Study of ossicular chain defects in patients with chronic otitis media

<p><strong>Background:</strong> Chronic otitis media (COM) is a long-standing disease of middle ear cleft and mastoid cavity having a permanent perforation in the tympanic membrane with or without discharge. It’s a worldwide health problem and it is still predominant in the modern antibiotic era. Aim<strong> </strong>was to determine the prevalence and types of ossicular chain defect in mucosal and squamosal type of COM. Also, to evaluate the hearing loss in relation to ossicular chain defect.</p><p><strong>Methods:</strong> The study was prospective observational study conducted in Bhopal over the duration of one year (January 2019 to June 2020). Patient aged 11-70 years reporting with COM were included in the study. Details regarding sociodemographic profile and extensive examination were recorded. Data was entered into MS excel 2007, analysis was done.</p><p><strong>Results:</strong> It was more prevalent in the age groups of 21-30years (39%) with female (53%) preponderance. Right sided ear was commonly involved (58%). Majority of the patients had tubo-tympanic disease (62%) whereas 38% had attico-antral disease. Ossicular chain was found intact in 33% cases. Average hearing loss was maximum (67.6 dBHL) when all ossicles are eroded. Hearing loss was minimum (33.6 dBHL) with isolated handle of malleus involvement.</p><p><strong>Conclusions:</strong> COM is one of the commonest causes of preventable hearing impairment in our society, hence early diagnosis and timely intervention is needed. Awareness among patients and doctors regarding the need for better ear hygiene is necessary.</p>

Atomic Scale Mechanisms Controlling the Oxidation of Polyethylene: A First Principles Study

Understanding the degradation mechanisms of aliphatic polymers by thermal oxidation and radio-oxidation is very important in order to assess their lifetime in a variety of industrial applications. We focus here on polyethylene as a prototypical aliphatic polymer. Kinetic models describing the time evolution of the concentration of chain defects and radicals species in the material identify a relevant step in the formation and subsequent decomposition of transient hydroperoxides species, finally leading to carbonyl defects, in particular ketones. In this paper, we first summarize the most relevant mechanistic paths proposed in the literature for hydroperoxide formation and decomposition and, second, revisit them using first principles calculations based on Density Functional Theory (DFT). Our results partially confirm commonly accepted reaction energies, but also propose alternative, more favourable, reaction paths. We highlight the influence of the environment—crystalline or not—on the outcome of some of the studied chemical reactions. A remarkable result of our calculations is that hydroxyl radicals play an important role in the decomposition of hydroperoxides. Based on our findings, it should be possible to improve the set of equations and parameters used in current kinetic simulations of polyethylene radio-oxidation.

Mitochondrial disease

Mitochondrial encephalomyopathies are caused by primary defects of the respiratory chain that lead to disturbed generation of adenosine triphosphate by aerobic metabolism. This characteristically impairs the function of high-demand tissues such as the brain, eye, cardiac, and skeletal muscle, as well as endocrine organs. The numerous proteins involved are encoded by genes in mitochondrial or nuclear DNA. Mutations in these genes can lead to clinical disorders. Disorders of intermediary metabolism (such as fatty acid β‎-oxidation or tricarboxylic acid cycle defects) involve mitochondrial enzymes, but the term ‘mitochondrial disease’ usually means a disease which is due to an abnormality of the final common pathway of energy metabolism—the mitochondrial respiratory chain, which is linked to the production of adenosine triphosphate by oxidative phosphorylation. The respiratory chain is essential for aerobic metabolism, and respiratory chain defects characteristically affect tissues and organs that are heavily dependent upon oxidative metabolism.