Fetal-type posterior cerebral artery is a common embryonic derivation type of the Willis.This article reviews the definition and typing of the fetal-type posterior cerebral artery,and its relationship with collateral circulation,ischemic stroke,and intracranial aneurysm,etc.

ObjectiveTo investigate the associations of fetal-type posterior cerebral artery (FTP) with infarction distribution and stroke severity in patients with acute ischemic stroke.MethodsThe patients with acute ischemic stroke were enrolled.They were divided into either a FTP group or a non-FTP group according to the results of magnetic resonance imaging.The former group was further divided into complete FTP (cFTP) and partial FTP (pFTP).According to the results of diffusion-weighted imaging, the infarction distribution was divided into the territory of the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA), and vertebrobasilar artery.According to the National Institutes of Health Stroke Scale (NIHSS), the stroke severity was assessed, <8 was defined as mild stroke, and ≥8 was defined as moderate to severe stroke.Multivariate logistic regression analysis was used to determine the associations of FTP with infarction distribution and stroke severity.ResultsA total of 647 patients with acute ischemic stroke were enrolled, and 201 (31.1%) had FTP, including 162 (25.0%) cFTP and 39 (6.0%) pFTP.Multivariate logistic regression analysis showed that cFTP and pFTP were the independent risk factors for MCA infarction (cFTP: odds ratio [OR] 24.714, 95% confidence interval [CI] 10.952-45.766, P<0.001;pFTP: OR 14.526, 95% CI 6.832-25.931, P<0.001), and the independent protective factors for PCA infarction (cFTP: OR 0.214, 95% CI 0.022-0.531, P<0.001;pFTP: OR 0.326, 95% CI 0.018-0.739, P<0.001), they were also the independent risk factor for the severity of acute ischemic stroke (cFTP: OR 22.138, 95% CI 12.492-64.067, P<0.001;cFTP: OR 19.510, 95% CI 8.956-23.514, P<0.001).ConclusionscFTP and pFTP are the independent risk factors for MCA infarction, and the independent protective factors for PCA infarction, and at the same time, they were also the independent risk factors for the moderate to severe stroke.FTP is associated with the infarction distribution and the stroke severity in acute ischemic stroke.

Objective To evaluate the clinical outcomes of external fixator with lumbopelvic distraction spondylodesis in treatment of vertically unstable pelvic fractures. Methods From January 2008 to March 2009, 9 patients (4 males and 5 females) with a vertically unstable pelvic fracture were treated with modular external fixator with lumbopelvic distraction spondylodesis. According to the classification of Tile, 9fractures were classified as type C. This fixation construct comprises a vertical lumbopelvic distraction component which fixed L4.5 and the posterior superior iliac spine and a transverse fixation which fixed anterior iliac spine with external fixator. Results All patients were followed up 12-18 months after surgery, with an average of 14.3 months. Postoperative X-ray showed satisfactory reduction of pelvic fracture. Pelvic fractures healed in all patients without loss of reduction 3-6 months after operation. According to Matta reduction evaluation criteria, 6 patients were excellent and 3 good. For the two patients with sacral neurological injuries,appropriate surgical decompression was performed to improve the symptom and minimize the deformity. No iatrogenic complications of neurovascular injury occurred. Patients now walk unassistedly without pain in the waist or legs, and with no shortening of lower limbs or claudication. By considering symptom and satisfactory scores, the Majeed functional assessment revealed that seven patients had excellent results and two good at one year. Conclusion External fixator with lumbopelvic distraction spondylodesis that allowed early mobilization and ambulation, with general applicability and definite safety, is an effective surgical technique for the treatment of vertically unstable pelvic fracture.

Nerve agent not only inhibit acetylcholinesterase ( AChE) at an early stage, but also induce prolonged and progressive neuroinflammation and delayed neurodegeneration.Recently, the US National Institute of Health ( NIH) has sponsored some major programs of toxic mechanisms and treatment of nerve agents, which aims at the development of quick and effective treatment to acute intoxication and delayed effect.The experimentally effective new antidotes mainly include AChE-targeting drugs, broad-spectrum reactivators and scavengers, antiinflamatory and nerve protection drugs.

Background and purpose:Previous studies have suggested Na+-Ca2+ exchanger isoform 1 (NCX1) as a key component of calcium homeostasis was involved in the tumorigenesis. However, the role of NCX1 and calcium signal in tumorigenesis of hepatocellular carcinoma (HCC) has not been explored. This study aimed to investigate the effect of NCX1 on cell proliferation and migration of HCC HepG2 cells in vitro and the possible mechanism.Methods:Both the real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot were applied to assess the expression of NCX1 mRNA and protein in normal hepatic cells (LO2), HCC cell line (HepG2), human normal hepatic tissues and hepatocellular carcinoma tissues. The change of intracellular calcium signal in LO2 and HepG2 cells via acti-vated NCX1 channel in the presence or absence of Na+ was examined by a confocal laser scanning microscope. The effects of NCX1 special inhibitor KB-R7943 on cell proliferation and migration of HepG2 cells were measured by MTT and cellscratch test.Results:Both mRNA and protein expression of NCX1 were higher in HCC tissues and cell line HepG2 than in the normal tissues and cell line LO2 (P<0.05). The activation of NCX1 channel induced a slight rise in cytoplasmic Ca2+concentration ([Ca2+]cyt) in normal cells, but caused a marked increase in cancer cells. And the NCX1 activation induced intracellular calcium increase was significantly reversed by NCX1 inhibitor KB-R7943 (P<0.05). Both NCX1-mediated proliferation and migration of HepG2 were also significantly attenuated by the KB-R7943 (P<0.05).Conclusion:NCX1 is up-regulated in HCC cells and tissues. The activation of NCX1 mediates intracellular calcium homeostasis. The inhibition of NCX1 activity can suppress the proliferation and migration of HepG2 cells. It is suggested that NCX1 may be involved in the development and progression of HCC.

