Objective To report the clinical and pathological features of chronic graft-versus-host disease-related polymyositis by summarizing the clinical data of the patient with chronic graft-versus-host disease-related polymyositis. Methods One patient with chronic graft-versus-host disease-related polymyositis was hospitalized in our hospital on December 29,2010.The patient,40 years old,female,underwent allogeneic haematopoietic stem cell transplantation because of acute granulocytic-monocytic leukemia.Fourteen months later she manifested as slowly progressive muscle weakness and myalgia in all limbs.Serum creatine kinase level was between 426-1948 U/L. Myositis antibody EJ was strongly positive.Electromyogram showed a neurogenic impairment and slow peripheral nerve conduction speed.Muscle biopsies were carried out in the left biceps brechii.In addition of standard histological and enzyme histochemical staining for the muscle sections,immunohistochemical workup was performed with mouse antiCDs,anti-CD20,anti-CD68 and anti major histocompatibility complex- Ⅰ ( MHC- Ⅰ ) monoclonal antibodies as first antibodies.Results The muscle biopsy showed large variation of fiber size,with muscle fiber necrosis,regeneration.Some angular fibers distributed in small cluster.The inflammatory cells infiltrated around the small vessel or in the endomysium,mainly CD8+ T-lymphocytes and CD6+8 macrophages.The most muscle fibers were MHC-Ⅰ positive. Conclusion The graft-versus-host disease-related polymyositis manifests as chronic myositis process with neurogenic lesions.

Objective It has been shown that adult brain is still capable of neurogenesis which can beinhibited by activation of NMDA receptor.Since lidocaine can inhibit NMDA-mediated excitatoryueurotransmission,we aimed to investigate the interaction between lidocaine and NMDA on the proliferation ofpheochromocytoma cells which are used as a model for central neuronal cells.Methods The PC 12 ceils culturedin vitro were divided into 6 groups:(1)control group,cultured in normal DMEM complete nutrient liquidmedium;(2)NMDA group,cultured in DMEM containing 400 ?mol?L~(-1) NMDA;(3)-(6)lidocaine group,cultured in DMEM medium containing 400 ?mol L~(-1) NMDA and 10,10~2,10~3 or 10~4 ?mol?L~(-1) lidocaine.After 5day incubation,the cell cycle progression was analysed using a flow cytometer.The percentage of cells in S-phase(S-phase fraction,SPF)was determined and proliferation activity(cells in S+G_2 phase/cells in M-phase)wascalculated.Results NMDA 400 ?mol?L~(-1) significantly decreased the SPF of PC12 cells in group 2 compared tocontrol group,and proliferation activity(S+G_2 phase/M-phase)was also significantly reduced(P0.05).The SPF of PC12 cell ingroup 3 and 6(10 and 10~4 ?mol?L~(-1) lidocaine)was also significantly higher than that in NMDA group butsignificantly lower than that in control group.Conclusion NMDA inhibits proliferation of PC12 cells whilelidocaine can antagonize the inhibitory effect of NMDA and promotes proliferation and differentiation of centralneuronal cells.

Objective To investigate the clinical and pathologic features in patients of microscopic polyangiitis (MPA) with peripheral nerve abnormality.Methods We collected clinical data of 6 patients with MPA that was confirmed by immunological,pathological and clinical findings.Electroneurophysiologic examinations and sural nerve biopsies were performed in these patients.Two normal controls were included in these studies.Results All of 6 patients developed asymmetric polyneuropathies.Electrodiagnostic studies showed reduced amplitudes of the sensory nerve action potential and compound motor action potential with mild impaired conductive velocities.The patients presented vasculitis changes with cell infiltration by monocytes and lymphocytes.Sural nerve biopsies found loss of myelinated fibers in all of the patients indicating axonal degeneration.Some of them associated with regeneration clusters of myelinated fibers.Conclusions Asymmetric neuropathy with sensory nerve injuries is the mainfeature in the MPA associated polyneuropathy.Electrodiagnostic examination indicated axonal lesions in mononeuritis multiplex.Sural nerve biopsies confirmed the active axonal lesions and vasculitis.

