[Clinical analysis of 10 patients of chronic subdural hematoma associated with arachnoid cyst].

Objective: To investigate the clinical characteristics, pathogenesis and surgical strategy for the chronic subdural hematoma associated with arachnoid cyst (AC). Method: Ten patients of chronic subdural hematoma associated with AC were retrospectively enrolled from the Neurosurgery Department of Tianjin Medical University General Hospital from January 2012 to September 2015, with a mean age of 27.5±5.6 years (range, 18-37 years). All patients simply performed a burr hole drainage of hematoma and left the AC intact, then followed up for 12 to 18 months after discharge respectively. Results: In this study, the AC in 8 of 10 cases occurs in the middle cranial fossa, and the other 2 cases root in the cerebral hemisphere.The AC of 10 patients all locate near the hematoma cavity.Nine patients had a full recovery, and only one patient had a recurrent subdural hematoma with a secondary operation, then recovery in 3 months postoperation.All patients lived completely free of neurological symptom and showed no recurrence in the follow-up period with a Barthel index more than 90. Conclusion: Simply burr hole drainage of hematoma and leave intact AC achieves satisfied outcome and provides a reliable therapy strategy for chronic subdural hematoma associated with arachnoid cyst.

[Application of hybrid operating room in the treatment of spinal dural arteriovenous fistulas].

Objective: To explore the experience in the treatment of spinal dural arteriovenous fistulas with application of hybrid operating room. Method: A retrospective analysis was performed among 22 patients with spinal dural arteriovenous fistulas admitted to Department of Neurosurgery of Tianjin Medical University General Hospital who received operation in the hybrid operating room from March 2011 to February 2016. Modified Aminoff-Logue scores (ALS) for myelopathy was used to evaluate the spinal function.All the 22 patients were followed up 6-12 months after the operation. Result: All the patients were diagnosed by spinal digital subtraction angiography (DSA). The modified ALS pre-operation and post-operation 6 months were (4.7±1.8) and (2.0±1.5), respectively, with significant difference (P<0.01). There were 15 cases with mild dysfunction, 6 cases with moderate dysfunction, severe dysfunction in 1 case before operation.Fifteen cases were cured, 4 cases improved, 1 case had no change after 6 months follow-up.The improvement rate was 95.45%. Conclusion: The application of hybrid operating room in the treatment of spinal dural arteriovenous fistulas achieves good outcome and provides a convenient and effective approach, which embodies the idea of precision medicine.

Predictive factors for in-stent restenosis after balloon-mounted stent placement for symptomatic intracranial atherosclerosis.

OBJECTIVES: We sought to evaluate whether clinical, lesion-related and procedural factors may predict in-stent restenosis (ISR) after intracranial stenting. METHODS: Sixty-one Chinese patients with 65 lesions treated with single bare metal balloon-mounted stent for symptomatic intracranial arterial stenosis underwent conventional angiographic follow-up after procedures between March 2004 and July 2009. Clinical, lesion-related and procedural factors were analysed for any predictive power for the ISR using univariate and multivariate analysis. ISR was defined as >50% stenosis within or at the edge of the stent or absolute luminal loss >20%. RESULTS: ISR was found in 18 patients (18/61, 29.5%) with 20 lesions (20/65, 30.8%) at a median follow-up of 7 months (range, 5-30 months). Univariate analysis revealed that diabetes, Mori classification, lesion length and stent diameter were associated with ISR. In addition, diabetes (hazard ratio (HR), 2.661; 95% confidence interval (CI), 1.044-6.787; P=0.040) and lesion length (HR, 1.206; 95% CI, 1.023-1.421; P=0.026) were detected as two independent predictors for ISR by stepwise multivariate Cox regression analysis. CONCLUSIONS: ISR after intracranial stenting with bare metal balloon-mounted stents in our series seems to be more frequent than those reported by the majority of the published case series. Diabetes and lesion length are associated with increased risk of ISR.

Human papillomavirus type 16 E7 peptide(38-61) linked with an immunoglobulin G fragment provides protective immunity in mice.