Objective To investigate the effect and mechanism of cell differentiation agent Ⅱ (CDA-Ⅱ) on the differentiation of human acute mycloid leukemia (APL) HL-60 cells.Methods The cell morphology and differentiation was detected by Wright-Giemsa staining,the expression of cell surface differentiation antigen CD11b of HL-60 was detected by flow cytometry,the differentially expressed genes were screened by gene expression profile chip (NimbleGen).Results The result of Wright-Giemsa staining showed that CDA-Ⅱ induced HL-60 differentiation towards mature stages in a time-dependent manner.After treated with CDA-Ⅱ,the percentage of CD11b-positive HL-60 cells significantly increased in a time-and dose-dependent manner.The result of gene expression profiling indicated differentially expressed genes including 113 up-regulation genes and 140 down-regulation genes.The up-regulation expression genes involved in six pathways including mineral absorption,complement and coagulation cascades,down-regulation expression genes involved in nine pathways including pyrimidine metabolism,RNA polymerase,purine metabolism and so on.Conclusion CDA-Ⅱ can induce HL-60 differentiation and make gene differentially expressed.The data provide the feasibility of CDA-Ⅱ in differentiation induction therapy for APL.

Objective To analyze the differential expression of D2 and D3 alternative splicing sites of human kinectin in human hepatocellular carcinoma (HCC) tissues, adjacent non-cancerous tissues and normal liver tissues, and to investigate a possible relationship between alternative splicing sites of kinectin and hepatocarcinogenesis. Methods The cDNA was obtained by RT-PCR in 45 coupled HCC cancerous and adjacent tissues, and 10 normal liver tissues. The difference in the expression of D2 and D3 alternative splicing sites in cDNA was examined by semi-quantitative PCR, and statistical analysis was performed. Results The ratio of D2L (long segment contains of the D2 region)/D2S (short segment that does not contain a D2 zone) in hepatocellular cancerous tissues was 2.709 ± 1.025, the ratio of D2L/D2S in adjacent non-cancerous tissues was 1.564 ± 0.357, and the ratio of D2L/D2S in normal liver tissues was 1.507 ± 0.499. The differences were statistically significant (F=29.698, P<0.05);the ratio of D2L/D2S in hepatocellular cancerous tissues was higher than that of adjacent non-cancerous tissues and normal liver tissues (P<0.05). The ratio of D3L (long segment contains of the D3 region)/D3S (short segment that does not contain a D3 zone) in hepatocellular cancerous tissues was 1.232 ± 0.041, the ratio of D3L/D3S in adjacent non-cancerous tissues was 1.156 ± 0.309, and the ratio of D3L/D3S in normal liver tissues was 1.282 ± 0.343. The ratio of D3L/D3S was not significantly different among hepatocellular cancerous tissues, adjacent non-cancerous tissues and normal liver tissues (F = 0.989, P > 0.05). Conclusion Variant containing D2 is over expressed in cancerous tissues and this alteration may be tumor associated.

Objective To study the clinical, laboratorial, histopathological, imaging features of two cases of hypothyroid myopathy. Method Clinical manifestations, thyroid function, electromyography, muscle MRI, muscle biopsy and follow-up results were collected, and analyzed with the literature. Result These two patients were middle-age to old age and the onset of disease was insidious. Their common clinical manifestations included subacute progressive weakness in the proximal muscles,myalgia after sports and reduction in tendon reflex.The blood test showed an increase in serum concentration of CK and TSH, and a decrease in FT3 and FT4. The electromyography showed suspicious myogenic damage.Muscle histopathological findings were largely nonspecific,such as type I fiber predominance and type 2 atrophy. The MRI revealed extensive muscular dystrophy and fatty filtration in the posterior group of thighs. Treatment of replacement therapy with L-T4 relieved the myopathic symptoms quickly. Conclusion When a patient presents with a subacute progressive weakness in the proximal muscles, the hypothyroidism should be consideration. Muscle histopathological findings may be nonspecific. The muscle MRI have a value of differential diagnosis and lesion assessment.

Radiotherapy combined with immunotherapy for the treatment of cancer can induce stronger abscopal effect (AE) and inhibit the growth of tumors outside of radiation field, but the occurrence of AE is distinctly uncommon and unpredictable in clinical practice. The complex molecular mechanism underlying AE remains to be in-depth understood. It has been reported that some new factors are involved in the regulation of AE induced by radiation, but the molecular mechanism has not been fully unravelled. In this article, the roles of macrophages, tumor draining lymph node, p53 and exosomes in the new mechanisms of AE were reviewed, aiming to provide a theoretical basis for the development of more effective cancer therapeutics.