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This study carries out a case study of maintenance costs in a multi-family residential building built in 1982 in a mid-size city in Brazil. The condominium's monthly cost reports (maintenance fees) were analyzed for 30 years, between 1991 and 2021. This long period of analysis unprecedented in the literature. Expenses were classified by system and type of maintenance (preventive, corrective or modernization renovation). We identified that maintenance on elevator systems and gardens  summed up the highest costs throughout the period, while envelope conservation, sewage systems and water tanks presented the lowest costs. Disregarding the extreme years and correcting for inflation, the average expenditure on maintenance in the last 5 years (2017–2021) was 175% higher than the first 5 years analyzed (1991–1995), with the condominium fee being 43.6% higher. If the (predictable) maintenance expenses over the years were considered from the beginning of the building's operation, current families could be paying around 15% less in condominium fees. In conclusion, for an efficient maintenance management system, construction professional must focus on maintenance from the project design stage, provide a financial reserve for future upkeeping and renovation from the beginning of occupation, and prepare a robust user manual.

Malaria-associated acute respiratory distress syndrome (MA-ARDS) and acute lung injury (ALI) are complications that cause lung damage and often leads to death. The MA-ARDS/ALI is associated with a Type 1 inflammatory response mediated by T lymphocytes and IFN-γ. Here, we used the Plasmodium bergheiNK65 (PbN)-induced MA-ALI/ARDS model that resembles human disease and confirmed that lung CD4+and CD8+T cells predominantly expressed Tbet and IFN-γ. Surprisingly, we found that development of MA-ALI/ARDS was dependent on functional CCR4, known to mediate the recruitment of Th2 lymphocytes and regulatory T cells. However, in this Type 1 inflammation-ARDS model, CCR4 was not involved in the recruitment of T lymphocytes, but was required for the emergence of TNF-α/iNOS producing dendritic cells (Tip-DCs) in the lungs. In contrast, recruitment of Tip-DCs and development of MA-ALI/ARDS were not altered in CCR2−/−mice. Importantly, we showed that NOS2−/−mice are resistant to PbN-induced lung damage, indicating that reactive nitrogen species produced by Tip-DCs play an essential role in inducing MA-ARDS/ALI. Lastly, our experiments suggest that production of IFN-γ primarily by CD8+T cells is required for inducing Tip-DCs differentiation in the lungs and the development of MA-ALI/ARDS model.

Malaria-associated acute respiratory distress syndrome (MA-ARDS) and acute lung injury (ALI) are complications that cause lung damage and often leads to death. The MA-ARDS/ALI is associated with a Type 1 inflammatory response mediated by T lymphocytes and IFN-γ. Here, we used the Plasmodium bergheiNK65 (PbN)-induced MA-ALI/ARDS model that resembles human disease and confirmed that lung CD4+and CD8+T cells predominantly expressed Tbet and IFN-γ. Surprisingly, we found that development of MA-ALI/ARDS was dependent on functional CCR4, known to mediate the recruitment of Th2 lymphocytes and regulatory T cells. However, in this Type 1 inflammation-ARDS model, CCR4 was not involved in the recruitment of T lymphocytes, but was required for the emergence of TNF-α/iNOS producing dendritic cells (Tip-DCs) in the lungs. In contrast, recruitment of Tip-DCs and development of MA-ALI/ARDS were not altered in CCR2−/−mice. Importantly, we showed that NOS2−/−mice are resistant to PbN-induced lung damage, indicating that reactive nitrogen species produced by Tip-DCs play an essential role in inducing MA-ARDS/ALI. Lastly, our experiments suggest that production of IFN-γ primarily by CD8+T cells is required for inducing Tip-DCs differentiation in the lungs and the development of MA-ALI/ARDS model.