9DTact: A Compact Vision-Based Tactile Sensor for Accurate 3D Shape Reconstruction and Generalizable 6D Force Estimation

The advancements in vision-based tactile sensors have boosted the aptitude of robots to perform contact-rich manipulation, particularly when precise positioning and contact state of the manipulated objects are crucial for successful execution. In this work, we present 9DTact, a straightforward yet versatile tactile sensor that offers 3D shape reconstruction and 6D force estimation capabilities. Conceptually, 9DTact is designed to be highly compact, robust, and adaptable to various robotic platforms. Moreover, it is low-cost and easy-to-fabricate, requiring minimal assembly skills. Functionally, 9DTact builds upon the optical principles of DTact and is optimized to achieve 3D shape reconstruction with enhanced accuracy and efficiency. Remarkably, we leverage the optical and deformable properties of the translucent gel so that 9DTact can perform 6D force estimation without the participation of auxiliary markers or patterns on the gel surface. More specifically, we collect a dataset consisting of approximately 100,000 image-force pairs from 175 complex objects and train a neural network to regress the 6D force, which can generalize to unseen objects. To promote the development and applications of vision-based tactile sensors, we open-source both the hardware and software of 9DTact, along with a comprehensive video tutorial, all of which are available at https://linchangyi1.github.io/9DTact.Comment: Project Website: https://linchangyi1.github.io/9DTact

Sustained Thromboresistant Bioactivity with Reduced Intimal Hyperplasia of Heparin-Bonded PTFE Propaten Graft in a Chronic Canine Femoral Artery Bypass Model

Background: Bypass graft thrombosis remains a significant mode of failure in prosthetic graft revascularization. The purpose of this investigation was to evaluate the long-term thromboresistant effect of heparin-bonded expanded polytetrafluoroethylene (ePTFE) graft using Carmeda BioActive Surface technology in a canine model. Methods: Bilateral femorofemoral artery bypass grafts with ePTFE grafts were performed in 25 adult grayhound dogs. In each animal, a heparin-bonded ePTFE graft (Propaten, WL Gore) was placed on one side, whereas a control nonheparin graft was placed on the contralateral side. The graft patency was assessed at 1, 6, 12, 18, and 24 months (n = 5 per group) following the bypass. Heparin bioactivity of the graft material was analyzed. The effect of intimal hyperplasia was also assessed. Results: All bypass grafts were patent at 1 month. Significantly greater patency rates were noted in the Propaten group compared to the control group at 12, 18, and 24 months, which were 84%, 80%, and 80% vs. 55%, 35%, and 20%, respectively (P 0.05). Conclusions: Heparin-bonded ePTFE graft provides a thromboresistant surface and reduced anastomotic intimal hyperplasia at 2 years. The stable heparin bioactivity of the Propaten graft confers an advantage in long-term graft patency

Surgical intervention for complications caused by femoral artery catheterization in pediatric patients

AbstractPurpose: This study evaluated the risk factors and surgical management of complications caused by femoral artery catheterization in pediatric patients. Methods: From January 1986 to March 2001, the hospital records of all children who underwent operative repairs for complications caused by femoral artery catheterization were reviewed. A prospective cardiac data bank containing 1674 catheterization procedures during the study period was used as a means of determining risk factors associated with iatrogenic femoral artery injury. Results: Thirty-six operations were performed in 34 patients (age range, 1 week-17.4 years) in whom iatrogenic complications developed after either diagnostic or therapeutic femoral artery catheterizations during the study period. Non-ischemic complications included femoral artery pseudoaneurysms (n = 4), arteriovenous fistulae (n = 5), uncontrollable bleeding, and expanding hematoma (n = 4). Operative repairs were performed successfully in all patients with non-ischemic iatrogenic femoral artery injuries. In contrast, ischemic complications occurred in 21 patients. Among them, 14 patients had acute femoral ischemia and underwent surgical interventions including femoral artery thrombectomy with primary closure (n = 6), saphenous vein patch angioplasty (n = 6), and resection with primary anastomosis (n = 2). Chronic femoral artery occlusion (> 30 days) occurred in seven patients, with symptoms including either severe claudication (n = 4) or gait disturbance or limb growth impairment (n = 3). Operative treatments in these patients included ileofemoral bypass grafting (n = 5), femorofemoral bypass grafting (n = 1), and femoral artery patch angioplasty (n = 1). During a mean follow-up period of 38 months, no instances of limb loss occurred, and 84% of children with ischemic complications eventually gained normal circulation. Factors that correlated with an increased risk of iatrogenic groin complications that necessitated surgical intervention included age younger than 3 years, therapeutic intervention, number of catheterizations (≥ 3), and use of 6F or larger guiding catheter. Conclusion: Although excellent operative results can be achieved in cases of non-ischemic complications, acute femoral occlusion in children younger than 2 years often leads to less satisfactory outcomes. Operative intervention can provide successful outcome in children with claudication caused by chronic limb ischemia. Variables that correlated with significant iatrogenic groin complications included a young age, therapeutic intervention, earlier catheterization, and the use of a large guiding catheter. (J Vasc Surg 2001;33:1071-8.

Sustained Thromboresistant Bioactivity with Reduced Intimal Hyperplasia of Heparin-Bonded PTFE Propaten Graft in a Chronic Canine Femoral Artery Bypass Model

Background: Bypass graft thrombosis remains a significant mode of failure in prosthetic graft revascularization. The purpose of this investigation was to evaluate the long-term thromboresistant effect of heparin-bonded expanded polytetrafluoroethylene (ePTFE) graft using Carmeda BioActive Surface technology in a canine model. Methods: Bilateral femorofemoral artery bypass grafts with ePTFE grafts were performed in 25 adult grayhound dogs. In each animal, a heparin-bonded ePTFE graft (Propaten, WL Gore) was placed on one side, whereas a control nonheparin graft was placed on the contralateral side. The graft patency was assessed at 1, 6, 12, 18, and 24 months (n = 5 per group) following the bypass. Heparin bioactivity of the graft material was analyzed. The effect of intimal hyperplasia was also assessed. Results: All bypass grafts were patent at 1 month. Significantly greater patency rates were noted in the Propaten group compared to the control group at 12, 18, and 24 months, which were 84%, 80%, and 80% vs. 55%, 35%, and 20%, respectively (P 0.05). Conclusions: Heparin-bonded ePTFE graft provides a thromboresistant surface and reduced anastomotic intimal hyperplasia at 2 years. The stable heparin bioactivity of the Propaten graft confers an advantage in long-term graft patency

Differences in responses of platelets to fluid shear stress in patients with peripheral artery disease (PAD) and coronary artery disease (CAD).

Information on differences in platelet function between patients with peripheral arterial disease (PAD) and patients with coronary artery disease (CAD) is limited. We sought to examine the differences in the platelets response to shear stress in patients with PAD compared to those with CAD. Men with symptomatic PAD (ankle brachial index [ABI] \u3c 0.9; n = 29) were compared with similarly aged men with CAD (post coronary artery bypass grafting; n = 40) but without PAD. All participants were on aspirin, and none were on clopidogrel. We measured changes in shear-induced platelet aggregation (SIPA) and shear-induced P-selectin expression (SIPE) under fluid shear rates of 5000 and 10,000 s(-1)which are typically found in arterioles and stenosed arteries, respectively. Aggregation was also induced by a combined stimulation of collagen, fluid shear stress, and adenosine diphosphate (ADP) or epinephrine using a platelet function analyzer (PFA-100) as well as optical aggregometry (arachidonic acid, collagen and epinephrine). Analyses of covariance adjusted for age, aspirin dose, and statin use were used to estimate differences between the groups. Values of SIPA at fluid shear rates of 5000 and 10,000 s(-1) were significantly higher in the PAD group, while there were no differences between the PAD and CAD groups in SIPE at both fluid shear rates. However, baseline shear-induced P-selectin expression was higher in patients with PAD than CAD (mean fluorescence intensity [MFI] = 2.93 +/- 1.37 vs.1.94 +/- 0.67; p = 0.01), while the percentage increases in SIPA and SIPE at fluid shear rates of 5000 and 10,000 s(-1) were significantly higher in patients with CAD when compared to PAD (p \u3c 0.001 for all comparisons). Although there were several similarities in platelet function between men with PAD and men with CAD, significant differences in platelet responses to shear stress were observed in men with PAD when compared to those with CAD. Although the mechanism for these observed differences are not clear, we hypothesize that in vivo platelet activation in PAD patients may contribute to the differences and will need to be further investigated

Role of Sua5 in tRNA modification and translational regulation

The ribosome is a highly efficient machine, synthesizing polypeptides at a rate of ~20 amino acids per second. Multiple levels of regulation are required to maintain a high rate of protein synthesis at a low error frequency. The incorporation of amino acids by transfer RNAs (tRNAs) is a critical aspect of faithful translation. tRNAs have to be properly processed and modified to function in translation. Despite their small size, tRNAs contain extensive posttranscriptional nucleoside modifications. The formation ofN6-threonylcarbamoyladenosine (t6A) at nucleoside 37 in tRNAs decoding ANN (N= any base) is conserved across all domains of life. t6A is present next to the anticodon and in vitro work has demonstrated that the modified base stabilizes the codon:anticodon interaction to prevent frameshifting during the decoding process. However, there is a paucity of in vivo data to support the in vitro findings. Recently, Sua5 was described as a conserved protein required for the formation of t6A. To understand the functional role of Sua5 and the relevance of t6A in translation, we employed a variety of translational reporter assays. Our results conclude that cells depleted of Sua5 exhibit aberrant translation in all three phases: initiation, elongation and termination. These data provide in vivo evidence to support the role of Sua5 and t6A in maintaining translational fidelity. When we further investigated the role of Sua5 in tRNA homeostasis, we found that it exhibited synthetic sickness with a deletion inMAF1, a negative regulator of Pol III. This is consistent with the idea that increasing the pool of hypomodified tRNAs compounds the defects in codon misreading. Another consequence of Sua5-depletion is the loss of 40S ribosomes. To date, Xrn1 is the only exonuclease found to degrade mature 18S ribosomal RNA (rRNA). We found that Sua5 exhibits a genetic interaction with Xrn1. We provide preliminary data to show that Sua5 depletion slows down the decay of mutant rRNAs. Further analyses on the turnover of wild type and mutant rRNAs not engaged in translation in Sua5-depleted cells will shed light on the process of rRNA degradation

The Sua5 Protein Is Essential for Normal Translational Regulation in Yeast ▿

The anticodon stem-loop of tRNAs requires extensive posttranscriptional modifications in order to maintain structure and stabilize the codon-anticodon interaction. These modifications also play a role in accommodating wobble, allowing a limited pool of tRNAs to recognize degenerate codons. Of particular interest is the formation of a threonylcarbamoyl group on adenosine 37 (t6A37) of tRNAs that recognize ANN codons. Located adjacent and 3′ to the anticodon, t6A37 is a conserved modification that is critical for reading frame maintenance. Recently, the highly conserved YrdC/Sua5 family of proteins was shown to be required for the formation of t6A37. Sua5 was originally identified in a screen by virtue of its ability to affect expression from an aberrant upstream AUG codon in the cyc1 transcript. Together, these findings implicate Sua5 in protein translation at the level of codon recognition. Here, we show that Sua5 is critical for normal translation. The loss of SUA5 causes increased leaky scanning through AUG codons, +1 frameshifting, and nonsense suppression. In addition, the loss of SUA5 amplifies the 20S RNA virus found in Saccharomyces cerevisiae, possibly through an internal ribosome entry site-mediated mechanism. This study reveals a critical role for Sua5 and the t6A37 modification in translational fidelity

Nitrotyrosine promotes human aortic smooth muscle cell migration through oxidative stress and ERK1/2 activation

AbstractNitrotyrosine is a new biomarker of atherosclerosis and inflammation. The objective of this study was to determine the direct effects of free nitrotyrosine on human aortic smooth muscle cell (AoSMC) migration and molecular mechanisms. By a modified Boyden chamber assay, nitrotyrosine significantly increased AoSMC migration in a concentration-dependent manner. For example, nitrotyrosine at 300 nM increased AoSMC migration up to 152% compared with l-tyrosine-treated control cells (P<0.01). Cell wound healing assay confirmed this effect. Nitrotyrosine significantly increased the expression of some key cell migration-related molecules including PDGF receptor-B, matrix metalloproteinase 2 (MMP2) and integrins αV and β3 at both mRNA and protein levels in AoSMC (P<0.01). In addition, nitrotyrosine increased reactive oxygen species (ROS) production in AoSMC by staining with fluorescent dye DCFHDA. Furthermore, nitrotyrosine induced transient phosphorylation of ERK2 by Bio-Plex luminex immunoassay and western blot analysis. AoSMC were able to uptake nitrotyrosine. Antioxidants including seleno-l-methionine and superoxide dismutase mimetic (MnTBAP) as well as ERK1/2 inhibitor PD98059 effectively blocked the promoting effect of nitrotyrosine on AoSMC migration and the mRNA expression of above cell migration-related molecules. Thus, nitrotyrosine directly increases AoSMC migration in vitro and the expression of migration-related molecules through overproduction of ROS and activation of ERK1/2 pathway. Nitrotyrosine may contribute to cardiovascular pathogenesis