Microstructure,Mechanical Properties,and Corrosion Behavior of Boron Carbide Reinforced Aluminum Alloy (Al-Fe-Si-Zn-Cu) Matrix Composites Produced via Powder Metallurgy Route

In this paper, Al-Fe-Si-Zn-Cu (AA8079) matrix composites with several weight percentages of B₄C (0, 5, 10, and 15) were synthesized by powder metallurgy (PM). The essential amount of powders was milled to yield different compositions such as AA8079, AA8079-5 wt.%B₄C, AA8079-10 wt.%B₄C, and AA8079-15 wt.%B₄C. The influence of powder metallurgy parameters on properties’ density, hardness, and compressive strength was examined. The green compacts were produced at three various pressures: 300 MPa, 400 MPa, and 500 MPa. The fabricated green compacts were sintered at 375 °C, 475 °C, and 575 °C for the time period of 1, 2 and 3 h, respectively. Furthermore, the sintered samples were subjected to X-ray diffraction (XRD) analysis, Energy Dispersive Analysis (EDAX), and Scanning Electron Microscope (SEM) examinations. The SEM examination confirmed the uniform dispersal of B₄C reinforcement with AA8079 matrix. Corrosion behavior of the composites samples was explored. From the studies, it is witnessed that the rise in PM process parameters enhances the density, hardness, compressive strength, and corrosion resistance.     

Spinal mepivacaine with fentanyl for outpatient knee arthroscopy surgery: a randomized controlled trial

Background

The foremost limitation of local anesthetic solutions for spinal anesthesia in the outpatient setting is prolonged motor blockade and delayed ambulation. The purpose of this study was to determine if the addition of intrathecal fentanyl to low-dose spinal mepivacaine provides adequate anesthesia with shorter duration of functional motor blockade for ambulatory knee surgery compared with spinal mepivacaine alone.

Methods

Following institutional review board approval and informed consent, 34 patients undergoing unilateral knee arthroscopy were enrolled in this study. The patients were randomly assigned to receive either 30 mg of isobaric mepivacaine 1.5% plus fentanyl 10 μg (M + F group) or 45 mg of isobaric mepivacaine 1.5% alone (M group) intrathecally. Postoperatively, the times to achieve sensory block regression to the S1 dermatome and to attain functional motor block recovery enabling ambulation were recorded. All assessments were blinded.

Results

The time to completion of Phase I recovery was shorter in the M + F group (104.6 ± 28.4 min) than in the M group (129.1 ± 30.4 min; P = 0.023). Regression of sensory blockade to S1 was earlier in the M + F group (118.4 ± 53.5 min) than in the M group (169.7 ± 38.9 min; P = 0.003). Patients in the M + F group (176.4 ± 40.3 min) were able to ambulate significantly earlier than those in the M group (205.6 ± 31.4 min; P = 0.025). No cases of transient or persistent neurological dysfunction were noted.

Conclusions

When compared with 45 mg isobaric mepivacaine 1.5%, an intrathecal dose of 30 mg isobaric mepivacaine 1.5% plus 10 μg fentanyl produces reliable anesthesia, hastens block regression, shortens stay in Phase I recovery, and enables earlier ambulation for patients undergoing unilateral knee arthroscopy (Registration no. NCT00803725).     

