Protein Z (PZ) is a vitamin K-dependent protein. As a cofactor for the protein Z-dependent protease inhibitor (ZPI), it inhibits coagulation factor X under the existence of phospholipid and calcium ion, and increases the ZPI activity by nearly 1000-fold, thus it plays a role in the process of thrombosis. ZPI inhibits coagulation factor Ⅺ a alone. ZPI activity is also consumed in the process of inhabiting factor Ⅹa and Ⅺa. This article reviews the biological characteristics of PZ and ZPI and their association with stroke.

To explore the characteristics and treatment of temporal bone fractures and its complications, clinical data of 48 cases of temporal bone fracture admitted to our hospital from January 1989 to November 1999 were retrospectively analyzed. The results showed that in these 48 patients temporal bone fracture caused by traffic accidents accounted for 66 67%. Forty three cases survived (89 58%) and 5 died (10 41%). Middle inner ear or craniocerebral injury held 77 08% and hearing loss or tinitus held 48%; The incidences of CSF otorrhea and facioplegia were 36 7% and 3%, respectively for the longitudinal fracture, while for the transversal fracture they were 25% and 37 5%, respectively. Our conclusions are: (1) Traffic injury is the most dangerous factor of temporal bone fracture; (2) The dangerous complication is injury to cranium and brain, or multiple organs, resulting in death; (3) Middle inner ear injury is the commonest complication in temporal bone fracture; (4) CSF otorrhea is common in the longitudinal fracture and facioplegia is common in the transversal fracture.

Objective To elucidate the clinical, electrophysiological, neuropathological features of two cases of hereditary neuropathy with liability to pressure palsies (HNPP) in one pedigree, and to review the literature of HNPP, so as to promote the understanding and diagnostic acuity of the disease. Methods Detailed electromyogram, motor and sensory conduction velocity, and distal motor latency were measured for clinically affected and unaffected nerves in the two patients. Sural nerve biopsy was performed for case one and the specimen was observed under light microscope and elcctronmicroscope. The cases reported in China up to the present were collected. Results Case one was an 18 year old male with a 9 year history of recurrent weakness and numbness of limbs precipitated by compression or stretch. Case two was his father. Although he had not experienced clinical episode of limb weakness and numbness, physiological examination revealed signs of peripheral neuropathy. Eletrophysiological study demonstrated diffuse peripheral nerve damage with decreased nerve conduction velocity, delayed distal motor latency, especially a decrease in motor conduction velocity at common entrapment sites, including clinical unaffected nerves. Sural nerve biopsy showed that myelin sheath of most myelinated fibers with normal axons was thickened. Some thickened myelin sheath was seen to invaginate into the axon. No onion bulb was found and unmyelinated fibers were relatively normal. Only 9 cases of HNPP were reported in China, but no DNA analysis was performed for any of them. Conclusions HNPP is a rare disease with autosomal dominant inheritance. Nerve conduction study is an important diagnostic method for screening. Its definite diagnosis relies on the typical pathological findings in nerve biopsy specimen. Sural nerve biopsy could be avoided for diagnosis if the family history were positive and nerve conduction study should show diffuse peripheral nerve damage

Objective To investigate the relationship betw een the serum bilirubin level and the severity of disease and short-term outcome in patient w ith acute ischemic stroke. Methods A total of 120 consecutive inpatients w ith acute ischemic stroke w ere enroled and 105 healthy subjects at the same time w ere used as a control group. The biochemical indicators, such as serum total bilirubin, direct bilirubin, indirect bilirubin, blood lipid, and blood glucose w ere measured w ithin 24 h after admission. The National Institutes of Health Stroke Scale ( NIHSS ) w as used to assess the neurological deficits on the day of admission. The NIHSS score <8 w as defined as mild stroke and ≥8 w as defined as moderate to severe stroke. At discharge or 14 d after onset, the modified Rankin Scale (mRS) w as used to evaluate the clinical outcomes, 0-2 w as defined as good outcome and > 2 w as defined as poor outcome. The levels of serum total bilirubin, direct bilirubin, and indirect bilirubin w ere measured again. Results The levels of serum total bilirubin, direct bilirubin, and indirect bilirubin in the moderate to severe stroke group w ere significantly higher than those in the mild stroke group ( P <0.01) and the control group ( P <0.01). Multivariate logistic regression analysis show ed that the increased levels of serum total bilirubin (odds ratio [OR] 1.855,95%confidence interval [CI] 1.390-2.475; P <0.01), indirect bilirubin ( OR 3.380, 95%CI 1.271-11.901; P <0.05), and direct bilirubin ( OR 3.51, 95%CI 1.062-11.473; P <0.01) had significantly independent correlation w ith baseline disease severity. Univariate analysis show ed that the increased serum total bilirubin level on admission w as associated w ith the short-term poor outcome ( P <0.05), but after adjustment for other confounding factors, there w as no statistical significance ( OR 2.411, 95%CI 0.803-7.243, P >0.05). Conclusions The serum bilirubin level show ed stress increase in patients w ith cerebral infarction in acute phase; and it w as significantly associated w ith the degree of neurological deficit, but it w as not associated w ith short-term outcome. It might be a defense response to the body for stroke events.