AIM: To observe the effect of microRNA-16 (miR-16) on the megakaryocytic differentiation of K562 cells, and to explore the potential mechanism.METHODS:miR-16 was over-expressed or silenced by transfection with miR-16 mimics or inhibitor in K562 cells.The level of miR-16 was detected by real-time PCR.The expression of CD41, CD42b and CD61, as megakaryocytic differentiation markers, was detected by flow cytometry.The effect of miR-16 on the expression of myeloblastosis oncogene ( MYB) was measured by Western blotting, and flow cytometry was performed to confirm whether the effect of miR-16 on expression of CD41, CD42b and CD61 was mediated by MYB.RESULTS:Transfection with miR-16 mimics dramatically elevated the level of miR-16 and the expression of CD41, CD42b and CD61 in the K562 cells.Transfection with miR-16 inhibitor decreased the level of miR-16 and the expression of CD41, CD42b and CD61 in the K562 cells (P<0.05).The expression of MYB was regulated by miR-16, and MYB silencing reversed the regulation of CD41, CD42b and CD61 induced by miR-16.CONCLUSION:miR-16 regulates the megakaryocytic dif-ferentiation of K562 cells by targeting MYB.

Objective To investigate the clinical, electrophysiological and pathological features of critical illness polyneuropathy and myopathy (CIPNM). Methods The clinical outcomes, electromyogram Results as well as pathological features in nerves and muscles of 3 patients with CIPNM were investigated and analyzed. Results 3 patients were all provided with assisted respiration after tracheal intubation. 7～10 d after intubation, all the patients emerged muscle strength and tendon reflexes of extremities weakening; while 14 days after that, 2 patients appeared amyotrophy of extremities. Electromyogram showed that the conduction of many motor and sensory nerves for extremities decreased, while the amplitude of compound muscle action potential (CMAP) of part of motor nerves decreased. Biopsy for nerves revealed decreased medullated nerve fibers and regeneration phenomenon of auxiliary fibers; while that for muscles showed neuralgic damage and myopathy-like changes. Conclusion CIPNM can complicate after tracheal intubation. The electrophysiological and pathological examinations for nerves and muscles can be helpful for the diagnosis.

Objective To investigate the value of functional MRI in the diagnosis and differential diagnosis of breast diseases.Methods Sixty-five patients with 68 lesions were enrolled in this study. Conventional T_1 WI and T_2 WI scan,dynamic contrast enhanced MRI,diffusion weighted imaging and ~1H single voxel MR spectroscopy were performed consequently.All lesions were verified by pathology,including 4 cases of breast adenosis,22 fibroadenomas,2 chronic inflammations,3 cysts,33 infitrating ductal carcinomas,1 intraductal carcinoma and 3 cystosarcoma phyllodes tumors.Morphological features,maximum enhancement ratio,time-intensity curve,apparent diffusion coefficient and Choline peak were analyzed. Results The detection rates of T_1 WI and T_2 WI were 14.7%(n=10)and 51.5%(n=35).The sensitivity,specificity,accuracy of dynamic contrast.enhanced MRI for the malignant tumor were 94.6%, 71.4% and 76.5% respectively.Retrospective study showed that diffusion weighted imaging,with the b value from 800 s/mm~2 to 1000 s/mm~2,could be used to differentiate various types of breast lesions.~1H signal voxel spectroscopy had a sensitivity of 51.4%,specificity of 82.6%,and accuracy of 67.6% for the malignent.The sensitivity,specificity and accuracy could reach 97.3%,90.0% and 92.6% respectively by combining conventional scan,dynamic contrast enhanced MRI and MR spectroscopy.Conclusion Functional MRI,with high sensitivity,specificity and accuracy,can be used widely in the diagnosis of malignant breast lesions.

Objectives To screen the differentially expressed proteins in serum of population chronically exposed to arsenic in drinking water,thus to provide candidate protein biomarkers for arsenic exposure and arsenicosis.Methods Subjects were selected from the drinking water type of endemic arsenicosis areas in Shanxi province,China.Demographic characteristics,history of arsenic exposure,cigarette smoking,alcohol drinking,health and other information were collected using questionnaire.The subjects were divided into low-arsenic group (with arsenic in drinking water ＜ 10 μg/L),medium-arsenic group( 10 - 50 μg/L),high-arsenic group( ＞ 50 μg/L),and arsenicosis group(the drinking water with arsenic ＞ 50 μg/L was replaced by low arsenic water ＜ 10 μg/L).The number of cases in each group was 30.The arsenicosis patients were diagnosed according to “Standard of Diagnosis for Endemic Arsenism” (WS/T 211-2001 ).With the principle of informed consent,blood samples were collected.Differentially expressed serum proteins of different arsenic exposure groups and arsenicosis group were screened by two-dimensional differential gel electrophoresis(2-D DIGE),and further identified by mass spectrometry (MS).Results An average of (1299 ± 167) protein spots were identified in 6 gel images and 688 protein spots were discovered repeatedly in at least 5 gels.There were 33 protein spots differentially expressed among low-,medium- and high-arsenic groups P ＜ 0.01).Fifty four protein spots were significantly different among low-,medium-,high-arsenic exposure groups and arsenicosis group(P ＜ 0.01 ).Twenty five protein spots were selected for MS analysis,and13 protein spots were identified.Compared with low-arsenic group,the expressions of apolipoprotein A-Ⅳ,retinol binding protein,and estrogen receptor hypothalamic isoform in medium- and higharsenic exposure groups were down regulated,and the expressions of component 4A and 4B were up regulated.Compared with low-,medium- and high-arsenic groups,the expressions of beta-2-glycoprotein Ⅰ,Keratin 1,hemopexin,complement C1r subcomponent,and ficolin-3 in arsenicosis group were down regulated,and the expressions of pigment epithelial-differentiating factor,alpha-1-microglobulin and carboxypeptidase N catalytic chain were up regulated.Conclusions Chronic arsenic exposure can significantly change population's serum protein expression.Differentially expressed proteins in arsenicosis patients will not decline with the decline of arsenic in a short term.Whether or not the differentially expressed proteins identified in this study can be used as biomarkers for arsenic exposure and arsenicosis needs to be further verified.