NAD(P)H Oxidase Mediates TGF-β1–Induced Activation of Kidney Myofibroblasts

TGF-β1 expression closely associates with activation and conversion of fibroblasts to a myofibroblast phenotype and synthesis of an alternatively spliced cellular fibronectin variant, Fn-ED-A. Reactive oxygen species (ROS), such as superoxide, which is a product of NAD(P)H oxidase, also promote the transition of fibroblasts to myofibroblasts, but whether these two pathways are interrelated is unknown. Here, we examined a role for NAD(P)H oxidase–derived ROS in TGF-β1–induced activation of rat kidney fibroblasts and expression of α-smooth muscle actin (α-SMA) and Fn-ED-A. In vitro, TGF-β1 stimulated formation of abundant stress fibers and increased expression of both α-SMA and Fn-ED-A. In addition, TGF-β1 increased both the activity of NADPH oxidase and expression of Nox2 and Nox4, homologs of the NAD(P)H oxidase family, indicating that this growth factor induces production of ROS. Small interfering RNA targeted against Nox4 markedly inhibited TGF-β1–induced stimulation of NADPH oxidase activity and reduced α-SMA and Fn-ED-A expression. Inhibition of TGF-β1 receptor 1 blocked Smad3 phosphorylation; reduced TGF-β1–enhanced NADPH oxidase activity; and decreased expression of Nox4, α-SMA, and Fn-ED-A. Diphenyleneiodonium, an inhibitor of flavin-containing enzymes such as the Nox oxidases, had no effect on TGF-β1–induced Smad3 but reduced both α-SMA and Fn-ED-A protein expression. The Smad3 inhibitor SIS3 reduced NADPH oxidase activity, Nox4 expression, and blocked α-SMA and Fn-ED-A, indicating that stimulation of myofibroblast activation by ROS is downstream of Smad3. In addition, TGF-β1 stimulated phosphorylation of extracellular signal–regulated kinase (ERK1/2), and this was inhibited by blocking TGF-β1 receptor 1, Smad3, or the Nox oxidases; ERK1/2 activation increased α-SMA and Fn-ED-A. Taken together, these results suggest that TGF-β1–induced conversion of fibroblasts to a myofibroblast phenotype involves a signaling cascade through Smad3, NAD(P)H oxidase, and ERK1/2.Progression of renal fibrosis involves expansion of interstitial myofibroblasts and extracellular matrix accumulation, resulting in the loss of function and ultimately renal failure.^1,2 The origin of myofibroblasts is under extensive investigation, and evidence indicates the cells may be derived from several sources, including an expansion of activated resident fibroblasts, perivascular adventitial cells, blood-borne stem cells that migrate into the glomerular mesangial or interstitial compartment, or tubular epithelial-to-mesenchymal transition and migration into the peritubular interstitial space. Regardless of their origin, there is common agreement that the myofibroblast is the cell most responsible for interstitial expansion and matrix accumulation during the course of renal fibrosis. TGF-β1 is the predominant growth factor responsible for matrix synthesis by mesenchymal cells such as fibroblasts in vitro and during renal fibrosis.^3,4 Indeed, there is a close correlation in the cellular expression of TGF-β1, a fibroblast transition to an activated, α-smooth muscle actin (α-SMA)-positive myofibroblast phenotype, and synthesis of an alternatively spliced isoform of fibronectin, Fn-ED-A.⁵ TGF-β1 differentially regulates the expression of Fn-ED-A in fibroblasts^6–8 and induces expression of α-SMA in a variety of mesenchymal cells in culture.^9,10 Indeed, a functional ED-A domain is mandatory for α-SMA induction by TGF-β1.^7,8,10 Moreover, TGF-β1 is frequently associated with a myofibroblast phenotype in liver, lung, and kidney disease,^1,11–13 and all three proteins frequently co-localize in these disease settings. In addition, a co-localization of α-SMA and Fn-ED-A is frequently observed in fibrotic disease as well as in glomerular and interstitial lesions in kidney diseases previously investigated in our laboratory.^14–17Accumulating evidence also indicates that reactive oxygen species (ROS), mainly in the form of superoxide, play a significant role in the initiation and progression of cardiovascular^18,19 and renal^20–25 disease. ROS are involved in distinct cell functions, including hypertrophy, migration, proliferation, apoptosis, and regulation of extracellular matrix.^25–28 More specific, the NAD(P)H oxidases of the Nox family have gained heightened attention as mediators of injury associated with vascular diseases, including hypertension, atherosclerosis, heart disease, and diabetes.^18,19,29,30 NAD(P)H oxidase generation of superoxide is recognized as an important mediator of cell proliferation in glomerulonephritis²² and matrix accumulation in diabetic nephropathy^25,31–33 and fibrosis.^21,24 Adventitial fibroblasts are also a major source of superoxide in the aorta,^19,34–36 therefore being highly relevant to renal disease. This is because the renal perivascular space is noticeably reactive and is the site where myofibroblasts may first appear during the course of renal disease and fibrosis.^17,37–39The observations that both TGF-β1 and ROS induce fibroblasts to α-SMA–positive myofibroblast phenotype^40–42 suggest that these two pathways are interrelated and may share signaling pathways in kidney disease. TGF-β signaling occurs through a well-established process involving two downstream pathways: Smad and extracellular signal–regulated kinase (ERK).^43–45 TGF-β/Smad signaling (Smad2 and Smad3) is tightly controlled by mitogen-activated protein kinase (MAPK; ras/MEK/ERK) signaling cascades.⁴⁶ A regulatory role for ROS in PDGF and angiotensin II–induced signal transduction has gained recognition^47,48; however, a role for ROS in TGF-β signaling is less well understood. It is also unknown whether kidney myofibroblasts express NAD(P)H oxidase homologs or generate ROS in response to TGF-β1. Given TGF-β1–induced myofibroblast activation and matrix synthesis during renal disease may be linked to ROS, we examined a role for NAD(P)H oxidase in TGF-β1–induced Smad3 and ERK signaling as well as kidney myofibroblast activation, as assessed by a switch to an α-SMA–positive phenotype and expression of Fn-ED-A expression in vitro.     

Intra-articular benign fibrous histiocytoma in the knee joint

We report a rare case of benign fibrous histiocytoma presenting as an intra-articular tumor in the knee joint causing pain and limitation of movements. This is the first case reported with no attachment to tendinous or ligamentous structures.     

Evaluation of BacT/Alert 3D automated unit for detection of nontuberculous mycobacteria requiring incubation at 30 degrees C for optimal growth

The reliability of the BacT/Alert 3D unit for automated detection of nontuberculous mycobacteria (NTM) that grow optimally at 30 °C was assessed. This system reliably maintained a temperature of 30 °C and detected 50% of the clinical NTM strains (5 Mycobacterium marinum and 3 Mycobacterium gordonae strains) faster than 37 °C culture.