OBJECTIVE: To explore whether the recombinant protein (Human papillomavirus (HPV) type16 E7 peptide(38-61) linked with an immunoglobulin G fragment) will generate protective immunity in mouse model. METHODS: In our study, we combined the HPV16 E7 peptide(38-61) with a murine IgG heavy chain constant region to construct a chimeric protein compound, which was highly expressed as inclusion bodies in a bacterial expression system with Escherichia coli. The purified chimeric protein was injected into C57BL/6 mice and the efficiency of the chimeric vaccine candidate was evaluated by antibody response assay, T cell proliferation assay, CTL assay, tumor challenge assay and therapeutic experiment. RESULTS: The chimeric vaccine candidate was able to induce anti-HPV antibodies as well as to elicit HPV16 E7-specific CTLs and T cell proliferation in a pre-clinical mouse model. It was also able to effectively protect mice against the challenge of HPV16-positive tumor cells, and to eradicate HPV16-expressing tumors in mice. CONCLUSIONS: The chimeric protein vaccine can induce E7-specific immune responses and protect mice against challenge of HPV16-positive tumor, even eradicate developed tumor. The results indicated a possibility to use the chimeric protein vaccine to protect human against HPV infection.

Interleukin-1 promotes expression and phosphorylation of neurofilament and tau proteins in vivo.

Slow-release, IL-1-impregnated pellets implanted in rat cerebral cortex to simulate chronic overexpression of IL-1 significantly increased relative tissue levels of tau mRNA and of tau immunoreactivity in neuronal cell bodies and in swollen dystrophic neurites that also overexpressed phosphorylated and nonphosphorylated neurofilament epitopes. In addition, rats with IL-1-impregnated pellets, but not control rats or those with sham pellets, showed focal immunoreactivity for hyperphosphorylated tau epitopes present in paired helical filaments. Our results are consistent with an important driving role for IL-1 in the pathogenesis of Alzheimer-type neuronal and neuritic changes.

Increased interleukin-1beta converting enzyme expression and activity in Alzheimer disease.

Increased expression of interleukin-1 in Alzheimer disease (AD) has been implicated as a driving force in neurodegenerative cascades that underlie the formation of neuritic plaques and neurofibrillary tangles, the spread of these neuropathological lesions across cerebral cortical regions, and the accompanying neuronal cell injury and loss. The beta isoform of interleukin-1 is generated from an inactive, 33-kDa precursor through the action of a specific interleukin-1beta converting enzyme (ICE), also known as caspase-1. We used mesial temporal tissue (hippocampus and parahippocampal cortex) obtained postmortem from Alzheimer and control patients for determinations of endogenous tissue ICE activity and for Western immunoblot analysis of tissue ICE concentrations. ICE activity in Alzheimer tissue was elevated 50-100% (p < 0.002, or better, at incubation times of 30 min to 10 h), and ICE protein level was elevated 180% (p = 0.01). Parahippocampal cortex of Alzheimer patients showed increased numbers of neurons with in situ evidence of DNA damage. Increased DNA degradation was also evident upon electrophoresis of isolated DNA. Overexpression and increased activity of ICE may contribute to neurodegeneration in AD through generation of biologically active interleukin-1, with consequent activation of interleukin-1-driven neurodegenerative cascades.

[Porencephaly. A report of 45 cases].

In 45 cases of porencephaly 35 were male and 10 female. Their age ranged from 80 days to 58 years (mean 14 years). In this series, symptoms were observed 80 days to 22 years before diagnosis. twenty-four cases were premature delivery, difficult labour or birth trauma. 14 cases had a history of head injury. 36 cases had congenital porencephalic cyst and 9 had post-traumatic porencephaly. The main symptoms and signs of porencephaly were dementia, speech defect, intracranial hypertension, hydrocephalus, epilepsy, ataxia or paralysis. etc. It is suggested that CT scan is very useful in the diagnosis of porencephaly, and section of cerebral cortex, opening of cyst, continuous drainage or shunting operation should be done as soon as the diagnosis was made.

Preliminary crystallographic analysis of deshexapeptide (B25-B30) insulin.

Satisfactory single crystals of deshexapeptide (B25-B30) insulin for X-ray crystal structure analysis have been grown in citrate buffer by the method of hanging-drop gas phase diffusion. The crystal belongs to the monoclinic system with space group C2. The unit cell constants are a = 42.6 A, b = 37.9 A, c = 27.2 A, beta = 125.4 degrees and there is only one molecule of deshexapeptide insulin in an asymmetric unit.

Lamotrigine protects against kainate but not ibotenate lesions in rat striatum.

