Laboratory experiments were carried out to investigate the effects of rotation on turbulent convection. The experimental facility was a bottom-heated, water-filled, cubical tank mounted on a turntable. The investigations were performed over a wide range of bottom buoyancy fluxes qo and rotation rates Q, including sd = 0; qo and Q were held constant during each experiment. The depth of the water column H was fixed for the entire experimental programme. For the non-rotating experiments, the r.m.s. velocity fluctuations were found to scale well with the convective velocity w* = (qoH)i, while the mean and r.m.s. fluctuations of buoyancy were found to scale with qo/w*. The spectra of temperature fluctuations were measured and were used to assess the applicability of two types of scaling, one of which is advanced in the present study.For the rotating experiments, the convective-layer growth is affected by the rotation a t a height h, x 4.5(q0 The r.m.s. horizontal velocity of the rotationally affected mixed layer is uniform throughout the mixed layer and is given by (.l")i x 1.7(qOQ-')4. The time growth law of the mixed-layer thickness h,, when h, > h,, is given by h, x 0.7(q0Q-3)iQt, where t is the time. The rotational effects become important when the Rossby number is given by Ro = (u'2)1/QZr x 1.5, where the integral lengthscale is estimated as 1, x 0.25hC.The mean buoyancy gradient in the mixed layer was found to be much higher than in the corresponding non-rotating case, and the r.m.s. fluctuations and mean buoyancies were found to scale satisfactorily with (qo Q)t. A spectral form for the temperature fluctuations in rotating convection is also proposed and is compared to the experimental results.

The coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an ongoing major threat to global health and has posed significant challenges for the treatment of severely ill COVID-19 patients. Several studies have reported that cytokine storms are an important cause of disease deterioration and death in COVID-19 patients. Consequently, it is important to understand the specific pathophysiological processes underlying how cytokine storms promote the deterioration of COVID-19. Here, we outline the pathophysiological processes through which cytokine storms contribute to the deterioration of SARS-CoV-2 infection and describe the interaction between SARS-CoV-2 and the immune system, as well as the pathophysiology of immune response dysfunction that leads to acute respiratory distress syndrome (ARDS), multi-organ dysfunction syndrome (MODS), and coagulation impairment. Treatments based on inhibiting cytokine storm-induced deterioration and occurrence are also described.

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Aging is an important factor affecting the deterioration of patients with coronavirus disease 2019 (COVID-19). The aging and degeneration of various tissues and organs in the elderly lead to impaired organ function. Underlying conditions such as chronic lung disease, cardiovascular disease, and diabetes in aged patients are associated with higher mortality. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily interacts with the cell surface receptor angiotensin-converting enzyme (ACE) 2 and other accessory proteins such as 78 kDa glucoseregulated protein 78 (GRP78) and CD147. Thus, altered receptor signals in aging and chronic disease play a role in SARS-CoV-2 infection, and are associated with a higher risk of deterioration in different organs. In this review, after a brief introduction to the link between aging and receptors for SARS-CoV-2, we focus on the risk of deterioration in different organs of COVID-19 patients considering aging as the main factor. We further discuss the structural and/or physiological changes in the immune system and organs (lung, heart, kidney, vessels, nerve system), as well as those associated with diabetes, in aging patients, and speculate on the most likely mechanisms underlying the deterioration of COVID-19 patients.