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Evidence from prospective studies on the association between eating speed and metabolic syndrome is limited. We prospectively investigated the association between eating speed and metabolic syndrome in a Japanese working population.

Participants were 1018 workers (ages 19-68 y) without metabolic syndrome at baseline who completed both baseline and 3-y follow-up surveys. Eating speed was self-reported and categorized as slow, medium, or fast. Metabolic syndrome was defined using criteria recommended in a joint interim statement from several international societies. A multiple logistic regression was used to estimate the odds ratio of metabolic syndrome according to eating speed with adjustment for covariates, including total energy intake.

At the 3-y follow-up, 67 workers (6.6%) were newly identified as having metabolic syndrome. Fast eating speed was significantly associated with increased odds of developing metabolic syndrome, with multivariable-adjusted odds ratios for eating fast of 2.13 (95% confidence intervals, 1.23-3.68) compared with medium eating speed with an adjustment for covariates, including total energy intake. The association remained statistically significant after an additional adjustment for body mass index (BMI) and BMI change between baseline and follow-up surveys (odds ratio 1.95; 95% confidence interval, 1.06-3.56).

Fast eating speed was associated with an increased likelihood of developing metabolic syndrome independently of total energy intake, BMI at baseline, and BMI change during the follow-up period.

Fast eating speed was associated with an increased likelihood of developing metabolic syndrome independently of total energy intake, BMI at baseline, and BMI change during the follow-up period.The COVID-19 pandemic has rapidly spread around the world with significant morbidity and mortality in a subset of patients including the elderly. The poorer outcomes are associated with 'cytokine storm-like' immune responses, otherwise referred to as 'hyperinflammation'. While most of the infected individuals show minimal or no symptoms and recover spontaneously, a small proportion of the patients exhibit severe symptoms characterized by extreme dyspnea and low tissue oxygen levels, with extensive damage to the lungs referred to as acute respiratory distress symptom (ARDS). The consensus is that the hyperinflammatory response of the host is akin to the cytokine storm observed during sepsis and is the major cause of death. Uncertainties remain on the factors that lead to hyperinflammatory response in some but not all individuals. Hyperinflammation is a common feature in different viral infections such as dengue where existing low-titer antibodies to the virus enhances the infection in immune cells through a process called antibody-dependent enhancement or ADE. ADE has been reported following vaccination or secondary infections with other corona, Ebola and dengue virus. Detailed analysis has shown that antibodies to any viral epitope can induce ADE when present in sub-optimal titers or is of low affinity. In this review we will discuss ADE in the context of dengue and coronavirus infections including Covid-19.Distinct populations of Trypanosoma cruzi interact with mammalian cardiac muscle cells causing different inflammation patterns and low heart functionality. During T. cruzi infection, the extracellular ATP is hydrolyzed to tri- and/or diphosphate nucleotides, based on the infectivity, virulence, and regulation of the inflammatory response. T. cruzi carries out this hydrolysis through the T. cruzi ectonucleotidase, NTPDase-1 (TcNTPDase-1). This study aimed to evaluate the role of TcNTPDase-1 in culture rich in metacyclic trypomastigote forms (MT) and cell culture-derived trypomastigote forms (CT) from Colombiana (discrete typing unit - DTU I), VL-10 (DTU II), and CL (DTU VI) strains of T. cruzi. For this, we measured TcNTPDase-1 activity in suramin-treated and untreated parasites and infected J774 cells and C57BL/6 mice with suramin pre-treated parasites to assess parasitic and inflammatory cardiac profile in the acute phase of infection. Our data indicated a higher TcNTPDase-1 activity for ATP in culture rich in metacyclic trypomastigote forms from Colombiana strain in comparison to those from VL-10 and CL strains. The cell culture-derived trypomastigote forms from CL strain presented higher capacity to hydrolyze ATP than those from Colombiana and VL-10 strains. Suramin inhibited ATP hydrolysis in all studied parasite forms and strains. Suramin pre-treated parasites reduced J774 cell infection and increased nitrite production in vitro. In vivo studies showed a reduction of inflammatory infiltrate in the cardiac tissues of animals infected with cell culture-derived trypomastigote forms from suramin pre-treated Colombiana strain. In conclusion, TcNTPDase-1 activity in trypomastigotes forms drives part of the biological characteristics observed in distinct DTUs and may induce cardiac pathogenesis during T. cruzi infection.Human pluripotent stem cells offer a limitless source of cells for regenerative medicine. They are also highly valuable as tools to study development and pathologies or as cellular substrates to screen and test new drugs. find more We generated human induced pluripotent stem cell (hiPSC) lines from two unrelated healthy control donors. Peripheral blood mononuclear cells (PBMCs) from these donors were reprogrammed by non-integrative viral transduction, had normal karyotypes and expressed pluripotency hallmarks.

It is well-established that sleep regulates immune functions. Immunological functions are dependent on circadian rhythms and regular sleep as both have an impact on the magnitude of immune responses following antigenic challenge (eg, in vaccination). Here we investigated whether nocturnal shift work can influence post-vaccination response.

Thirty-four healthy workers (23 females) working either nocturnal or diurnal shifts (17 in each group) received the meningococcal C meningitis vaccine. Sleep was recorded polysomnographically (PSG) and with actigraphy. Humoral and cellular responses were assessed after vaccination.

Night workers showed decreased N3 stage and REM sleep duration, increased inflammatory mediators (TNF-α and IL-6 levels), and a weak specific humoral response to vaccination associated with reduced CD4 T lymphocytes, reduced plasmacytoid dendritic cells, reduced prolactin levels, increased T

and increased IL-10 levels. In addition, the decrease in total sleep time and circadian rhythm alterations were associated with a reduced humoral response post-vaccination.