Objective To observe effects for exercise and diet on learning and memory ability in mice with encephalon aging induced by D-galactose(D-gal).Methods The model of mice with encephalon aging was made by D-gal.The learning and memory ability of mice was determined by Morris water maze.Results There was significant difference between high fat feed encephalon aging group and restrict food on normal feed encephalon aging group,normal feed and exercise encephalon aging group,high fat feed and exercise encephalon aging group,high fat feed normal group,normal feed and exercise group,normal feed group(all P<0.05).In spatial probe test,there was significant difference between restrict food on normal feed encephalon aging group and normal feed encephalon aging group(all P<0.05).Conclusion Exercise and restrict food can improve the learning and memory function in the mice;feed with high fat can promote encephalon aging.

To report the clinical, radiological and neuropathological findings of a patient with rheuma-toid meningitis. The patient was a 71-year-old Chinese man with a two-year history of rheumatoid arthritisand no other significant medical history, who presented to our hospital recurrent weakness of his left ex-tremities, dysarthria and a continuous bilateral hand tremor. Cerebrospinal fluid (CSF) and serumexam-inations were normal apart from a mildly raised serum perinuclear antineutrophil cytoplasmic autoantibody(p-ANCA). Brain magnetic resonance imaging (MRI) showed leptomeningeal enhancementin both fron-tal and parietal lobes, in addition to several old white matter infarcts. Meningeal biopsy showed numerousinfiltrating macrophages and lymphocytes within the leptomeninges. The patient responded clinically andradiologically to corticosteroid and cyclophosphamide therapy. The patient subsequently developed herpeszoster over his left chest as a complication of his immunosuppressive treatment. His cyclophosphamidewas ceased and intravenous immunoglobulin (IVIG) therapy was commenced, with good clinical responseto both the herpes zoster and meningitis. According to the result of the biopsy, aseptic meningitis wasconsidered the MRI results and the patient’s clinical history were given, and a diagnosis of rheumatoidmeningitis was made. The patientwas p-ANCApositive. Although there was no evidence for cerebral vas-culitis on biopsy, it remains a possibility that the patient’s recurrent minor cerebral infarcts visible onMRI were vasculitic in nature.

Objective To investigate the expression and significance of Smad 7,Smurf 1 and Smurf 2 in basal cell carcinoma and squamous cell carcinoma.Methods Biopsy specimens were resected from 14 patients with basal cell carcinoma,19 patients with squamous cell carcinoma and 30 normal controls.Quanti- tative real-time PCR and immunohistochemical techniques were utilized to assess the expression of Smad 7, Smurf 1 and Smurf 2 in these specimens.Results The gray scale for staining of Smad 7,Smurf 1 and Smurf 2 was 166.61?7.11,166.08?8.71,and 166.25?8.15 respectively in basal cell carcinoma,161.66?5.52,166.84?9.27,and 169.98?9.48 respectively in squamous cell carcinoma.The expression levels of Smad 7,Smurf 1 and Smurf 2 were all significantly increased in basal cell carcinoma and squamous cell car- cinoma in comparison with normal controls.Conclusions The over-expression of Smad 7,Smurf 1 and Smurf 2 may interfere with transforming growth factor?signaling transduction pathway through several links,therefore prevent the inhibitory effect of transforming growth factor?on epidermal proliferation,and accelerate the abnormal proliferation in above epidermal tumors.

Hemorrhage of the basal ganglia is common in hypertensive patients, and most of the cases are spon- taneous unilateral hemorrhage. Traumatic basal ganglia hemorrhage is uncommon, while bilateral hemorrhage of the basal ganglia after trauma is an extremely rare entity. This report described a rare case of bilateral hemorrhage of the basal ganglia after head trauma. We also analyzed the mechanisms and reviewed relative literatures.
Basal Ganglia Hemorrhage ; diagnostic imaging ; etiology ; Craniocerebral Trauma ; complications ; Female ; Humans ; Middle Aged ; Tomography, X-Ray Computed

Objective: To observe the impact of vareniline tartrate on vascular endothelial function and inlfammatory factor releasing in acute coronary syndrome (ACS) patients with nicotine dependence after smoking withdrawal treatment.
Methods: We recruited the in-hospital ACS patients who were smoking ≥10 cigarettes/day for more than 10 years with at least moderate nicotine dependence, and randomly divided them into 2 groups: Varenicline group, the patients received oral medication for 2 weeks and Self withdrawal group, the patients without medication assistance.n=52 in each group. All patients received (10-30) min daily mission and consulting for quit smoking for 2 weeks. The basic information was recorded and blood levels of NO, IL-6 and ET-1 were compared before and after withdrawal treatment.
Results: Compared with they were before, after 2 weeks withdrawal treatment, in Varenicline group, blood levels of ET-1 decreased as (33.950 ± 1.439) ng/L vs (170.198 ± 12.602) ng/L and IL-6 decreased as (0.103 ± 0.020) ng/L vs (0.307 ± 0.051) ng/L; in Self withdrawal group, ET-1 decreased as (60.795 ±7 .036) ng/L vs (170.511 ± 12.374) ng/L, all P<0.05; while NO levels were similar,P>0.05. After treatment, ET-1 level in Varenicline group (33.950 ± 1.439) ng/L was lower than Self withdrawal group (60.795 ± 7.036) ng/L and IL-6 level in Varenicline group (0.103 ± 0.020) ng/L was also lower than Self withdrawal group (0.258 ± 0.042) ng/L, allP<0.05; while NO levels were similar between 2 groups,P>0.05.
Conclusion: Compared with self withdrawal, varenicline tartrate may effectively inhibit inlfammatory factor releasing in ACS patients with nicotine dependence, and therefore improve the vascular endothelial function.

