Effect of ultrasonic surface impact on the microstructural characterization and mechanical properties of 316L austenitic stainless steel.

In the present study, effect of ultrasonic impact treatment (UIT) on the microstructural characterization and mechanical properties of 316L stainless steel (hereinafter referred to as 316L) was investigated experimentally. The fatigue fracture mechanism of 316L before and after UIT was revealed. The experimental results indicated that the martensitic grain size induced at the impact edge was about 2.00 Å. The surface modified 316L formed a gradient nanostructure and induced a martensitic phase transformation. The hardness of the surface layer of the modified 316L was twice the hardness of its matrix. The tensile strengths of 316L before and after UIT were 576 MPa and 703 MPa, respectively. The stretching stripes of 316L were more disordered after UIT. The fatigue strengths of 316L before and after UIT were 267 MPa and 327 MPa, respectively. The fatigue cracking of 316L started from the austenite grain boundaries. The fatigue fracture surface was relatively rough. The fatigue crack sources of the modified 316L came from internal inclusions. The inclusions were oxides dominated by SiO2. As the stress range increased, the crack initiation site migrated to the interior and the fatigue fracture surface became flatter.

Experimental study on pore structure characteristics and thermal conductivity of fibers reinforced foamed concrete.

The pore structure characteristics and thermal conductivity of foamed concrete (FC) reinforced with glass fibers (GF), polyvinyl alcohol fibers (PVAF) and polypropylene fibers (PPF) were investigated experimentally in this article. Firstly, GF, PVAF or PPF with different mass fractions (0%, 1%, 1.5% and 2%) were added to the Portland cement, fly ash and plant protein foaming agent to prepare the FC. Then, SEM tests, dry density tests, porosity tests, and thermal conductivity tests were carried out on FRFC. Later, the adhesion of GF, PVAF and FFF with different mass fractions to the cementitious base was investigated by SEM images of FRFC. The pore size distribution, shape factor and porosity of FRFC were analyzed using Photoshop software and Image Pro Plus (IPP) software. Finally, the effects of different mass fractions and lengths of three types of fibers on the thermal conductivity of FRFC were discussed. The results indicated that proper fiber mass fraction can play a role of refining small pores and separating large pores, improving the structural compactness, reducing the pore collapse phenomenon and optimizing the pore structure of FRFC. The three types of fibers can promote the optimization of cellular roundness and increase the proportion of pores with diameters below 400 µm. The FC with larger porosity had smaller dry density. As the fiber mass fraction increased, the thermal conductivity performed a phenomenon of first decrease and then increase. The three types of fibers with 1% mass fraction achieved relatively low thermal conductivity. Compared with the FC without fibers, the thermal conductivities of GF reinforced FC, PVAF reinforced FC and PPF reinforced FC with 1% mass fraction were decreased by 20.73%, 18.23% and 7.00%, respectively.

Cathepsin K Knockout Exacerbates Haemorrhagic Transformation Induced by Recombinant Tissue Plasminogen Activator After Focal Cerebral Ischaemia in Mice.

Severe haemorrhagic transformation (HT), a common complication of recombinant tissue plasminogen activator (rtPA) treatment, predicts poor clinical outcomes in acute ischaemic stroke. The search for agents to mitigate this effect includes investigating biomolecules involved in neovascularization. This study examines the role of Cathepsin K (Ctsk) in rtPA-induced HT after focal cerebral ischaemia in mice. After knockout of Ctsk, the gene encoding Ctsk, the outcomes of Ctsk+/+ and Ctsk-/- mice were compared 24 h after rtPA-treated cerebral ischaemia with respect to HT severity, neurological deficits, brain oedema, infarct volume, number of apoptotic neurons and activated microglia/macrophage, blood-brain barrier integrity, vascular endothelial growth factor (VEGF) expression and Akt-mTOR pathway activation. We observed that haemoglobin levels, brain oedema and infarct volume were significantly greater and resulted in more severe neurological deficits in Ctsk-/- than in Ctsk+/+ mice. Consistent with our hypothesis, the number of NeuN-positive neurons was lower and the number of TUNEL-positive apoptotic neurons and activated microglia/macrophage was higher in Ctsk-/- than in Ctsk+/+ mice. Ctsk knockout mice exhibited more severe blood-brain barrier (BBB) disruption, with microvascular endothelial cells exhibiting greater VEGF expression and lower ratios of phospo-Akt/Akt and phospo-mTOR/mTOR than in Ctsk+/+ mice. This study is the first to provide molecular insights into Ctsk-regulated HT after cerebral ischaemia, suggesting that Ctsk deficiency may disrupt the BBB via Akt/mTOR/VEGF signalling, resulting in neurological deficits and neuron apoptosis. Ctsk administration has the potential as a novel modality for improving the safety of rtPA treatment following stroke.

