To investigate the influence of the extent of attrition of teeth in the elderly and to provide a basis for the treatment, 5 527 teeth of 249 elderly, aged from 60 to 92 years, were examined. The results indicated that the occurrence rate of attrition was 100%, 54.6% of them was slight and 45.4% of them was severe. About 16% of them showed symptoms, and hypersensitivity of teeth was the most common one. The authors tried to individualize the treatment. The teeth with severe attrition were repaired by making plastic-metal plate and occlusive rehabilitation. After treatment all patients′ symptoms were resolved, and masticatory efficiency was improved.

To investigate the influence of the extent of attrition of teeth in the elderly and to provide a basis for the treatment, 5 527 teeth of 249 elderly, aged from 60 to 92 years, were examined. The results indicated that the occurrence rate of attrition was 100%, 54.6% of them was slight and 45.4% of them was severe. About 16% of them showed symptoms, and hypersensitivity of teeth was the most common one. The authors tried to individualize the treatment. The teeth with severe attrition were repaired by making plastic-metal plate and occlusive rehabilitation. After treatment all patients′ symptoms were resolved, and masticatory efficiency was improved.

The feasibility of using cord blood mesenchymal stem/progenitor cells (CB-MSPCs) to regenerate cardiomyocytes and the optimal inducing conditions were investigated. The CB mononuclear cells were cultured in low serum DMEM medium to produce an adherent layer. After expansion, the adherent cells were added into cardiomyocyte inducing medium supplemented with 5-azacytidine. Cardiogenic specific contractile protein troponin T staining was performed to identify the cardiomyocyte-like cells. The results showed that the frequency of CB-MSPCs clones in CB mononuclear cells was 0.5 x 10(-6) and about 1.3 x 10(7)-fold expansion was achieved within 20 sub-cultivation. After cardiogenic induction, 70% CB-MSPCs was differentiated into cardiomyocyte-like cells. It was indicated that low serum culture could expand CB-MSPCs extensively and the expanded CB-MSPCs could be induced to differentiate into cardiomyocyte-like cells in high efficiency.
Azacitidine/pharmacology ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Fetal Blood/*cytology ; Fluorescent Antibody Technique ; Mesenchymal Stem Cells/*cytology ; Myocytes, Cardiac/*cytology ; Troponin T

Objective To investigate the expression and cellular localization of cyclin-dependent kinase 5 (Cdk5) in cerebral cortex after subarachnoid hemorrhage (SAH) in rats.Methods Fifty-two male Sprague Dawley (SD) rats were randomly divided into either a sham operation group (n =12) or a SAH group (n =40).The latter was randomly redivided into 6,12,24 h,and day 2 and 3 subgroups (n =8 in each group).A rat SAH model was induced by injecting fresh blood into the prechiasmatic cistern.Western blot and immunohistochemistry were used to detect the expression of Cdk5 in rat brain cortex.Double labeling immunofluorescence staining was used to detect the cellular localization of Cdk5 protein in cerebral cortex.Neuronal nuclear antigen labeled neurons,and glial fibrillary acidic protein labeled astrocytes.Results Western blot showed that the expression of Cdk5 protein was up-regulated at 12 hours after SAH (t =3.709,P =0.001),and it reached the peak on day 1 (t =3.475,P=0.002).Immunohistochemistry showed that the proportion of Cdk5 positive cell was also increased gradually after SAH,and the changes of time course were consistent with the results of Western blot,and it reached the peak on day 1 (t =4.320,P =0.000).Double labeling immunofluorescence showed that Cdk5 was mainly expressed in the neuronal cytoplasm in the sham operation group,and Cdk5 shifted to the neuronal nuclei in the SAH group.Cdk5 was mainly colocalized between astrocytes and neurons.Conclusions SAH up-regulates the expression of Cdk5 protein in cerebral cortex.Cdk5 may be involved in early brain injury after SAH.