Objective To explore clinical and muscular pathological features of statin-induced myopathy.Methods Nine patients were enrolled in this study,who were diagnosed as statin-induced myopathy by muscle biopsy in Peking University First Hospital from April,2012 to October,2014.The clinical data and pathological findings were analyzed.Results The exposure time to statins varied from 4 days to 4 years in the total of 9 patients,6 males and 3 females,with the average age of 63 ± 6 (55 to 74) years old.Three patients suffered from myalgia and 6 patients complained of weakness mainly at the proximal limbs,while no symptoms occured in 3 patients.Serum creatine kinase (CK) increased in all patients with the maximum value varied from 468 to 8 000 U/L.Serum myositis antibodies were tested in 7 patients and all were negative.Electromyogram was performed in six patients with myogenic damage found in 2 patients.MRI of bilateral thigh muscle was carried out in six patients with muscle edema and mild fatty infiltration found in 2 patients.All patients underwent skeletal muscle biopsy with histochemical and immunohistochemical staining.The main muscular pathological features were muscle fiber atrophy,necrosis,regeneration and increased lipid droplets.Ragged blue fiber,cytochrome C oxidase-negative muscle fibers and decreased NADH activity were observed in some patients.MHC-Ⅰ expressed in the sarcolemma of muscle fibers at various levels.Mild C5b-9 staining was found in the endomysium,capillary and cytoplasm.Symptoms and the level of CK were improved in 7 patients after discontinuing statins or changing to another statin,while the immunosuppressive therapy were used in 2 patients and shown to be effective.Conclusions Statin induced myopathy is self-limiting in most patients,with improvement after discontinuation of statins.Few patients with autoimmune necrotic myopathy need immunosuppressive therapy.

Objective:To report thigh muscle magnetic resonance imaging (MRI)tests of four Chinese patients with dystrophinopathy with edema changes in adductor longus muscles that mimics adductor en-thesopathy.Methods:Four boys,who were from four unrelated families and aged from 5 to 11 years, were investigated because of the clinical manifestations including myalgia or muscle weakness or the inci-dental findings of elevated serum creatine kinase levels,and were diagnosed with dystrophinopathy by gene test of Duchenne muscular dystrophy (DMD).Their creatine kinase levels were increased from 4 087 IU /L to 32 700 IU /L (Normal range:75 -175 IU /L).The muscle biopsy of three patients all demonstrated a dystrophic pattern including necrosis,regeneration,hypertrophy,atrophy and connective tissue proliferation,with different proportions of dystrophin-negative muscle fibers.The gene test of DMD showed an out-frame deletion of exons in three of the four patients,involving either exons 45 or exons 49 -52 deletion or exon 62 duplication,and c.2665 C >T with nonsense mutation in the other one. Muscle MRI tests of the bilateral thighs were performed with T1 weighed sequence and slow tau inversion recovery sequence.The degree of fatty infiltration changes was scored.Results:MRI of the thigh mus-cles showed mild to severe fatty infiltration changes in T1 weighed sequence with the total scores from 2 to 13.The most severe fatty infiltration changes were in the long head of biceps femoris and adductor mag-nus.Obvious hyperintensities appeared mainly in the adductor longus muscles on slow tau inversion re-covery (STIR)images in all the patients without any abnormal signals in the attachment of the ligament, indicating edema changes of the adductor longus muscles which mimiced adductor enthesopathy.Two of the four patients presented with edema changes in the bilateral adductor longus muscles,while the other two were with only unilateral changes.Furthermore,other thigh muscles,including adductor magnus, semitendinosus,sartorius and rectus femoris muscles,could also have mild edema changes in two of the four patients.Conclusion:Dystrophinopathy can manifest as edema changes in the adductor longus mus-cles in thigh muscle MRI tests,which is a typical lesion in adductor enthesopathy.The adductor longus muscles in the dystrophinopathy patients may be easy to be impaired due to traction injury during sports.

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.

Objective To describe the changes of cell development associated contracture and structure proteins in vascular smooth muscle cells (VSMCs) in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Methods The clinical manifestation of probands in 6 families showed the recurrent cerebral ischemic event. A part of patients showed dementia. The genetic analysis in all probands showed Notch3 gene mutation. All probands received the sural nerve biopsy. The primary antibodies against α-smooth muscle actin, smooth muscle myosin heavy chain, desmin and vimenfin were used in immunohistochemistry staining on all of them. Results VSMCs showed hypertrophy or atrophy in the arterioles with different caliber. The granular osmiophilic material (GOM) could be found within the basal lamina of arteriole VSMCs in all of the probands. The expressions of α-smooth muscle actin and smooth muscle myosin heavy chain were partly lost, negative or unevenly distributed in the VSMCs in the arteriole. The expression of desmin showed also unregular distribution or partial loss. The expression of vimentin was partly enhanced. Conclusions The VSMCs show the physiological features of synthetic configuration, indicating the hypoplasia of VSMCs in the arterioles of CADASIL. The VSMCs of the larger arteriole were more severely involved.