Aurora-A is a novel predictor of poor prognosis in patients with resected lung adenocarcinoma.

BACKGROUND: The Aurora-A (Aur-A) gene, a key regulator of mitosis, has been proved as an oncogene in a variety of cancers. The Aur-A overexpression has been proved correlated with aggressiveness of cancer cells. However, the frequency of Aur-A protein overexpression, as well as its association with clinicopathologic parameters and prognosis remain unclear in lung adenocarcinoma (ADC). This study tried to clarify the clinical significance of Aur-A in patients with resected lung ADC. PATIENTS AND METHODS: A total of 142 informative patients with surgically resected lung ADC and 20 normal lung tissues were enrolled. Western blot and immunohistochemistry (IHC) were utilized to assess protein expression of Aur-A. RESULT: The expression of Aur-A was elevated in most of tumor tissues compared with the adjacent tissues by western blot. The IHC results showed that Aur-A protein was over-expressed in 98 of 142 (69.0%) tumor sections, while Aur-A was low-expressed in all normal lung sections. A positive correlation between Aur-A overexpression rate and ascending pathologic stages was observed (P<0.05). Kaplan-Meier analysis demonstrated that patients with Aur-A high expression had significantly inferior survival compared to those with Aur-A low expression. Both overall survival (OS) and disease-free survival (DFS) of positive overexpression patients were shorter than the negative group (P=0.036, P=0.041, respectively). Multivariate analysis confirmed that Aur-A expression, as an independent and significant factor for both DFS and OS, could predict a poor prognosis in patients with resected lung ADC (P=0.022, P=0.049, respectively). CONCLUSIONS: Aur-A was overexpressed in lung ADC and overexpression of Aur-A might be a novel predictor for poor prognosis and potential therapeutic target in lung ADC.

A sensitive flow injection chemiluminescence method for the determination of progesterone.

A sensitive flow injection (FI) chemiluminescence (CL) method was developed for the determination of trace amounts of progesterone. This method was based on the luminescent properties of the tris(1,10-phenanthroline) ruthenium(II) - potassium permanganate (KMnO4 ) - progesterone in acidic medium sensitized by Na2 SO3 . With the peak height as a quantitative parameter applying optimum conditions, the relative CL intensity was linear with progesterone concentration in the range of 1.0 × 10(-10) ∼ 6.0 × 10(-9) g·ml(-1) and 6.0 × 10(-9) ∼ 4.0 × 10(-8) g·ml(-1) with a detection limit of 7.1 × 10(-11) g·ml(-1) . The relative standard deviation (RSD) was 2.79% for 1.0 × 10(-8) g·ml(-1) progesterone (n = 11). The proposed method held low detection limit and was successfully applied to determination of progesterone in pharmaceutical preparations. The possible CL reaction mechanism was also discussed.

Effects of ischemic preconditioning on ischemia/reperfusion-induced arrhythmias by upregulatation of connexin 43 expression.

BACKGROUND: The susceptibility of hypertrophied myocardium to ischemia-reperfusion injury is associated with increased risk of postoperative arrhythmias. We investigate the effects of ischemic preconditioning (IP) on post-ischemic reperfusion arrhythmias in hypertrophic rabbit hearts. METHODS: Thirty-three rabbit models of myocardial hypertrophy were randomly divided into three groups of 11 each: non-ischemia-reperfusion group (group A), ischemia-reperfusion group (group B), and ischemic preconditioning group (group C). Another ten healthy rabbits with normal myocardium served as the healthy control group. Rabbit models of myocardial hypertrophy were induced by abdominal aortic banding. Surface electrocardiogram (ECG) was recorded and Curtis-Ravingerova score was used for arrhythmia quantification. Connexin 43 (Cx43) expression was assessed by immunohistochemistry. RESULTS: Ratios of heart weight to body weight and left ventricular weight to body weight increase significantly in the three groups compared with the healthy control group (p < 0.05). Arrhythmia incidence in group C is significantly lower than group B (p < 0.05). Curtis-Ravingerova score in group C is lower than group B (p < 0.05). Cx43 expression area in group A is smaller by comparison with the healthy control group (p < 0.05). Cx43 expression area and fluorescence intensity in group B are reduced by 60.9% and 23.9%, respectively, compared with group A (p < 0.05). In group C, Cx43 expression area increases by 32.5% compared with group B (p < 0.05), and decreases by 54.8% compared with group A (p < 0.05). CONCLUSIONS: The incidence of ischemia/reperfusion-induced arrhythmias in hypertrophic rabbit hearts decreases after IP, which plays an important protecting role on the electrophysiology of hypertrophied myocardium by up-regulating the expression of Cx43.

