Hypertensive retinopathy (HR) often coexist with carotid lesions in hypertensive patients.Carotid lesions are closely associated with cardiovascular and cerebrovascular diseases,as well as end events,offering early important evidence to screening high risk patients.HR has significant value to predict target organ damage (TOD) of hypertension including carotid lesion.In addition,hypertensive retinopathy and carotid lesions-related ischemic ocular diseases will cause serious vision function damage.This article is going to summarize the value and correlation between hypertensive retinopathy and carotid lesions in terms of clinical manifestations,pathological physiological mechanism and target organ damage.

Objective To investigate the effect of hypoxia micro?environment on anoikis in human high?metastatic cell line 95D of giant cell carci?noma of lung. Methods Suspension technology was used to culture 95D to establish the model of anoikis?resistant 95D cells. Hypoxic culture was conducted in the experimental group,and regular culture was conducted in the control group. The effect of hypoxia on proliferation of anoikis?resis?tant 95D was investigated by MTT and the apoptosis in the two groups were detected by flow cytometer. The invasive ability of the cells was assessed by Transwell test. The effect of hypoxia on the expression of HIF?1α,VEGF and MMP?2 in anoikis?resistant 95D was detected by Western blot. Re?sults The growth rate of the anoikis?resistant 95D cells treated with hypoxia was 52.9%,and the apoptosis rate of these cells was higher than that in the non?hypoxic group(40.4%vs 21.7%,P<0.05). The treatment of hypoxia down?regulated the invasive ability,the number of migration cells un?der hypoxia was higher than that in the control group,with statistical significance(40.1±6.7 vs 12.5±7.9,P<0.05). The up?regulation of HIF?1α, the down?regulation of VEGF and MMP?2 were observed in the group of hypoxia. Conclusion During anoikis of human high?metastatic lung can?cer cell line 95D,hypoxia inhibited the survival ability and the metastasis ability of anoikis?resistant cells,which,however,might be the early mani?festation of hypoxia.

Serum anti-M2 mitochondrial antibody (AMA-M2) was screened with immune colloidal gold technique in 6 008 individuals aged over 60 years who underwent health check-up in Xuhui District of Shanghai,the positive samples were retested with ELISA method.The results showed that 1.31％ (79/6 008) individuals were AMA-M2 positive; the positive rate was 0.82％ (18/2 186) in males and 1.60％ (61/3 822) in females.Eleven subjects with positive AMA-M2 underwent further investigation,8 cases were diagnosed as primary biliary cirrhosis (PBC) and the remaining 3 were highly suspected as PBC.All 11 individuals were abnormal in biochemical tests of liver function and/or clinical symptoms.

Objective To explore microbic distribution feature of acute rhinitis pafienta' nasal cavity and dependabihty research of respiratory infection.Methods 436 acute rhinitis pafienta were randomly divided tO infection group(314)and non-infection group(122)depended on whether accompanying respiratory infection.Take blenna narium and carry out nasal cavity microbiological detection,meanwhile take blood and mesasure the content of serum IL-4 and IFN-γ.Results The staphylococcus aureus taked the most proportion(58.6%and 3 1.2%)of nasal cavity bacterial distribution in infection group and non-infection group,the following bacterium were the staphylococcus epidermidis(44.9%and 46.7%),bacillus meningitidis purulentae(7.9%and 4.9%)and bacillus coli(3.5%and 1.6%),the major eumycete were the peptostreptococcus asaeeharolyticus(1.9%and 1.6%),eubacterium lentum (1.6%and 0)and eubacterium mucus(0.9%and 0.8%),the major virus were the syncytial virus,the rhinoviru8es,adenodrus,influenza virus,parainfluenze virus and coronaviruses.The respiratory tract infection patients' content of serum IL-4 Were significant higher(P＜0.05)than the non-infection group,but the content ofIFN-γ were signifieanfly reduced(P＜0.05).Conclusion The staphylococcus aureus,syncytial virus,rhinoviruses,adenovirus and influenza virus have the close relation with the infection of the respiratory tract,which can cause the disorder of organism immune function.

