Introduction. SARS-CoV-2 infection causes immune disorders that create conditions for the reactivation of human herpesviruses (HHVs). However, the estimates of the HHVs effect on the course and ...outcome of COVID-19 are ambiguous. Аim – to study the possible relationship between the HHV reactivation and the adverse outcome of COVID-19. Materials and methods. Postmortem samples from the brain, liver, spleen, lymph nodes and lungs were obtained from 59 patients treated at the Moscow Infectious Diseases Hospital No.1 in 2021–2023. The group 1 comprised 39 patients with fatal COVID-19; group 2 (comparison group) included 20 patients not infected with SARS-CoV-2 who died from various somatic diseases. HHV DNA and SARS-CoV-2 RNA were determined by PCR. Results. HHV DNA was found in autopsy samples from all patients. In group 1, EBV was most often detected in lymph nodes (94%), HHV-6 in liver (68%), CMV in lymph nodes (18%), HSV in brain (16%), VZV in lung and spleen (3% each). The detection rates of HHVs in both groups was similar. Important differences were found in viral load. In patients with COVID-19, the number of samples containing more than 1,000 copies of HHV DNA per 100,000 cells was 52.4%, in the comparison group – 16.6% (p 0.002). An association has been established between the reactivation of HSV and HHV-6 and the severity of lung damage. Reactivation of EBV correlated with increased levels of liver enzymes. Conclusion. Reactivation of HHVs in patients with fatal COVID-19 was associated with severe lung and liver damages, which indicates a link between HHV reactivation and COVID-19 deaths.
Aquaporins represent proteins contributed to water transport through cell membrane. They are involved in formation and resolution of edema, cell migration and inflammatory reaction. There are only few ...studies linking the genetic polymorphism of aquaporin 5 (rs3759129 AQP5) and sepsis. At the same time, the apparent heterogeneity of patients along the foci of infection may limit finding the most significant association of AQP5 genotypes with the course of infectious complications of critical conditions and restrict further development of rs3759129 AQP5 as a potentially strong marker of sepsis outcome.The purpose of the study was to determine whether the preferential localization of the infection affects the prognostic value of the genetic marker AQP5 (1364A/C, rs3759129) in outcome prediction in sepsis (SEPSIS-3, 2016) patients.Materials and methods. Study groups (n=339) included ICU patients with abdominal sepsis (AS, including pancreatitits, peritonitis, cholecystitis, appendicitis; n=94) sepsis patients with other sources of infections (n=65) and ICU patients without sepsis (n=180). AQP5 polymorphism was studied by analyzing PCR products in a 2% agarose gel using a AQP5 1364A/C specific tetra primer set.Result. Distribution of alleles (A and C) and genotypes (AA, AC and CC) AQP5 1364A/C in patients with sepsis or sepsis subgroups (sepsis with no septic shock and sepsis shock patients) versus control group (healthy volunteers) did not differ. Although there was a trend to preferential survival of sepsis patients with genotype C AQP5 despite the source of infection, only patients with AQP5 CC or AC genotype and abdominal sepsis (Sepsis-3), or a subgroup of the same AQP5 genotype experiencing septic shock, demonstrated increased 30day survival versus AA homozygotic patients (P=0.002).Conclusion. The informative value of detecting the AQP5 CC or AC genotype for prognosis of 30-day survival versus AA homozygotic patients is most significant only in abdominal sepsis patients.
Previously the problem of the heat flux distribution at the semiconductor-substrate interface in the semiconductor-substrate transistor structure with adiabatic boundary condition on top of ...semiconductor was solved analytically. The method of images for two cases of a point and a linear heat sources located on the top of semiconductor layer was used to solve this problem. The substrate was considered as a half-space adjacent to the bottom of the semiconductor layer unlimited on the sides. It has been shown that even in the case of a perfect heat sink into substrate, the heat flow transverse dimension at the semiconductor-substrate interface has the order of thickness of the semiconductor layer. And with decreasing thermal conductivity of the substrate, this transverse dimension increases substantially. In our work, so far only for the case of a point heat source, a solution of a more general problem of heat propagation in the passivation-semiconductor-substrate transistor structure is obtained. Using the method of images, we calculate the transverse dimension of the heat flux at the semiconductor-substrate interface depending on the value of the thermal conductivity of the substrate for different values of the thermal conductivity of passivation. According to our study, the appearance of the heat sink into passivation leads to an increase in the transverse dimension of the heat flow at the semiconductor-substrate interface, although the proportion of heat going into the substrate decreases. Our research should help to optimize the design of transistor structures taking into account the heat transfer into passivation, which is relevant, for example, for high-power transistors based on wide band gap semiconductors, such as GaN and SiC, when the heat dissipation in the active region of the device, located close to passivation, is very high. In addition, our results confirm the previously developed practical recommendation for TCAD simulations with accounting for self-heating effect.
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