OBJECTIVE To report the investigation on validating clinical moist sterilizer by applying wireless thermo-loggers in accordance with the advanced Euro and British standards.METHODS The validation had been implemented with microbiological tests and thermometric tests to measure the temperature distribution of the chamber of sterilizer,the temperature and time relation inside the tested package of small and challenge loads,the pressure of the chamber and the temperature beside the drainage.RESULTS The measurements presented the relation between temperature and time measurements of the spots inside the chamber of the tested sterilization loads.CONCLUSIONS The measurement results indicate directly the operation condition and the temperature-time relation inside sterilization loads.These measurements are helpful for controlling sterilization quality.The results of microbiological tests are negative,which are consistent with that of thermomeric tests.

Cleidocranial Dysplasia ; pathology ; Diagnosis, Differential ; Dwarfism ; Humans ; Maxillofacial Abnormalities ; Osteosclerosis ; pathology ; Pycnodysostosis ; diagnostic imaging ; etiology ; pathology ; therapy ; Radiography ; Tooth Abnormalities

Faciliysyion techniques were used to help improve the extremity motor functions of 43 elderly and 79 middle aged or youthful stroke patients. The Fugl-Meyer scale was employed for thc assessment of the functional status. The results showed that the motor function of upper extremty of thc elderly patients was not improved. but the motor function of lower extremity was improved significantly. The motor functions of upper and lower extremities were all improved significantly in the middle-aged or youthful patients. In early rehabilitation group the Increased motor function marks of the upper extremity of the elderly stroke patients were less than that of the middle-aged or youthful stroke patients. the increased motor function marks of the lower extremity of The elderly stroke patients were less significantly than that of the middle-aged or youthful stroke patients also. In late rehahilitation group the increased motor function marks of the lower extremity in elderly stroke patients were more than that in the middle-aged or youthful stroke patients.

OBJECTIVETo observe the effect of bone morphogenetic protein-7 (BMP-7) on the transdifferentiation of cultured human tubular epithelial cell (HKC) induced by TGF-beta1 and to elucidate its possible mechanism.

METHODSThe cultured HKC cells were divided into 5 groups: serum-free group (negative control); single TGF-beta1 treated group (positive control); single BMP-7 treated group; combined TGF-beta1 and BMP-7 treated group; and BMP-7 pre-treated group. Expression of keratin of HKC cells was assessed by indirect enzyme immunohistochemistry (IEI), expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin by immunohistological method, percentage of alpha-SMA positive HKC cells by flow cytometry, and mRNA expression of alpha-SMA, TGF-beta1, and TGF-beta type II receptor by reverse transcription PCR.

RESULTSThe expression of alpha-SMA and the percentage of alpha-SMA positive HKC cells markedly increased after having been treated by TGF-beta1 while the expression of E-cadherin and keratin decreased. In the group pre-treated with BMP-7 (50 ng/ml) and then added with TGF-beta1 (8 ng/ml), expression of alpha-SMA was significantly lower than in the positive control group, while expression of E-cadherin and keratin significantly higher than in the positive control group. Measurement of the percentage of alpha-SMA positive HKC found significant deference between the combined TGF-beta1 and BMP-7 treated group and the positive control group (9.7% vs 19.8%; 5.8% vs 19.8%; P < 0.05). Significant difference existed between the BMP-7 (50 ng/ml) pre-treated group and the positive control group (8.7% vs 19.8%, P < 0.05). mRNA expression of alpha-SMA was measured by RT-PCR and the results showed that it significantly decreased in the group treated or pre-treated with BMP-7 (50 ng/ml) (15% and 12% of the results in the positive control group, respectively). The mRNA expression levels of both TGF-beta1 and its type II receptor significantly decreased (28% and 19%; 47% and 36%, compared with the positive control group, respectively).

CONCLUSIONTransdifferentiation of cultured renal epithelial cell induced by TGF-beta1 can be inhibittd by certain levels of BMP-7, cultured together with TGF-beta1 or pretreated. BMP-7 can prevent and inhibit the mRNA expression of TGF-beta1 and its type II receptor, which may be an important mechanism by which BMP-7 inhibit the transdifferentiation of renal tubular epithelial cell.