Cyclooxygenase-2 up-regulates vascular endothelial growth factor via a protein kinase C pathway in non-small cell lung cancer.

BACKGROUND: Vascular endothelial growth factor (VEGF) expression is up-regulated via a cyclooxygenase-2 (COX-2)-dependent mechanism in non-small cell lung cancer (NSCLC), but the specific signaling pathway involved is unclear. Our aim was to investigate the signaling pathway that links COX-2 with VEGF up-regulation in NSCLC. MATERIAL AND METHODS: COX-2 expression in NSCLC samples was detected immunohistochemically, and its association with VEGF, microvessel density (MVD), and other clinicopathological characteristics was determined. The effect of COX-2 treatment on the proliferation of NSCLC cells (A549, H460 and A431 cell lines) was assessed using the tetrazolium-based MTT method, and VEGF expression in tumor cells was evaluated by flow cytometry. COX-2-induced VEGF expression in tumor cells was monitored after treatment with inhibitors of protein kinase C (PKC), PKA, prostaglandin E2 (PGE2), and an activator of PKC. RESULTS: COX-2 over-expression correlated with MVD (P = 0.036) and VEGF expression (P = 0.001) in NSCLC samples, and multivariate analysis demonstrated an association of VEGF with COX-2 expression (P = 0.001). Exogenously applied COX-2 stimulated the growth of NSCLCs, exhibiting EC50 values of 8.95 × 10(-3), 11.20 × 10(-3), and 11.20 × 10(-3) µM in A549, H460, and A431 cells, respectively; COX-2 treatment also enhanced tumor-associated VEGF expression with similar potency. Inhibitors of PKC and PGE2 attenuated COX-2-induced VEGF expression in NLCSCs, whereas a PKC activator exerted a potentiating effect. CONCLUSION: COX-2 may contribute to VEGF expression in NSCLC. PKC and downstream signaling through prostaglandin may be involved in these COX-2 actions.

[Protective effects of metallothionein induced by dexamethasone against ischemia/reperfusion injury of myocardium of isolated rat heart].

OBJECTIVE: To investigate the protective effects of metallothionein (MT) induced by dexamethasone (DEX) against ischemia/reperfusion (I/R) injury of myocardium of isolated rat heart. METHODS: Thirty-two Sprague-Dawley (SD) rats were divided randomly into the DEX and control groups. In the former group, the rats were pretreated with DEX, and in latter group distilled water was given before their hearts were isolated for Langendorff perfusion and I/R. MT was assessed by Western blotting. The left ventricular developed pressure (LVDP), maximal change rate of intraventricular pressure rise/down (+/-dp/dt max), coronary artery flow (CF) and reperfusion arrhythmias were observed dynamically before ischemia and during 60-minute reperfusion following 30-minute ischemia, The hearts were perfused with triphenyltetrazolium (TTC) after 60-minute reperfusion. The myocardial infarct size was measured with Adobe Photoshop. The levels of MB isoenzyme of creatine kinase (CK-MB), malonaldehyde (MDA), total superoxide dismutase (T-SOD), CuZn-SOD, catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATPase, Ca2+-Mg2+-ATPase were detected. RESULTS: Compared with control group, the expression of MT was significantly increased (3.085+/-1.065 vs. 1.028+/-0.016, P<0.05), the LVDP, +/-dp/dt max and CF were greatly improved (all P<0.05), the accumulated point of ventricular arrhythmia and the infarct size were significantly reduced in DEX group [(2.00+/-1.41) scores vs. (6.63+/-4.24) scores and (28.38+/-11.22)% vs. (47.39+/-8.30)%, respectively, both P<0.01]. The level of CK-MB was significantly lowered in the DEX group compared with control group [(8.69+/-4.16)U/g vs. (18.15+/-5.59) U/g, P<0.01], and myocardium MDA content was decreased (P<0.05). Moreover, the levels of T-SOD, CuZn-SOD, CAT, GSH-Px, and the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased (P<0.05 or/and P<0.01) in DEX group. CONCLUSION: DEX induces upregulation of MT, which attenuates I/R injury in rat heart.