OBJECTIVETo investigate whether programmed death ligand 1 (PD-L1) expressed in the periodontal tissue of chronic periodontitis and the correlativity of PD-L1 and different degrees of chronic periodontitis, provide experience for immunoregulation mechanism, clinical treatment and prognosis of chronic periodontitis.

METHODSGingiva and periodontal tissue of healthy people and chronic periodontitis patients were collected. Based on clinical probing, periodontal tissue were classified into three groups: periodontal tissues of healthy people, periodontal tissue of mild chronic periodontitis, periodontal tissue of severe chronic periodontitis. Fluorescent quantitation polymerase chain reaction was applied to explore the expression of PD-L1 mRNA in the periodontal tissue of the different groups. Western blot and immunohistochemistry method were utilized to test the expression of PD-L1 protein in the periodontal tissue of the different groups. Combining with clinical image data, the relationship between differentially expressions of PD-L1 and different degrees of chronic periodontitis was analyzed.

RESULTSThe relative expression quantity of PD-L1 in the periodontal tissue of the mild chronic periodontitis was significantly higher that of the severe chronic periodontitis (P<0.01). The relative expression quantity of PD-L1 in the periodontal tissue of healthy subjects and severe chronic periodontitis had no statistical significance (P>0.05).

CONCLUSIONThe expression of PD-L1 in the periodontal tissue negativelv regulates inflammatory periodontal tissue damage.

During fermentation, it is often difficult to detect the abnormalities, for example, caused by contamination on-line. Instead, the faults were detected usually by off-line laboratory analysis or other ways, which in most cases, is too late to remedy the situation. In this paper, a simple three-layers BP network was used for the early prediction of the amount of product, based on the difference in prediction errors between normal and abnormal charges and other accessorial information, such as profit function and pH value. In addition, three indications characteristic to abnormal charge are incorporated in practical operation. The prediction for Cephalosporin C Fed-batch Fermentation in a Chinese pharmaceutical factory was studied in details as an example and the result shows the abnormal charge can be discovered early successfully using the method.
Bioreactors ; microbiology ; Cephalosporins ; biosynthesis ; Culture Media ; Fermentation ; Hydrogen-Ion Concentration ; Models, Biological ; Neural Networks (Computer)

Objective To describe the chnical, neuroimagine, pathological and genetic features in a case with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS)/Leigh overlap syndrome.Methods The ease was a 22-year-old woman with recurrent headache, loss of visual acuity and general seizures over 11 years.MRI demonstrated symmetrical high T2-weighted signals in occipital and parietal lobes, in the late stage of the disease, the above imagine changes on MRJ were also shown in the bilateral basal ganglion and brainstem.She died of status epilepticus at age of 22.Brain autopsy and mitochondrial DNA (mtDNA) analysis were performed in the patient.Results The main neuropathological findings were muhifocal and lamilar spongiform in the cortex of the whole brain, the basal ganglion and middle brain.Gliosis, macrophagie reaction and capillary endothelial proliferation were observed in these areas.All 6 layers of the cortex and subcortical white matter in occipital and parietal lobes were severely affected.GI3513A mutation was found in the gene of mitochondria encoded NADH dehydrogenase subunit 5 (MTNDS).Conclusions MELAS/Leigh overlap syndrome presents the symptoms predominantly affecting the cerebral cortex.Neuroimagines suggested that the lesion initially involves the cerebral cortex and in the late stage implicates the basal ganglion and the brainstem, possibly caused by pathological changes of spongiform with capillary proliferation in these areas.