhibition and apoptosis, the mechanism may be related to cell cycle arrest, decrease of P-gp protein expression, inhibition of BCR/ABL gene expression.

Endovascular treatment of an intracranial aneurysm with a ruptured bleb.

OBJECTIVE: To study the features and approaches of endovascular treatment for intracranial aneurysms with a ruptured bleb. METHODS: This retrospective study was carried out from June 2007 to June 2009 in Jilin University, Jilin, China. Thirty patients with intracranial aneurysms with ruptured blebs were included. The aneurysms were diagnosed by digital subtraction angiography (DSA), and the endovascular treatment was planned according to the relationship between the aneurysm body and the ruptured bleb. The aneurysms were classified into 4 types (type I, II, III, IV) based on the size of the neck of the aneurysm connected with the parent artery, the size of the body of the aneurysm, and the size of the junction formed between the aneurysm and bleb. Endovascular treatment for each type of aneurysm was performed. RESULTS: Type IV aneurysms were the most difficult operation performed, easily resulting in rupture and bleeding during surgery, whereas embolization of a type III aneurysm was relatively simple. Type I and II aneurysms resulted in better prognosis. Statistical analysis showed that the outcome of the treatment of type I and II aneurysms was better than that in type III and IV aneurysms, the outcome of type I, II, and III was better than that in type IV. CONCLUSION: The outcome of the endovascular treatment of an intracranial aneurysm with a ruptured bleb was related to the aneurysm type. Treatment in a type-dependent manner is therefore recommended.

Inhibitory effect of histone deacetylase inhibitor LBH589 on multiple myeloma MM1R cells in vitro / 中国实验血液学杂志

This study was purposed to explore the effect of a new generation of histone deacetylase inhibitor LBH589 alone or combined with bortezomib (Bor) on multiple myeloma cells (MM1R) in vitro. The effect of LBH589 (10, 20, 50 nmol/L) alone or combined with Bor (10, 20 nmol/L) on MM1R proliferation was detected by MTT method; the effect of LBH589 on cell cycle and apoptosis of MM1R cells were determined by flow cytometry; the histone H4 acetylation level of MM1R cells treated with LBH589 (10, 20, 50 nmol/L) for 24 h was analyzed by Western blot. The results showed that the LBH589 alone or combined with Bor all could inhibit the proliferation of MM1R cells in a concentration- and time-dependent manner. After MM1R cells were treated with drugs for 48 h, the cells in G(0)/G(1) phase increased, the cells in G(2)/M and S phase decreased, suggesting the arrest of cells in G(0)/G(1) phase, at the same time, the apoptosis rate of MM1R cells treated with drugs increased in a concentration-dependent manner, while the effect of LBH589 combined with Bor was more obvious than that of LBH589 alone (P < 0.001). Western blot analysis showed that the histone H4 acetylation level was enhanced in concentration-dependent manner after MM1R cells were treated with different concentrations of LBH589 for 24 h. It is concluded that the LBH589 can inhibit the proliferation of MM1R cells, block the cell cycle, induce cell apoptosis, moreover LBH589 combined with Bor has synergistic effect on MM1R cells.