Actins ; biosynthesis ; genetics ; Bone Morphogenetic Protein 7 ; Bone Morphogenetic Proteins ; pharmacology ; Cell Differentiation ; drug effects ; Cells, Cultured ; Epithelial Cells ; cytology ; Humans ; Kidney Tubules ; cytology ; metabolism ; Polymerase Chain Reaction ; RNA, Messenger ; biosynthesis ; genetics ; Transforming Growth Factor beta ; pharmacology ; Transforming Growth Factor beta1

OBJECTIVE To analyze the preliminary regulation between the skin cell toxicity of EOs and drug property char-acteristics of Chinese materia medica(CMM)on the same platform.METHODS The physicochemical parameters of 33 kinds of EOs were measured.MTT assays were applied to evaluate the cell toxicity of EOs on human HaCaT keratinocytes.Finally, data mining technique was applied to analyse experimental data for the purpose to illustrate the relationship between skin cell toxicity of EOs and drug properties of CMMs.RESULTS By non-linear canonical correlation analysis,high correlation(P=0. 041 1<0.05)was found between skin cell toxicity of EOs and channel tropism property of CMMs.EOs with the properties of liver,lung,stomach,kidney and large intestine channel possess lower skin cell toxicity.However,EOs with the properties of heart,pericardium,spleen,bladder,san-jiao and gall bladder channel possess higher skin cell toxicity.A mathematical model between drug property including four mature,five flavor,channel tropism of CMMs and skin cell toxicity of EOs was estab-lished based on non-linear canonical correlation analysis.In the model,significant correlation was found(P=0.041 4<0.05). EOs from CMMs with the properties of cool nature,bitter flavor plus liver or lung or kidney or large intestine channel might be superior in safety towards the skin cells.On contrary,EOs from CMMs with the properties of hot nature,sweet flavor plus heart or pericardium or spleen or bladder or san-jiao or gall bladder channel might be superior in toxicity towards the skin cells. CONCLUSION The skin cell toxicity of EOs is affected by drug property characteristics of CMMs,especially channel tropism property.

OBJECTIVETo investigate the in vitro effect of caffeic acid phenethyl ester (CAPE), a NF-κB inhibitor, on the apoptosis of osteoarthritic (OA) chondrocytes and on the regulation of the gelatinases matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9).

METHODSAnnexin V-FITC/propidium iodide (PI) labeling and western blotting were used to observe and determine the apoptosis in TNFα-stimulated primary cultured osteoarthritic chondrocytes. Also, gelatin zymography was applied to examine MMP-2 and MMP-9 activities in supernatants.

RESULTSIt was confirmed by both flow cytometry and western blotting that chondrocytes from OA patients have an apoptotic background. Use of CAPE in combination with 10 ng/mL of TNFα for 24 h facilitated the apoptosis. MMP-9 in the supernatant could be autoactivated (from proMMP-9 to active MMP-9), and the physiologic calcium concentration (2.5 mmol/L) could delay the autoactivation of MMP-9. The activities of MMP-2 and MMP-9 in the fresh supernatant increased significantly in response to stimulation by 10 ng/mL of TNFα for 24 h. The stimulatory effect of TNFα just on proMMP-9 was counteracted significantly by CAPE.

CONCLUSIONNF-κB could prevent chondrocytes apoptosis though its activation was attributed to the increase of proMMP-9 activity induced by TNFα (a pro-apoptotic factor). Therefore, therapeutic NF-κB inhibitor was a 'double-edged swords' to the apoptosis of chondrocytes and the secretion of MMP-9.