OBJECTIVETo investigate the effect of quercetin on apoptosis and feedback regulation of MDM2-p53 in multiform glioblastoma U87 cells in vitro.

METHODSU87 cells exposed to different concentrations of quercetin (50, 100, and 150 µmol/L) were examined with flow cytometry, RT-PCR and Western blotting for detecting the cell apoptosis, MDM2 mRNA expression, and p53 and caspase-3 expressions.

RESULTSQuercetin induced obvious apoptosis in U87 cells in a concentration-dependent manner, with apoptosis rates of (12.40∓0.70)% at Q0, (22.53∓0.72)% at Q50, (29.06∓0.81)% at Q100, and (31.5∓0.45)% at Q150. Quercetin significantly increased the expressions of MDM2 mRNA and active caspase-3 protein but decreased the expression of p53 in the cells.

CONCLUSIONQuercetin promotes the apoptosis of multiform glioblastoma U87 cells mediated by caspase-3 and influences the feedback balance of MDM2-p53.

Apoptosis ; Caspase 3 ; metabolism ; Cell Line, Tumor ; drug effects ; Glioma ; metabolism ; pathology ; Humans ; Proto-Oncogene Proteins c-mdm2 ; metabolism ; Quercetin ; pharmacology ; Tumor Suppressor Protein p53 ; metabolism

Background:Circular RNAs(circRNAs)are covalently closed single-stranded RNAs with multiple biological functions.CircRNA.0007127 is derived from the carbon catabolite repression 4-negative on TATA-less(CCR4-NOT)complex subunit 2(CNOT2),which was found to regulate tumor cell apoptosis through caspase pathway.Methods:Potential circRNA.0007127 target microRNAs(miRNAs)were analyzed by miRanda,TargetScan,and RNAhybrid software,and the miRNAs with binding sites for apoptosis-related genes were screened.The roles of circRNA.0007127 and its downstream target,microRNA(miR)-513a-5p,were validated by quantitative real-time polymerase chain reaction(qPCR),flow cytometry,mitochondrial membrane potential,immunofluorescence,western blot,and caspase-8(CASP8)protein activity in vitro in H2O2-induced K-562 cells.The circRNA.0007127-miR-513a-5p and CASP8-miR-513a-5p interactions were verified by luciferase reporter assays.Results:Silencing circRNA.0007127 decreased cell apoptosis by inhibiting CASP8 pathway activation in K-562 cells.Compared with the control group,the expression of CASP8 was reduced by 50％and the 43-kD fragment of CASP8 protein was significantly reduced(P≤0.05).The luciferase reporting assay showed that circRNA.0007127 combined with miR-513a-5p or CASP8,with extremely significant differences(P≤0.001).The overexpression of miR-513a-5p inhibited the gene expression level of CASP8 in a human myeloid leukemia cell model(75％change)and the level of a 43-kD fragment of CASP8 protein(P≤0.01).The rescue experiment showed that cotransfection with circRNA.0007127 small-interfering RNA(siRNA)and the miR-513a-5p inhibitor increased CASP8 gene expression and the apoptosis rate,suggesting that the miR-513a-5p inhibitor is a circRNA.0007127 siRNA antagonist.Conclusions:CircRNA.0007127 regulates K-562 cell apoptosis through the miR-513a-5p/CASP8 axis,which can serve as a novel powerful molecular target for K-562 cells.

OBJECTIVETo investigate the influence of exposure to different concentrations of ethanol on neural progenitor cells and the differentiation of neurons and glial cells in zebrafish embryos.

METHODSZebrafish embryos were exposed to 1%, 2%, and 2.5% (V/V) ethanol at 5 hpf by adding ethanol to the egg water. In situ hybridization and real-time PCR were used to detect the changes in the mRNA expression profiles of the markers of different cells to examine the effects of alcohol on neural development.

RESULTSThe number of neural precursor cells, neurons and mature glial cells was significantly reduced in the zebrafish embryos following ethanol exposure, and this reduction became more prominent as the ethanol concentration increased. The expression of the early glial marker slc1a3a was down-regulated in the spinal cord but increased in the brain after exposure to increased ethanol concentrations. The expression of the mature glial markers was significantly lowered in response to exposure to increasing ethanol concentrations.