Objective Subarachnoid hemorrhage ( SAH) is a devastating disease with high fatality and morbidity and micro-glia/macrophage ( M/M) plays a vital role in SAH brain injury with complicated pathophysiological mechanism .This study was to ob-serve the effect of Nrf2 deficiency on M/M activation and M1 polarization after subarachnoid hemorrhage in mice . Meth ods We col-lected 70 wild-type ( WT) ICR mice and 35 Nrf2-knockout ( KO) mice to establish the SAH model by injecting fresh autologous blood into pre-chiasmatic cistern.WT mice were arranged into four groups: sham operation group, post operative day 1 (POD1) group, POD3 group and POD5 group.Then WT mice and Nrf2 Nrf2-knockout mice were divided into sham operation WT group , sham opera-tion KO group, SAH WT group and SAH KO group.Western blotting (WB) and immunohistochemistry (IHC) were applied to observe the activation and proliferation of M/M after SAH on WT mice .Difference in activation and M 1 polarization were observed by detecting Iba1 expression in WB and CD 16/32 +Iba1 +cells in immunofluorescence between WT and KO mice . Results Gray scale values of Iba1 expression by WB in WT mice are 0.491 ±0.039, 0.657 ± 0.069, 0.930 ±0.046 and 0.926 ±0.046;average optical intensity values of Iba1 expression by IHC in WT mice are 0.412 ±0.122, 0.625 ±0.135, 0.963 ±0.213 and 0.978 ±0.224.The data indica-ted that Iba1 expression increased in SAH KO group in comparison to SAH WT group on 1, 3, 5 day after SAH (P<0.05).Moreover, Nrf2 deficiency promoted the activation and polarization of M /M by increased Iba1 protein expression and CD16/32 +Iba1 +cells after SAH ( P<0.05). Conclusion SAH induces M/M activation and proliferation in mice, and Nrf2 deficiency promotes the activa-tion, proliferation and M1 polarization after SAH .

Pim kinases contribute to tumor formation and development of lymphoma, which shows enhanced DNA replication, DNA recombination and repair. Endothelial cells^(ECs) express all the three members of Pim kinase gene family. We hypothesized that DNA repair gene would regulate Pim expression in ECs. Human umbilical vein endothelial cells (HUVECs) were isolated and maintained in M199 culture medium. The cellular distribution of Pim-3 in ECs was determined by immunofluorescent staining. The siRNA fragments were synthesized and transfected by using Lipofectamine LTX. The total cellular RNA was extracted from the cells by using Trizol reagent. cDNAs were quantified by semi-quantity PCR. The effects of LY294002 and wortmannin on RNA stability in ECs were also examined. Our data showed that LY294002 and wortmannin, phosphatidylinositol 3-kinase (PI3K) and PI3K-like kinase inhibitors, increased Pim mRNA expression in ECs without altering the mRNA stability. RNA interference (RNAi) targeting DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated (ATM) increased mRNA expression of Pim-3 and Pim-1, respectively. Silencing of Akt decreased Pim-1 instead of Pm-2 and Pim-3 gene expression in ECs. But etoposide, a nucleoside analogue, which could activate DNA-PKcs and ATM, increased Pim expression in ECs. Our study indicates that the expression of Pim kinases is physiologically related to DNA-PKcs and ATM in ECs.

Objective Subarachnoid hemorrhage ( SAH) is a devastating disease with a high mortality.This study was to in-vestigate the effect of Nrf2 on secondary brain injury following SAH and its action mechanism in mice. Methods SAH models were established in wild-type ( WT) and Nrf2 knockout ( KO) ICR male mice by injecting fresh blood drawn from the femoral artery into the pre-chiasmatic cistern.The animals were divided into four groups, WT sham, WT SAH, KO sham, and KO SAH.At 24 hours after modeling, the expression levels of malondialdehyde ( MDA) , GSH/GSSG, TNF-αand IL-1β, the volume of brain water, and content of Evans blue were measured, the activity scores obtained, and cerebral vasospasm of the anterior and middle cerebral arteries ( ACA and MCA) detected. Results At 24 hours, the expressions of MDA, TNF-α, and IL-1βwere (3.299 ±0.335), (1.187 ± 0.436), and (59.330 ±21.787) mg/g in the WT sham group, (4.339 ±0.328), (2.432 ±0.434), and (121.584 ±21.675) mg/g in the WT SAH group, (3.488 ±0.634), (1.170 ±0.312), and (58.497 ±15.608) mg/g in the KO sham group, and (5.335 ±0.499), (3.132 ±0.548), and (171.117 ±50.479) mg/g in the KO SAH group, markedly increased in the SAH groups as compared with the sham controls (P<0.05), while the GSH/GSSG levels were significantly higher in the former two groups than in the latter (0.553 ±0.100 and 0.375 ±0.068 vs 0.714 ±0.091, 0.761 ±0.114, P<0.01).The contents of brain water and Evans blue were (0.784 ±0.005) and (7.055 ±1.046) μg/g in the WT sham group, (0.808 ±0.004) and (7.230 ±1.192) μg/g in the WT SAH group, (0.784 ±0.004) and (9.620 ±1.290) μg/g in the KO sham group, and (0.819 ±0.004) and (11.628 ±1.040)μg/g in the KO SAH group, remarkably increased in the SAH groups in comparison with the sham groups (P<0.05).The apoptosis rate 8.916 and 82.100 ±6.870 vs 70.833 ±8.750 and 51.767 ±13.006), ACA radius/wall thickness value (13.885 ±3.360 and 14.212 ±3.2545 vs 8.024 ±2.780 and 6.861 ±2.702), MCA radius/wall thickness value (18.648 ±2.893 and 19.435 ±2.775 vs 6.337 ±3.993 and 5.107 ±3.805), and activity score (2.733 ±0.450 and 2.767 ±0.430 vs 1.967 ±0.928 and 1.433 ±0.679) (all P<0.01). Conclusion Nrf2 knockout increases oxidative stress and inflammatory reaction following SAH and consequently aggravates secondary brain injury.Nrf2 has a protective effect against SAH-induced brain injury.