Aged ; Apoptosis ; drug effects ; Caffeic Acids ; pharmacology ; therapeutic use ; Calcium ; physiology ; Cells, Cultured ; Chondrocytes ; drug effects ; enzymology ; secretion ; Drug Evaluation, Preclinical ; Female ; Humans ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Middle Aged ; NF-kappa B ; antagonists & inhibitors ; Osteoarthritis ; drug therapy ; enzymology ; Phenylethyl Alcohol ; analogs & derivatives ; pharmacology ; therapeutic use ; Tumor Necrosis Factor-alpha ; pharmacology

Phytoestrogens, a group of plant-derived non-steroidal compounds that can behave as estrogens by binding to estrogen receptors, have drawn great attention for their potentially beneficial effects on human health. However, there are few studies investigating the potential side effects of phytoestrogens on the reproductive system. The present study was to elucidate the effects of 17β-estradiol (E2), progesterone (P4), and phytoestrogens genistein (Gen), resveratrol (Res), and phloretin (Phl) on eosinophilic infiltration of the ovariectomized rat uterus and endometrial vascular permeability, and to analyze the underlying mechanisms. The ovariectomized rats received daily subcutaneous injections of E2, E2+P4, P4, Gen, Res, Phl, or an equivalent volume of vehicle for 21 days, and sham-operated animals (Sham rats) were used as the controls. Hematoxylin-eosin staining revealed a marked increase in uterine eosinophilic infiltrations in ovariectomized rats treated with E2, E2+P4 or P4, which was associated with increased expression of vascular endothelial growth factor (VEGF), nuclear factor-κB (NF-κB), and tumor necrosis factor-α (TNF-α) proteins as determined by immunohistochemical and Western blot analysis. However, all three phytoestrogens had no markedly effect on the uterine eosinophilic infiltration and the expressions of VEGF, NF-κB, and TNF-α in the uterus of ovariectomized rats. Our data demonstrate that E2 alone or in combination with P4 increases uterine eosinophilic infiltration which is related with vascular hyperpermeability caused by VEGF, NF-κB and TNF-α, whereas phytoestrogens Gen, Res, and Phl, have no such an effect.
Animals ; Endothelium, Vascular ; drug effects ; Eosinophils ; cytology ; Estradiol ; pharmacology ; Estrogens ; pharmacology ; Female ; Genistein ; pharmacology ; NF-kappa B ; metabolism ; Ovariectomy ; Permeability ; Phloretin ; pharmacology ; Phytoestrogens ; pharmacology ; Progesterone ; pharmacology ; Rats ; Stilbenes ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism ; Uterus ; drug effects ; Vascular Endothelial Growth Factor A ; metabolism

Autophagy is a conserved and programmed catabolic process that degrades damaged proteins and organelles. But the underlying mechanism and functions of autophagy in the ischemia-reperfusion (IR)-induced injury are unknown. In this study, we employed simulated IR of N2a cells as an in vitro model of IR injury to the neurons and monitored autophagic processes. It was found that the levels of Beclin-1 (a key molecule of autophay complex, Beclin-1/class III PI3K) and LC-3II (an autophagy marker) were remarkably increased with time during the process of ischemia and the process of reperfusion after 90 min of ischemia, while the protein kinases p70S6K and mTOR which are involved in autophagy regulation showed delayed inactivation after reperfusion. Administration of 3-methyladenine (3MA), an inhibitor of class III PI3K, abolished autophagy during reperfusion, while employment of rapamycin, an inhibitor of mTORC1 (normally inducing autophagy), surprisingly weakened the induction of autophagy during reperfusion. Analyses of mitochondria function by relative cell viability demonstrated that autophagy inhibition by 3-MA attenuated the decline of mitochondria function during reperfusion. Our data demonstrated that there were two distinct dynamic patterns of autophagy during IR-induced N2a injury, Beclin-1/class III PI3K complex-dependent and mTORC1-dependent. Inhibition of over-autophagy improved cell survival. These suggest that targeting autophagy therapy will be a novel strategy to control IR-induced neuronal damage.
Adenine ; analogs & derivatives ; pharmacology ; Animals ; Apoptosis Regulatory Proteins ; genetics ; metabolism ; Autophagy ; Beclin-1 ; Cell Line, Tumor ; Cell Survival ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Mitochondria ; metabolism ; Multiprotein Complexes ; antagonists & inhibitors ; metabolism ; Neurons ; drug effects ; metabolism ; Neuroprotective Agents ; pharmacology ; Phosphatidylinositol 3-Kinases ; antagonists & inhibitors ; metabolism ; Reperfusion Injury ; metabolism ; Sirolimus ; pharmacology ; TOR Serine-Threonine Kinases ; antagonists & inhibitors ; metabolism

