Animals ; Base Sequence ; Capsid Proteins ; genetics ; Carcinoma ; Genes, Tumor Suppressor ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Molecular Sequence Data ; Nasopharyngeal Neoplasms ; genetics ; therapy

Aim: To establish an analytical method for the simultaneous determination of norfloxacin,ofloxacin,pefloxacin,ciprofloxacin,lomefloxacin,danofloxacin,enrofloxacin,sarafloxacin and difloxacin in eggs using solid-phase extraction-LC-MS/MS.Methods: Egg samples were deproteinized with acetonitrile,followed by defatting with hexane.Then the samples were processed by solid-phase extraction and analyzed by LC-MS/MS using an electrospray source.The separation was carried out on a Shimadzu Shim-pack VP-ODS C_(18) column,with a mobile phase consisting of acetonitrile-0.1% formic acid(13: 87).Results: The validated method was proved to be of high specificity,accuracy and sensitivity.Conclusion: The established method is suitable for the routine residual monitoring of fluoroquinolones.

OBJECTIVETo investigate the effects of ginkgolides injection on experimental cerebral ischemia and its related mechanism of action.

METHODThe middle cerebral artery occlusion (MACO) model was induced by the FeCl3-occluding method to explore the protective effects of ginkgolides injection on the score of neurological deficits, the rate of cerebral infarction and the histomorphology of cerbral ischemia in rats. Thrombosis formation in vivo was induced by adrenaline-collagen in mice to explore the antithrombotic effect. Platelet aggregation was induced by ADP and hemorrheological parameters with hyper-viscosity by dextran T-500 were used to explore the effects of antiplatelet aggregation and decreasing viscosity of blood.

RESULTGinkgolides injection could markedly decrease the infarct size and behavior deficits score, inhibit the thrombus formation in mice, decrease blood viscosity and ameliorate hemorrheological parameters in rat.

CONCLUSIONGinkgolides injection has the protective effects on focal cerebral ischemia, and its mechanism may be relative to its inhibition of platelet-dependent thrombosis and amelioration of hemarheological partments.

Animals ; Behavior, Animal ; drug effects ; Blood Viscosity ; drug effects ; Brain ; pathology ; Female ; Ginkgo biloba ; chemistry ; Ginkgolides ; administration & dosage ; isolation & purification ; pharmacology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Injections ; Intracranial Thrombosis ; pathology ; Male ; Mice ; Neuroprotective Agents ; administration & dosage ; isolation & purification ; pharmacology ; Platelet Aggregation ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Objective:To evaluate the endothelial functions and autoregulation capacity of cerebral blood flow in patients with Fabry disease .Methods:Brachial artery vasodilation was assessed in 8 pa-tients with Fabry disease and 14 healthy controls by means of flow-mediated dilation ( FMD) and Nitro-glycerin-mediated dilation ( NMD) .Cerebrovascular reactivity was calculated in terms of breath-holding index ( BHI) and vascular motor reactivity ( VMR) by TCD-CO2 test in 4 patients and 14 healthy con-trols.Results:Compared with the controls , brachial artery vasodilation experiment showed no difference (the patients:FMD 15.94%±5.03% and NMD 23.92%±7.23%, the controls: FMD 14.57%± 5 .84% and NMD 22 .64%±6 .96%) , there was no relationship between FMD or NMD and the age , course of disease , MSSI or enzyme activity .In respect of cerebrovascular autoregulation capacity , there was no difference in anterior circulation , while cerebrovascular reactivity tended to be impaired in posteri-or circulation .Conclusion:Endothelial function showed no decline in patients with Fabry disease , but cerebrovascular autoregulation capacity tended to be impaired in posterior circulation .

Child ; Humans ; Lupus Nephritis ; complications ; Male ; Nephritis, Interstitial ; etiology ; Prognosis

Adenoma ; pathology ; Brain Neoplasms ; secondary ; Chromogranin A ; metabolism ; Diagnosis, Differential ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Neoplasm Recurrence, Local ; Pituitary Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Reoperation ; Synaptophysin ; metabolism ; Temporal Lobe ; pathology

Objectives To report clinical,electrophysiological and pathological features of myopathy with tubular aggregates.Methods The onset of the disease was between 5-50 years old in the 6 sporadic male cases.Skeletal muscle biopsy was performed for all cases.Specimens were examined histochemically,enzymhistochemically and electromicroscopically.Results Case 1 and 2 presented with limb girdle myasthenic syndrome.The case 1 developed exercise-induced cramps in the late stage.Case 3 complained about persistent weakness and Dopa-responsive dystonia.Case 4 and 5 were characterized by periodic paralysis.Case 6 showed exercise-induced cramps.Serum potassium was normal in all patients. Slight elevation of serum creatine kinase appeared in 3 cases.Electromyography showed neurogenic pattern in case 1 and 6,myogenic changes in case 4 and 5,and no abnormality in other 2 cases.Marked decrement of active potential amplitude was noted with low frequency repetitive nerve stimuli in case 1 and 2.Four percent to forty percent of muscle fibers showed focal material accumulation in the fibers,which involved mainly type 2 fibers in all cases.The material was stained bright red material with modified gomori trichrome,intensive staining with nicotinamide adenine dinucleotide-tetrazolium reductase,lack activity of succinate dehydrogenase and ATPase.Electron microscopy confirmed bundles of parallel micro-tubular structure in the muscle fiber.Conclusions Myopathy with tubular aggregates has various clinical subtypes and electromyographic pattern.Dystonia or other systemic symptoms could be noted in this disease.The limb girdle myasthenic syndrome can also be accompanied with exercise-induced cramps.