Objective To investigate the risk factors, clinical and angiographic features of women aged 50 or less with coronary artery disease(CAD). Methods One hundred and seventy-three female CAD patients comifrmed by coronary angiographic aged 50 or less were classiifed as group A, while another 494 non-CAD women aged 50 or less as group B. The differences in CAD risk factors, clinical and angiographic features between the 2 groups were analyzed. Results There were more women with diabetes, positive CAD family history, dyslipidemia or hypertension (especially diastolic hypertension) in group A than in group B. Patient in group A had higher diastolic pressures and serum glucose level than those in group B but both groups had similar body weights, systolic pressures and menopause ages. The serum total cholesterol and triglyceride levels were higher in patients in group A than those in group B while high-density-lipoprotein (HDL) cholesterol and apolipoprotein A levels were lower in group A. The low-density-lipoprotein (LDL) and apolipoprotein B were higher in group A than in group B but without signiifcance. There were more women with positive urine protein in group A than in group B. In group A, more than 50%of patients were with single diseased artery while another 15%with slight coronary artery atherosclerosis or even normal arteries. Most of the lesions were found in left anterior descending artery (LAD) and its branches. Conclusions Risk factors of CAD included diabetes, positive CAD family history, dyslipidemia, hypertension(especially diastolic hypertension) and positive urine protein in women aged 50 or less Menopause alone, without other CAD risk factors, would not lead to CAD. Single vessel disease was more commonly found in this group of patients.

BACKGROUND: Adipose tissues were initially introduced as energy storages, but recently they have become famous as an endocrine organ which produces and secretes various kinds of molecules to make physiologic and metabolic changes in human body. It has been studied that these molecules are secreted in abundance as the adipose tissue becomes bigger along with obesity. Furthermore, it has been found that they are mediating systemic inflammation and generation of metabolic diseases such as type 2 diabetes and atherosclerosis. On the basis of these, we studied previous papers which have been researched about the interaction between preadipocytes and macrophages, adipose tissues and lymph nodes, and adipose tissue secreting molecules. RESULTS: Firstly, preadipocytes and macrophages are expressing similar transcriptomes and proteins, and preadipocytes can be converted to mature macrophages which have phagocytic activity. Moreover, the monocytes, which initially located in the bone marrow, are filtrated to the adipose tissue by monocyte chemotatic protein-1 and are matured to macrophages by colony stimulating factor-1. Secondly, adipose tissues and their associated lymph nodes are interacting each other in terms of energy efficiency. Lymph nodes promote lipolysis in adipose tissues, and polyunsaturated fatty acids in adipocytes become energy sources for dendritic cells. Lastly, adipose tissues produce and secrete proinflammatory molecules such as leptin, adiponectin, TNF-alpha, IL-6, and acute phase proteins, which induce the inflammation and potentially generate metabolic diseases. CONCLUSION: According to these, we can link adipose tissues to inflammation, but we need to affirm the actual levels and roles of adipose tissue-derived proinflammatory molecules in human body.
Acute-Phase Proteins ; Adipocytes ; Adiponectin ; Adipose Tissue* ; Atherosclerosis ; Bone Marrow ; Dendritic Cells ; Fatty Acids, Unsaturated ; Human Body ; Immune System* ; Inflammation ; Interleukin-6 ; Leptin ; Lipolysis ; Lymph Nodes ; Macrophages ; Metabolic Diseases ; Monocytes ; Negotiating ; Obesity ; Transcriptome ; Tumor Necrosis Factor-alpha

AIM: To screen and identify the differentially expressed genes in lymphocytes of patients with unstable angina in order to find the molecular mechanism of unstable angina. METHODS: Suppression subtractive hybridizations (SSH) and dot blot hybridizations were performed to screen the relatively differentially expressed genes in lymphocyte RNA between the patients with unstable angina pectoris and stable angina pectoris. The obtained expressed sequence tags (ESTs) were used as probes to perform Reverse Northern blot with forward and reverse suppression products. And the positive ESTs were performed RNA slot hybridization with unstable and stable angina group. The obtained ESTs were sequenced and analyzed using BLAST (nr) at NCBI. RESULTS: Three up-regulated ESTs in the unstable angina group, and one down-regulated EST in the stable angina group were obtained. All of them are sequences of known genes. CONCLUSION: All these ESTs may be associated with the unstablization of plaque of coronary artery in patients with unstable angina.