Clinical and Experimental Medicine

We sought to explore the relationship between body mass index (BMI) and neurologic outcomes following acute COVID-19 infection. We conducted a retrospective electronic medical record-based cohort study enrolling adults with laboratory-confirmed acute COVID-19 infection who presented to 1 of 12 academic and community hospitals in Southwestern Ontario, Canada between April 1, 2020 and July 31, 2021. Primary subjective (anosmia, dysgeusia, and/or headache) and objective (aseptic meningitis, ataxia, delirium, encephalopathy, encephalitis, intracranial hemorrhage, ischemic stroke, and/or seizure) composite neurologic outcomes were assessed, comparing obese and overweight individuals to those with underweight/normal BMI indices, adjusting for baseline characteristics. Secondary outcomes (severity of illness, length of hospital stay, SARS-CoV-2 viral load, mortality) were similarly analyzed. A total of 1437 enrolled individuals, of whom 307 (21%), 456 (32%), and 674 (47%) were underweight/normal, overweight, and obese, respectively. On multivariable analysis, there was no association between BMI category and the composite outcome for subjective (odds ratio [OR] 1.17, 95% CI 0.84–1.64, Bonferroni p = 1.00 for obese; OR 1.02, 95% CI 0.70–1.48; Bonferroni p = 1.00 for overweight) and objective (OR 0.74, 95% CI 0.42–1.30, p = 0.29 for obese; OR = 0.80, 95% CI 0.45–1.43, p = 0.45 for overweight) neurologic manifestations. There was no association between BMI category and any secondary outcome measure and no evidence of effect modification by age or sex. This study demonstrates the absence of an association between BMI and neurologic manifestations following acute COVID-19 illness. Prospective studies using standardized data collection tools and direct measures of body fat are warranted to obtain more valid effect estimates.

We intend to evaluate the relationship between the rates of global SARS-CoV-2 vaccination and the number of COVID-19 confirmed cases, as well as the mortality rate after the declaration of a pandemic. Of the data from 191 countries at the time of data retraction, we selected 111 countries that have SARS-CoV-2 vaccination reports. We stratified countries into high-income and non-high-income countries (HIC and non-HIC) based on World Bank income-group. We used a fixed-effects model (FEM) and performed a longitudinal analysis. The number of confirmed cases decreased as the vaccination rates increased in both non-HICs (B =  − 0.027, T =  − 2.0) and HICs (B =  − 0.207, T =  − 17.5). The number of deaths decreased as the vaccination rates increased in both non-HICs (B =  − 0.151, T =  − 2.3) and HICs (B =  − 0.230, T =  − 40.9). For full vaccination, this measure had a negative association with daily confirmed cases and daily deaths in both non-HICs and HICs. In non-HICs, daily cases and daily deaths decreased as the first vaccination and full vaccination coverages increased. However in HICs, daily cases and daily deaths decreased as the first vaccination and full vaccination coverages increased in the early phase, but after a certain period, they tended to increase again. We observed a significant association between the increase in vaccination coverage in the real world and reduced daily confirmed cases and deaths. However, as the confirmed cases and deaths have rebounded in HICs, our findings indicate that COVID-19 is not completely prevented through vaccine distribution.

Residual HCV-RNA can persist in liver tissue and peripheral blood mononuclear cells (PBMCs) long after antiviral therapy of chronic hepatitis C in patients repeatedly negative for viral RNA in serum. This occult infection associates with impaired immune response and the risk of lymphoproliferative disorders or progressive liver disease. There are currently no monitoring strategies for patients after treatment. We investigated if serum inflammation markers and interferon lambda (IFNL) genotype can be predictors of the presence of HCV-RNA and the replicative HCV-RNA (−) strand in patients who reached sustained virological response after interferon-free therapy. Forty-two consecutive patients who remained HCV-RNA negative in serum 24 weeks after the end of treatment (EOT) and during the follow-up were enrolled. Total HCV-RNA and HCV-RNA (−) strand were detected using ultrasensitive RT-PCR in PBMCs collected 12–15 months after EOT. Polymorphisms within IFNL3–IFNL4 region (rs12979860 and ss469415590) were genotyped with allele-specific PCR. Viral RNA was found in PBMCs from 31 (74%) patients, and of those 29 (69%) were also positive for HCV-RNA (−). Neither normalization of alanine aminotransferase nor IFNL genotype predicted the presence of residual HCV-RNA. A significantly higher neutrocyte-to-lymphocyte ratio (NLR) 24 weeks after the start of treatment predicted elimination of replicative HCV-RNA strand (OR 0.23; 95% CI 0.10–0.86; P = 0.019). Patients with no HCV-RNA (−) in PBMCs showed a greater increase in neutrocyte count between EOT and baseline (P = 0.028). Lack of significant elevation of NLR after therapy with direct-acting antivirals could predict the presence of residual replicative HCV-RNA strand in PBMCs.

The function of the epithelial-to-mesenchymal transition (EMT) during hepatocellular carcinoma (HCC) progression is well established. However, the regulatory mechanisms modulating this phenomenon remain unclear. Homeobox B9 (HOXB9) has been proposed as an oncogene in many cancer developments, but its function and underlying mechanisms in HCC metastasis remain unknown. HOXB9 modulates EMT through the transforming growth factor-β1 (TGF-β1) pathway, which is a recognized regulator of EMT in HCC cells. The knockdown of HOXB9 decreased the migration and invasion of HCC cells. Conversely, the HOXB9 overexpression led to an increase in the above-mentioned phenotypes in HCC cells. Further analysis of HOXB9-regulated cellular functions showed the ability of this transcription factor to induce EMT. Moreover, we demonstrated that the TGF-β1 pathway is important in HOXB9-induced EMT in HCC cells. These findings define a novel cellular mechanism regulated by HOXB9, which controls EMT phenotype in HCC. This study is the first to illustrate the pivotal function of HOXB9 in regulating the metastatic behavior of HCC cells.

The background of this article is as follows: Few data are available about the persistence of serum-specific IgG antibodies to L. infantum after acute VL. The objective of this article is to evaluate the persistence of antibodies against L. infantum in patients healed from acute VL, and the kinetic of the same antibodies observed in 2 cases of VL relapse and 2 cases of resistance to therapy. The methods which we used to obtain our objective are the following: 55 apparently immunocompetent, HIV-negative patients were examined for antibodies to L. infantum by IFAT over 14 years period, and we got the following results: Serum-specific IgG antibodies titers decrease slowly, but constantly. In the patients with a diagnosis of VL relapse, the kinetic of antibodies was characterized by an initial reduction, and a subsequent antibody levels rapidly increase, while in the patients with a clinical and parasitological diagnosis of VL not responding to specific therapy, we demonstrated persistent high level of antibodies to L. infantum. Finally, we conclude that specific antibodies to L. infantum might persist for many years, and decrease slowly, but steadily. The persistence of these specific antibodies is not related to poor therapeutic response or prognosis, but an acute increase in their levels might be a sentinel of a VL relapse, while persistence of high antibody levels could suggest a resistance to therapy.