Broussardbagger3918

South America is the current epicenter of COVID-19 pandemic. Yet, the epidemiological and clinical features of the disease have not been described in Brazil, the third most affected country in the world.

In this retrospective study, we describe the demographics, epidemiology and clinical features of the first 557 consecutive patients positive for SARS-CoV-2 living in Pernambuco state, Northeast Brazil.

The first COVID-19 cases occurred in the high income population. The age of infected patients ranged from 27 days to 97 years with a median of 47 years. The ratio of males to female in the SARS-CoV-2-infected group was 0.831. The most common symptom was cough (74.51%), followed by fever (66.79%), dyspnea (56.01%), sore throat (28.19%) and O

saturation <95% (24.42%). 86.44% of the lethal cases were patients older than 51 years. The median time from illness onset to diagnosis was 4.0 days (range 0-39 days) Severe patients diagnosed after 14 days of symptoms onset had higher viral load than patients with mild disease.

Our study provides important information about COVID-19 in the tropics and will assist physicians and health officials to face the current pandemics as SARS-CoV-2 continues to spread in the human population.

Our study provides important information about COVID-19 in the tropics and will assist physicians and health officials to face the current pandemics as SARS-CoV-2 continues to spread in the human population.

This study aims to explore the role of M2a polarization and formyl peptide receptor (FPR) regulation in the reactivation of Mycobacterium tuberculosis (Mtb) infection.

M1/M2a monocyte percentage and FPR1/2/3 protein expression of blood immune cells were measured in 38 patients with sputum culture (+) active pulmonary TB disease, 18 subjects with latent TB infection (LTBI), and 28 noninfected healthy subjects (NIHS) using flow cytometry method.

M1 percentage was decreased in active TB versus either NIHS or LTBI group, while M2a percentage and M2a/M1 percentage ratio were increased. FPR1 expression on M1/M2a, FPR2 expression on M1, and FPR3 expression of M1 were all decreased in active TB versus LTBI group, while FPR1 over FPR2 expression ratio on NK T cell was increased in active TB versus either NIHS or LTBI group. In 11 patients with active TB disease, M1 percentage became normal again after anti-TB treatment. In vitro Mtb-specific antigen stimulation of monocytic THP-1 cells resulted in M2a polarization in association with increased FPR2 expression on M2a.

Increased M2a and decreased M1 phenotypes of blood monocyte may serve as a marker for active TB disease, while decreased FPR1 on blood monocyte may indicate LTBI status.

Increased M2a and decreased M1 phenotypes of blood monocyte may serve as a marker for active TB disease, while decreased FPR1 on blood monocyte may indicate LTBI status.Perfluorooctanoic acid (PFOA) has attracted widespread research attention as it is very stable, bioaccumulates, and causes reproductive toxicity. Data from several animal experiments and epidemiological studies indicate that female fertility may decline because of ovarian granulosa cell (GC) apoptosis as oocyte quality is positively associated with effective gap junctional intercellular communication (GJIC) between GCs. To the best of our knowledge, however, no previous trials have been conducted or reported on the effects of PFOA exposure on apoptosis induction in human GCs. Moreover, the roles of GJIC in GC survival and in the induction of apoptosis in GCs by PFOA remain unclear. To test this, we cultured human GCs in vitro and treated them with 0 μM, 0.3 μM, 3 μM, or 30 μM PFOA for 24 h. We also treated a human ovarian GC line (KGN) with various combinations of PFOA, retinoic acid (RA, 10 μM), and carbenoxolone disodium (CBX, 50 mM). Ruboxistaurin Our findings showed that PFOA lowered human GC viability and increased apoptosis. The effects of CBX resemble those of PFOA. The combination of PFOA and CBX enhances the inhibition of GJIC by PFOA and promotes apoptosis. The effects of RA are the opposite to those of PFOA. The combination of RA and PFOA mitigates PFOA-induced GJIC inhibition and reduces apoptosis. The observed expression levels of apoptosis-related proteins were consistent with the aforementioned findings. Hence, our study demonstrated that PFOA may induce human ovarian GC apoptosis by inhibiting GJIC.Deficient or excessive quantities of essential trace elements (ETEs)1 in the fetal environment can compromise developmental processes. We investigated whether concentrations of zinc (Zn), manganese (Mn), selenium (Se), cobalt (Co), molybdenum (Mo), and nickel (Ni) in umbilical cord tissue are associated with risk for neural tube defects (NTDs). Umbilical cord tissues from 166 cases of NTD cases and 166 matched controls were collected and element concentrations were measured using inductively coupled plasma-mass spectrometry. Associations between ETE concentrations and the risk for NTDs were estimated using multivariate logistic regression while adjusting for potential confounders. Bayesian kernel machine regression (BKMR) was used to examine the joint effects of these ETEs. We found that median concentrations of Ni were higher but those of Mo and Co were lower in the NTD group than in the control group. Co was the only element that was associated with NTD risk after adjusting for confounders (OR 0.31, 95 % CI 0.12-0.79 for the second and OR 0.37, 95 % CI 0.15-0.91 for the top tertile relative to the lowest tertile). The association between Co and NTD risk was confirmed with the BKMR model. In addition, a joint effect of the six ETE mixture on NTD risk was observed the risk decreased with the levels of the mixture from 25th percentile through 75th percentile. In conclusion, higher levels of Co were associated with lower risk for NTDs, and NTD risk decreased with the levels of the six ETEs as a co-exposure mixture, suggesting a protective effect.Investment in phenotypic drug discovery has led to increased demand for rapid and robust target deconvolution to aid successful drug development. Although methods for target identification and mechanism of action (MoA) discovery are flourishing, they typically lead to lists of putative targets. Validating which target(s) are involved in the therapeutic mechanism of a compound poses a significant challenge, requiring direct binding, target engagement, and functional studies in relevant physiological contexts. A combination of orthogonal approaches can allow target identification beyond the proteome as well as aid prioritisation for resource-intensive target validation studies.