BACKGROUNDThe synovial fluid concentrations of adiponectin are significantly higher in patients with rheumatoid arthritis (RA) than in patients with osteoarthritis (OA). Accumulating evidence suggests that adiponectin may be an inducer of inflammation in arthritis, but the mechanism remains unclear. The objectives of this study were to compare the expression levels of adiponectin receptors in rheumatoid arthritis synovial fibroblasts (RASF) and osteoarthritis synovial fibroblasts (OASF), evaluate the roles of adiponectin receptors in adiponectin-induced prostaglandin E(2) (PGE(2)) production, and then investigate the effects of a nonsteroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX)-2-selective inhibitor on adiponectin-induced PGE(2) release.

METHODSThe expressions of adiponectin receptor 1 (AdipoR1) and AdipoR2 mRNA and protein in synovial fibroblasts from seven patients with RA and eight patients with OA undergoing total knee replacement were evaluated by real-time polymerase chain reaction, immunofluorescence microscopy and Western blotting analysis. Adiponectin-induced PGE(2) production was detected by enzyme-linked immunosorbent assay. RNA interference against the AdipoR1 and AdipoR2 genes was performed to investigate the effects of the adiponectin receptors on adiponectin-induced PGE(2) production in both RASF and OASF.

RESULTSAdipoR1 and AdipoR2 mRNA and protein were expressed by both RASF and OASF. Compared with OASF, RASF exhibited higher levels of AdipoR1, but there was no significant difference for AdipoR2. Adiponectin induced the production of PGE(2) by the synovial fibroblasts in a concentration-dependent manner, and this was more obvious in RASF. RNA interference showed that the difference may be mediated by the diverse distribution of AdipoR1. The adiponectin-induced PGE(2) production was efficiently relieved by the NSAID and COX-2-selective inhibitor.

CONCLUSIONThe present findings suggest that AdipoR1 may mediate the difference in adiponectin-induced PGE(2) production in RASF and OASF.

Adiponectin ; pharmacology ; Arthritis, Rheumatoid ; metabolism ; Blotting, Western ; Cells, Cultured ; Dinoprostone ; metabolism ; Female ; Fibroblasts ; drug effects ; metabolism ; Humans ; Immunoassay ; Male ; Microscopy, Fluorescence ; Middle Aged ; Osteoarthritis ; metabolism ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Receptors, Adiponectin ; genetics ; metabolism ; Synovial Membrane ; cytology

BACKGROUNDThe diagnostic value of virtual imaging combined with three-dimensional computed tomographic angiography (3D-CTA) for intracranial aneurysms has not been fully elucidated yet. This study aimed to evaluate the value of combined application of virtual imaging techniques and 3D-CTA in diagnosing patients with aneurismal subarachnoid hemorrhage (SAH) at the acute stage.

METHODSEighty patients with non-traumatic SAH received 3D-CTA examinations. The raw CT data of these patients were reconstructed and transferred into the 3D mode through the surgical plan system based on virtual reality (VR) image, and the 3D virtual images of skulls and brain blood vessels were acquired. The location, size and shape of aneurysms and their anatomic relationship with adjacent tissues were measured from many points of view.

RESULTSSeventy-three aneurysms were detected in 68 of the 80 patients, but 2 aneurysms were detected in 2 of the 5 patients who had been found free of aneurysms previously and had received 3D-CTA examinations for a second time one month later. The 3D virtual images produced by the virtual imaging system were clear and vivid, and they could reveal the location and size of the aneurysm and its relations to the parent artery and skull directly.

CONCLUSIONSThe imaging of 3D-CTA is convenient, reliable and fast in diagnosing intracranial aneurysms and can be regarded as the first choice for the diagnosis and treatment of ruptured intracranial aneurysms. Combined with the surgical plan system based on the VR image, 3D-CTA may obtain more imaging information about aneurysms.

Adolescent ; Adult ; Aged ; Angiography ; methods ; Female ; Humans ; Imaging, Three-Dimensional ; methods ; Intracranial Aneurysm ; diagnostic imaging ; surgery ; Male ; Middle Aged ; Tomography, X-Ray Computed ; methods ; Young Adult