Here we report the clinical,radiological and neuropathological findings of a patient with tumor-like inflammatory demyelinating diseases of the central nervous system.The patient was a 51-year-old man with a four-month history of inflammatory pseudotumor and no other significant medical history,who presented to our hospital recurrent relapse numbness and weakness of his right extremities,dysarthria and memory deterioration.Brain magnetic resonance imaging(MRI) showed mass focal lesion in white matter of left parietal lobes.The biopsy showed numerous infiltrating macrophages and lymphocytes within the perivascular.The patient responded clinically to corticosteroid and intravenous immunoglobulin(IVIG) therapy.According to the results of the biopsy and the MRI,a diagnosis of inflammatory pseu-dotumor of the central nervous system was made.The vascular dysfunction may act in the pathogenesis of inflammatory pseudotumor of the central nervous system.

Objective To investigate the effect of α-galactosidase A (GLA) gene mutation on cell autophagy and to elucidate its mechanism preliminarily.Methods Two families were diagnosed by ultrastructural pathological examination,GLA gene activity test and GLA gene mutation screening.Mutant type recombinant expression plasmid of two pedigrees (pcDNA3.1-GFP-ex1 (EX1 group),pcDNA3.1-GFP-ex3 (EX3 group)) and wild type recombinant expression plasmid of GLA (pcDNA3.1-GFP-GLA,GLA group) were constructed.Hela cell line (control group) was transiently transfected with recombinant expression plasmid according to lipofectin transfection.The relative gene expression of Beclin-1 was measured with real-time PCR,and protein expression level of LC3-Ⅱ/LC3-Ⅰ,Beclin-1 and P62/SQSTM1 was examined by Western blotting.Results The LC3 protein values of groups EX1,EX3,GLA and control were 1.495 ± 0.064,1.490 ± 0.020,1.285 ± 0.021,1.260 ± 0.042,respectively;P62/ SQSTM1 values were 0.555 ± 0.086,0.480 ± 0.084,0.785 ± 0.439,0.980 ± 0.278,respectively;Beclin-1 mRNA 2-△Ct values were 0.011 ±0.003,0.008 ±0.002,0.005 ±0.001,0.003 ±0.001,respectively;Beclin-1 protein values were 1.178 ±0.098,1.209 ±0.092,0.931 ±0.100,0.796 ±0.184,respectively.Compared with the wide type group,the level of LC3-Ⅱ/LC3-Ⅰ protein was significantly higher in the mutant type groups(t =5.118,4.984;P =0.007,0.008),though no statistically significant difference was found in the expression levels of P62/SQSTM1 (t =1.052,1.400;P =0.323,0.199).Besides,the expression levels of Beclin-1 mRNA (t =3.800,2.445;P =0.005,0.040) and protein (t =2.424,2.729;P =0.042,0.026) were significantly higher in the mutant type groups.Conclusions GLA gene mutation can induce cell autophagic dysfunction,and signaling pathway of autophagic activation may be Beclin-1 dependent.

Objective To report the clinical and peripheral neuropathological findings in two patients with autosomal recessive Charcot-Marie-Tooth disease 2K(AR-CMT2K).Methods Case one was a nine year-old girl.She had distal weakness of lower limbs for six years, with calf atrophy and contracture of Achilles tendon for three years.Case two was an eight year-old boy.He had distal weakness of lower limbs with contracture of Achilles tendon and calf muscle atrophy for three years, and proximal weakness of low limbs for two years.The motor nerve conduction velocities in median nerves were 48.1 m/s in case one and 47.6 m/s in case two.The compound motor action potential amplitude of median nerves decreased by 46% in case one and 69% in case two.Sural nerve biopsies and gene targeted next-generation sequencing were performed in both patients.Results Density of myelinated fibers was 8 407/mm2 in case one and 7 714/mm2 in case two.The ratio of myelinated fibers with diameter over 8 μm was 2.6% in case one and 0 in case two.Both patients had small regenerating cluster of myelinated fibers.Thin myelinated fibers appeared in case one.In case two, atypical onion bulb formations with focal folded myelin appeared, and electromicroscopy revealed mitochondrial aggregate in axons.Compound heterozygous mutations of ganglioside-induced differentiation associated protein 1 gene were detected in both patients, including c.767A>G(p.H256R) and c.466G>A (p.A156T) in case one and c.767A>G and 845G>A(p.R282H) in case two.Conclusions Contracture of Achilles tendon may appear in early childhood of AR-CMT2K patients.The main pathological changes in sural nerve are loss of large myelinated fibers, mitochondrial aggregate in axons and myelin abnormalities.