Objective To establish mouse models of intracerebral hemorrhage using autologous arterial blood,to study the physiological property of hippocampal neurons,brain edema changes and learning ability in the mouse models after intracerebral hemorrhage.Methods Eighty male C57/BL6 mice were randomly divided into intracerebral hemorrhage group and control group (n=40); 20 μL arterial blood from the tail arteries or normal saline were injected into the caudate nucleus of intracerebral hemorrhage group and control group by stereotactic technique,respectively.One,three,five and seven d after injection,the neurological impairment was scored; the behavioral changes of the mice in the Morris water maze (navigation test and space exploration experiment) were observed; brain edema was measured by wet and dry weight method and electrophysiological differences of hippocampal neurons were recorded by whole-cell patch-clamp technique and computer software.Results As compared with those in the control group,significantly increased neurological deficit scores one,three,five and seven d after injection,statistically decreased residence time in the platform on the fifth d of training,obviously increased water content around the brain edema one,three,five and seven d after injection,and significantly decreased resting membrane potential and input resistance in the hippocampal CA1 pyramidal cells five d after injection of mice in the intracerebral hemorrhage group were noted (P＜0.05).Conclusion The hippocampus-dependent spatial leaming ability of intracerebral hemorrhage mice is decreased,and the permeability of potassium channels is enhanced.

Objective·To explore the role of advanced platelet-rich fibrin(A-PRF)in osteochondral regeneration.Methods·Bone-marrow mesenchymal stem cells(BMSCs)and knee joint chondrocytes were obtained from New Zealand rabbits.A-PRF was obtained by low-speed centrifugation of the heart blood of rabbits.The histological structure of A-PRF was observed by an optical microscope.The release of growth factors in A-PRF was detected by ELISA,including platelet-derived growth factor,transforming growth factor-β,insulin-like growth factor,vascular endothelial growth factor,epidermal growth factor and fibroblast growth factor.A-PRF's cytotoxicity and capability for promoting the proliferation of rabbit BMSCs were detected by live/dead double staining and MTT methods.The effect of A-PRF on the gene expression of type Ⅱ collagen,aggrecan,alkaline phosphatase(ALP)and osteocalcin(OCN)in rabbit BMSCs was detected by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR).Transwell chambers were used to determine the effect of A-PRF on the migration ability of rabbit BMSCs and the chondrocytes.Rabbit knee osteochondral defect models were established,and 18 rabbits were randomly divided into 3 groups.The A-PRF group(n=6)was implanted with A-PRF in the defect,the A-PRF+BMSCs group(n=6)was implanted with rabbit BMSCs on A-PRF,and the control group(n=6)did not undergo implantation.The rabbits were sacrificed 12 weeks after surgery and the knee joint specimens were stained with hematoxylin-eosin(H-E),toluidine blue and safranin O/fast green.Based on the surface morphology and histology of the knee joints,the International Cartilage Repair Society(ICRS)scoring system was used for macroscopic and histological scoring.Results·A-PRF had a loose network structure and can slowly release growth factors.No cytotoxicity to rabbit BMSCs was observed after adding A-PRF,and the the capability for promoting the proliferation of rabbit BMSCs was significantly increased at 24,48 and 72 h after adding A-PRF(all P<0.05).Chondrogenesis-related gene Ⅱ collagen and aggrecan,as well as osteogenesis-related genes ALP and OCN were significantly up-regulated(all P<0.05).After adding A-PRF,the migration abilities of rabbit BMSCs and chondrocytes were significantly enhanced(both P<0.05),and the migration ability of rabbit BMSCs was significantly higher than that of chondrocytes(P=0.025).The joint surface morphology in the rabbit knee joint defect models was observed.It can be seen that the defects in the A-PRF group and the A-PRF+BMSCs group were basically restored,while the the defects in the control group were only covered by soft tissue.In the ICRS macroscopic score,there was no statistical difference between the A-PRF group and the A-PRF+BMSCs group,but the scores of the two groups were all significantly higher than those of the control group(all P<0.05).According to the histological results,both the A-PRF group and the A-PRF+BMSCs group formed osteochondral repair,but the cartilage in the A-PRF group was more mature,while the control group formed fibrous repair.In the ICRS histological score,there was no statistical difference between the A-PRF group and the A-PRF+BMSCs group,but the scores of both the groups were significantly higher than those of the control group(both P<0.05).Conclusion·Autologous A-PRF has good biocompatibility and the capability for promoting the proliferation of BMSCs.It can promote the repair of cartilage and subchondral bone both in vitro and in vivo.

Activation of the heart normally begins in the sinoatrial node (SAN). Electrical impulses spontaneously released by SAN pacemaker cells (SANPCs) trigger the contraction of the heart. However, the cellular nature of SANPCs remains controversial. Here, we report that SANPCs exhibit glutamatergic neuron-like properties. By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse, we found that SANPCs co-clustered with cortical neurons. Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system, expressing genes encoding glutamate synthesis pathway (Gls), ionotropic and metabotropic glutamate receptors (Grina, Gria3, Grm1 and Grm5), and glutamate transporters (Slc17a7). SANPCs highly expressed cell markers of glutamatergic neurons (Snap25 and Slc17a7), whereas Gad1, a marker of GABAergic neurons, was negative. Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca