Delivery actuator for a transcervical sterilization device

The use of delivery systems in the human body for positioning and deploying implants, such as closure devices, dilation balloons, stents, coils and sterilization devices, are gaining more importance to preclude surgical incisions and general anesthesia. The majorities of the non-surgical medical devices are delivered in a low profile into human body form and subsequently require specialized operations for their deployment and release. An analogous procedure for permanent female sterilization is the transcervical approach that does not require either general anesthesia or surgical incision and uses a normal body passage. The objective of this paper is to detail the design, development and verification of an ergonomic actuator for a medical application. In particular, this actuator is designed for the deployment and release of an implant to achieve instant permanent female sterilization via the transcervical approach. This implant is deployed under hysteroscopic visualization and requires a sequence of rotary and linear operations for its deployment and release. More specifically, this manually operated actuator is a hand held device designed to transmit the required forces in a particular sequence to effect both implant deployment and release at a target location. In order to design the actuator and to investigate its mechanical behavior, a three-dimensional (3D) Computer Aided Design (CAD) model was developed and Finite Element Method (FEM) was used for simulations and optimization. Actuator validation was performed following a number of successful bench-top in-air deployments and in-vitro deployments in animal tissue and explanted human uteri. During these deployments it was observed that the actuator applied the required forces to the implant resulting in successful deployment. Initial results suggest that this actuator can be used single handedly during the deployment phase. The ongoing enhancement of this actuator is moving towards “first-in- man” clinical trials

Pb2+ tolerance by Frankia sp. strain EAN1pec involves surface-binding

Several Frankia strains have been shown to be lead-resistant. The mechanism of lead resistance was investigated for Frankia sp. strain EAN1pec. Analysis of the cultures by scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDAX) and Fourier transforming infrared spectroscopy (FTIR) demonstrated that Frankia sp. strain EAN1pec undergoes surface modifications and binds high quantities of Pb +2 . Both labelled and unlabelled shotgun proteomics approaches were used to determine changes in Frankia sp. strain EAN1pec protein expression in response to lead and zinc. Pb 2+ specifically induced changes in exopolysaccharides, the stringent response, and the phosphate (pho) regulon. Two metal transporters (a Cu2+-ATPase and cation diffusion facilitator), as well as several hypothetical transporters, were also upregulated and may be involved in metal export. The exported Pb2+ may be precipitated at the cell surface by an upregulated polyphosphate kinase, undecaprenyl diphosphate synthase and inorganic diphosphatase. A variety of metal chaperones for ensuring correct cofactor placement were also upregulated with both Pb+2 and Zn+2 stress. Thus, this Pb+2 resistance mechanism is similar to other characterized systems. The cumulative interplay of these many mechanisms may explain the extraordinary resilience of Frankia sp. strain EAN1pec to Pb+2. A potential transcription factor (DUF156) binding site was identified in association with several proteins identified as upregulated with heavy metals. This site was also discovered, for the first time, in thousands of other organisms across two kingdoms

Bioremediation of Heavy Metals

Exposure to lead (Pb), zinc (Zn), cadmium (Cd), copper (Cu), and selenite (SeO3−2) consider the main heavy metals that threat human health. These heavy metals can interfere with the function of vital cellular components. Soil heavy metal contamination represents risks to humans and the ecosystem through drinking of contaminated groundwater, direct ingestion or the food chain, and reduction in food quality. Bioremediation means cleanup of polluted environment via transformation of toxic heavy metals into less toxic form by microbes or its enzymes. Otherwise, bioremediation by microbes has limitations like production of toxic metabolites. The efflux of metal ions outside the cell, biosorption to the cell walls and entrapment in extracellular capsules, precipitation, and reduction of the heavy metal ions to a less toxic state are mechanisms to metals’ resistance

Liver Adiposity and Metabolic Profile in Individuals with Chronic Spinal Cord Injury

Purpose. To quantify liver adiposity using magnetic resonance imaging (MRI) and to determine its association with metabolic profile in men with spinal cord injury (SCI). Materials and Methods. MRI analysis of liver adiposity by fat signal fraction (FSF) and visceral adipose tissue (VAT) was completed on twenty participants. Intravenous glucose tolerance test was conducted to measure glucose effectiveness (g) and insulin sensitivity (i ). Lipid panel, fasting glucose, glycated hemoglobin (HbA1c), and inflammatory cytokines were also analyzed. Results. Average hepatic FSF was 3.7% ± 2.1. FSF was positively related to TG, non-HDL-C, fasting glucose, HbA1c, VAT, and tumor necrosis factor alpha (TNF-). FSF was negatively related to i and testosterone. FSF was positively related to VAT ( = 0.48, = 0.032) and TNF- ( = 0.51, = 0.016) independent of age, level of injury (LOI), and time since injury (TSI). The associations between FSF and metabolic profile were independent of VAT. Conclusions. MRI noninvasively estimated hepatic adiposity in men with chronic SCI. FSF was associated with dysfunction in metabolic profile, central adiposity, and inflammation. Importantly, liver adiposity influenced metabolic profile independently of VAT. These findings highlight the significance of quantifying liver adiposity after SCI to attenuate the development of metabolic disorders

Cell–cell signaling drives the evolution of complex traits: introduction—lung evo-devo

Physiology integrates biology with the environment through cell–cell interactions at multiple levels. The evolution of the respiratory system has been “deconvoluted” (Torday and Rehan in Am J Respir Cell Mol Biol 31:8–12, 2004) through Gene Regulatory Networks (GRNs) applied to cell–cell communication for all aspects of lung biology development, homeostasis, regeneration, and aging. Using this approach, we have predicted the phenotypic consequences of failed signaling for lung development, homeostasis, and regeneration based on evolutionary principles. This cell–cell communication model predicts other aspects of vertebrate physiology as adaptational responses. For example, the oxygen-induced differentiation of alveolar myocytes into alveolar adipocytes was critical for the evolution of the lung in land dwelling animals adapting to fluctuating Phanarezoic oxygen levels over the past 500 million years. Adipocytes prevent lung injury due to oxygen radicals and facilitate the rise of endothermy. In addition, they produce the class I cytokine leptin, which augments pulmonary surfactant activity and alveolar surface area, increasing selection pressure for both respiratory oxygenation and metabolic demand initially constrained by high-systemic vascular pressure, but subsequently compensated by the evolution of the adrenomedullary beta-adrenergic receptor mechanism. Conserted positive selection for the lung and adrenals created further selection pressure for the heart, which becomes progressively more complex phylogenetically in tandem with the lung. Developmentally, increasing heart complexity and size impinges precociously on the gut mesoderm to induce the liver. That evolutionary-developmental interaction is significant because the liver provides regulated sources of glucose and glycogen to the evolving physiologic system, which is necessary for the evolution of the neocortex. Evolution of neocortical control furthers integration of physiologic systems. Such an evolutionary vertical integration of cell-to-tissue-to-organ-to-physiology of intrinsic cell–cell signaling and extrinsic factors is the reverse of the “top-down” conventional way in which physiologic systems are usually regarded. This novel mechanistic approach, incorporating a “middle-out” cell–cell signaling component, will lead to a readily available algorithm for integrating genes and phenotypes. This symposium surveyed the phylogenetic origins of such vertically integrated mechanisms for the evolution of cell–cell communication as the basis for complex physiologic traits, from sponges to man

Frankia as a Biodegrading Agent

The Frankia actinorhizal plant symbiosis plays an important role in colonization of soils contaminated with toxic aromatic hydrocarbons. Our understanding of the bacterial partner, Frankia, in the actinorhizal symbiosis has been greatly facilitated by the availability of sequenced genomes. The analysis of these Frankia genomes has suggested that these bacteria are metabolically diverse and have potential for toxic aromatic hydrocarbon degradation. In this chapter, we explore what is known about that metabolic potential

Life Threatening haemoptysis in primary lung cancer-signet ring cell carcinoma

© 2020 The Author(s) Primary signet ring cell carcinoma of the lung is a rare non-small cell carcinoma of the lung with extremely aggressive features and poor prognosis. The diagnosis mainly required tissue biopsy with immunohistochemical analysis and gene mutation studies. We describe a unique case of primary signet ring cell carcinoma of the lung presenting with life threatening haemoptysis along with literature review of prognosis and management of this rare clinical entity