Pretreatment of rats with 8-16 mg/kg of lamotrigine 1 h before intrastriatal injections of 2 nm of kainic acid significantly attenuated the neurotoxicity as evidenced by measurements of striatal choline acetyltransferase and glutamate decarboxylase activities. No significant effect was seen on the toxicity of intrastriatal injections of quinolinic acid or ibotenic acid. These differential effects are further evidence that these neurotoxins act at different excitatory amino acid receptors and that the neurotoxicity of kainate is uniquely dependent on neuronally released glutamate.

Immunostaining of human brain capillaries by antibodies to very late antigens.

Normal and neurologically diseased brain tissue was stained with antibodies directed against very late antigens (VLAs) 1, 2, 3, 5, 6, their common beta 1-subunit, and three extracellular proteins: collagen type IV, laminin and fibronectin. Strong staining of capillaries was obtained in both normal and pathological tissue with antibodies to collagen type IV and its putative receptor VLA-1; laminin and its putative receptor VLA-6; and the common VLA beta 1-subunit. Only residual plasma in vessels was stained with the antibody to fibronectin. Negative staining was obtained with antibodies to the fibronectin receptor VLA-5 and VLA-3. Trace staining was obtained with the antibody to VLA-2.

gamma-Glutamyltransferase activity is unchanged in acutely quinolinate-lesioned rat neostriatum but is elevated in Huntington's disease caudate.

gamma-Glutamyltransferase (GGT; gamma-glutamyl transpeptidase) was measured in the neostriata of rats 5-7 days after local injections of 0-150 nmol of quinolinic acid. In contrast to the high levels seen in studies on the caudate in a few Huntington's disease cases, GGT activity showed no significant relation to the amount of quinolinic acid injected or to the extent of neuronal loss, as indicated by assays of choline acetyltransferase and glutamate decarboxylase on the same striatal homogenates. The chronicity of the degenerative disease, contrasted with the acuteness of the lesion, may explain the difference.

Effect of MK-801, kynurenate, glycine, dextrorphan and 4-acetylpyridine on striatal toxicity of quinolinate.

Measurements of striatal choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities indicated that systemic administration of 4-8 mg/kg of MK-801 to rats completely blocked neuronal damage due to intrastriatal injections of 75-150 nmol of quinolinic acid. Similar experiments with 0-2 mg/kg MK-801 suggested the ED50 might be between 1 and 1.5 mg/kg for protection against 50 nmol of intrastriatal quinolinic acid, and between 2 and 3 mg/kg for 75 nmol. Repeated pretreatment with kynurenate (3 x 300 mg/kg) gave significant but not complete protection against similar doses of quinolinic acid, with the protective effect being greater for GAD than for ChAT. Glycine appeared to potentiate the effect of high doses of quinolinic acid on ChAT and the other pretreatments tested (dextrorphan, dextromethorphan, 4-acetylpyridine) had no significant effect.

Tetrahydroaminoacridine potentiates neurotoxicity of quinolinic acid in rat striatum.

Intraperitoneal injection of 5 mg/kg of tetrahydro-9-amino-acridine (THA) in rats 1 h before intrastriatal injection of 50-150 nmol of quinolinic acid potentiated the local neurotoxicity as indicated by measurements of striatal levels of glutamate decarboxylase and choline acetyltransferase. A larger dose (10 mg/kg) THA had no significant effect. The results are discussed in terms of THA's binding to various elements of the NMDA/sigma receptor complex and reported data on such binding are confirmed.

Gene amplification in Tetrahymena thermophila: formation of extrachromosomal palindromic genes coding for rRNA.

Tetrahymena thermophila contains in the macronucleus multiple copies of extrachromosomal palindromic genes coding for rRNA (rDNA) which are generated from a single chromosomal copy during development. In this study we isolated the chromosomal copy of rDNA and determined the structure and developmental fate of the sequence surrounding its 5' junction. The result indicates that specific chromosomal breakage occurs at or near the 5' junction of rDNA during development. The breakage event is associated with DNA elimination and telomeric sequence addition. Similar results were also found previously for the 3' junction of this gene. These results could explain how the extrachromosomal rDNA is first generated. Near both junctions of the chromosomal rDNA, a pair of 20-nucleotide repeats was found. These sequences might serve as signals for site-specific breakage. In addition, we found a pair of perfect inverted repeats at the 5' junction of this gene. The repeats are 42 nucleotides long and are separated by 28 nucleotides. The existence of this structure provides a simple explanation for the formation of the palindromic rDNA.