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The fuel called biogas is obtained through anaerobic digestion of different types of organic waste, providing a way to tap the energy stored in organic matter. The use of this fuel is also attractive from the standpoint of global warming because its application does not register a net emission of carbon dioxide into the atmosphere. One possible use for this fuel is to feed the spark-ignition internal combustion engines. In the present, there is little information available about the process of combustion in internal combustion engines fueled by biogas. The combustion process of an internal combustion engine ignition powered by biogas is characterized in terms of the duration of combustion, i.e., depending on the time elapsed while the reactants (methane and oxygen) are transformed into products (mainly carbon dioxide and water). This study numerically evaluates the way in which the geometrical parameters such as the compression ratio and operating parameters like engine speed, the excess air, the time of spark timing and carbon dioxide content of biogas affect the evolution of the combustion process. To carry out this study, a five factors and two levels experiment was designed and conducted, based on which, the most influential parameters were identified. Equations expressing the combustion characteristic parameters, as a function of the geometric and operation parameters of a spark ignited engines, are delivered as a result

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In the modern diet, excessive fructose intake (>50 g/day) had been driven by the increase, in recent decades, of the consumption of sugar-sweetened beverages. This phenomenon has dramatically increased within the Caribbean and Latin American regions. Epidemiological studies show that chronic high intake of fructose related to sugar-sweetened beverages increases the risk of developing several non-communicable diseases, such as chronic obstructive pulmonary disease and asthma, and may also contribute to the exacerbation of lung diseases, such as COVID-19. Evidence supports several mechanisms—such as dysregulation of the renin–angiotensin system, increased uric acid production, induction of aldose reductase activity, production of advanced glycation end-products, and activation of the mTORC1 pathway—that can be implicated in lung damage. This review addresses how these pathophysiologic and molecular mechanisms may explain the lung damage resulting from high intake of fructose.