CONCLUSIONSEthanol can reduce neural precursor cells and inhibits neuronal and glial differentiation in zebrafish embryos.

Animals ; Brain ; Cell Differentiation ; drug effects ; Embryo, Nonmammalian ; drug effects ; Ethanol ; adverse effects ; Neural Stem Cells ; drug effects ; Neurogenesis ; drug effects ; Neuroglia ; drug effects ; Neurons ; drug effects ; Spinal Cord ; Zebrafish ; embryology

Background: Blackened intestines in slaughtered pigs have been commonly observed in China in recent years. However, no cause has been reported. Objectives: We attempted to determine whether the blackening of the pig intestine was related to an excess of copper (Cu) in their feed. Methods: In this study, we observed and collected porcine intestines in small- and large-scale pig slaughterhouses in Shandong province from May to October 2018. Twelve types of metal ions were detected in the black intestinal samples. Results: The Cu level in the intestine samples was mostly higher than the Chinese national limit for food. Further study showed that Cu supplementation in most commercial porcine feed also exceeded the national standard. An animal model (mouse) that could mimic the intestinal blackening in pigs was established. Compared to control mice, Cu accumulated in the liver and intestines of mice fed an excessive Cu level, confirming the excessive Cu in the feed may be considered the major cause of blackened porcine intestines. Microscopic examination revealed that black intestines had many particles containing Cu in the lamina propria of the intestinal mucosa, and the intestinal mucosal epithelial cells showed degeneration and necrosis. Conclusions In conclusion, overuse of Cu in animal feed can lead to animal poisoning and Cu accumulation in animal products. Such overuse not only harms the health of livestock but can also affect public health.

Background: Blackened intestines in slaughtered pigs have been commonly observed in China in recent years. However, no cause has been reported. Objectives: We attempted to determine whether the blackening of the pig intestine was related to an excess of copper (Cu) in their feed. Methods: In this study, we observed and collected porcine intestines in small- and large-scale pig slaughterhouses in Shandong province from May to October 2018. Twelve types of metal ions were detected in the black intestinal samples. Results: The Cu level in the intestine samples was mostly higher than the Chinese national limit for food. Further study showed that Cu supplementation in most commercial porcine feed also exceeded the national standard. An animal model (mouse) that could mimic the intestinal blackening in pigs was established. Compared to control mice, Cu accumulated in the liver and intestines of mice fed an excessive Cu level, confirming the excessive Cu in the feed may be considered the major cause of blackened porcine intestines. Microscopic examination revealed that black intestines had many particles containing Cu in the lamina propria of the intestinal mucosa, and the intestinal mucosal epithelial cells showed degeneration and necrosis. Conclusions In conclusion, overuse of Cu in animal feed can lead to animal poisoning and Cu accumulation in animal products. Such overuse not only harms the health of livestock but can also affect public health.

Objective To investigate the correlations of serum cystatin C level with severity of stroke and short-term outcome in patients with acute ischemic stroke.Methods Patients with first-ever acute ischemic stroke aged ≥50 years who did not receive thrombolysis and took a visit within 3 d after onset were selected prospectively.The serum cystatin C level was detected within 24 h after admission and various clinical data were collected.The National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological deficits on the day of admission.The NIHSS score ＜8 was defined as mild stroke and ≥8 was defined as moderate to severe stroke.The modified Rankin Scale (mRS) was used to evaluate the short-term outcome at discharge or 14 d after onset,0-2 was defined as good outcome and ＞2 was defined as poor outcome.Results A total of 188 patients were enrolled,including 93 (49.5％) females and 95 (50.5％) males,their mean age was 65.4 ±9.2 years old (range 50-87).There were 120 patients with mild stroke (63.8％),68 with moderate to severe stroke (36.2％);106 patients (56.4％) had good outcome and 82 (43.6％) had poor outcome.Univariate analysis showed that serum cystatin C level in the moderate to severe stroke group was significantly higher than that in the mild stroke group (1.36 ± 0.29 mg/L vs.1.21 ±0.23 mg/L;t =3.902,P ＜ 0.001),the serum cystatin C level in the poor outcome group was significantly higher than that in the good outcome group (1.38 ± 0.25 mg/L vs.1.22 ± 0.25 mg/L;t =4.101,P =0.001).Multivariate logistic regression analysis showed that the serum cystatin C level was an independent risk factor for stroke severity (odds ratio 12.182,95％ confidence interval 11.163-13.202;P ＜ 0.001) and short-term poor outcome (odds ratio 9.025,95 ％ confidence interval 8.202-9.848;P ＜ 0.001).Conclusion The serum cystatin C level is significantly correlated with the severity of stroke and the short-term outcome in patients with acute ischemic stroke.