To ensure adequate intensive care unit (ICU) capacity for SARS-CoV-2 patients, elective neurosurgery and neurosurgical ICU capacity were reduced. Further, the Finnish government enforced strict restrictions to reduce the spread. Our objective was to assess changes in ICU admissions and prognosis of traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) during the Covid-19 pandemic.

Retrospective review of all consecutive patients with TBI and aneurysmal SAH admitted to the neurosurgical ICU in Helsinki from January to May of 2019 and the same months of 2020. The pre-pandemic time was defined as weeks 1-11, and the pandemic time was defined as weeks 12-22. The number of admissions and standardized mortality rates (SMRs) were compared to assess the effect of the Covid-19 pandemic on these. Standardized mortality rates were adjusted for case mix.

Two hundred twenty-four patients were included (TBI n = 123, SAH n = 101). There were no notable differences in case mix between TBI and SAH patients admitted during the Covid-19 pandemic compared with before the pandemic. No notable difference in TBI or SAH ICU admissions during the pandemic was noted in comparison with early 2020 or 2019. SMRs were no higher during the pandemic than before.

In the area of Helsinki, Finland, there were no changes in the number of ICU admissions or in prognosis of patients with TBI or SAH during the Covid-19 pandemic.

In the area of Helsinki, Finland, there were no changes in the number of ICU admissions or in prognosis of patients with TBI or SAH during the Covid-19 pandemic.

Adherence is a critical issue in the treatment of obstructive sleep apnea with continuous positive airway pressure (CPAP). Approximately 40% of patients treated with CPAP are at risk of discontinuation or insufficient use (< 4 h/night). Assuming that the first few days on CPAP are critical for continued treatment, we tested the predictive value at day 14 (D14) of the Philips Adherence Profiler™ (AP) algorithm for adherence at 3 months (D90).

The AP™ algorithm uses CPAP machine data hosted in the database of EncoreAnywhere™. This retrospective study involved 457 patients (66% men, 60.0 ± 11.9 years; BMI = 31.2 ± 5.9 kg/m

; AHI = 37.8 ± 19.2; Epworth score = 10.0 ± 4.8) from the Pays de la Loire Sleep Cohort. At D90, 88% of the patients were adherent as defined by a mean daily CPAP use of ≥ 4 h.

In a univariate analysis, the factors significantly associated with CPAP adherence at D90 were older age, lower BMI, CPAP adherence (≥ 4 h/night) at D14, and AP™ prediction at D14. In a multivariate analysis, only older age (OR 2.10 [1.29-3.41], p = 0.003) and the AP™ prediction at D14 (OR 16.99 [7.26-39.75], p < 0.0001) were significant predictors. CPAP adherence at D90 was not associated with device-derived residual events, nor with the levels of pressure or leakage except in the case of very significant leakage when it persisted for 90 days.

Automatic telemonitoring algorithms are relevant tools for early prediction of CPAP therapy adherence and may make it possible to focus therapeutic follow-up efforts on patients who are at risk of non-adherence.

Automatic telemonitoring algorithms are relevant tools for early prediction of CPAP therapy adherence and may make it possible to focus therapeutic follow-up efforts on patients who are at risk of non-adherence.The current study evaluated the outcome of dietary folate modulations on the expression of tumor suppressor genes (TSGs) during developmental stages of hepatocellular carcinoma (HCC) in a Wistar rat model. In addition to dietary folate modulations, male rats were administered diethylnitrosamine (DEN) intraperitoneally once a week upto 18 weeks to induce HCC. Serum folate levels were found to be decreased and increased in folate deficiency (FD) and folate-oversupplemented (FO) groups respectively when compared to folate normal (FN) rats. Apoptosis was observed in FD in fibrosis and HCC stages. mRNA expression analysis by RT-PCR of TSGs (DPT, p16, RUNX3, RASSF1A and SOCS1) and protein expression by western blot (RASSF1A, RUNX3 and p16) depicted differential expression in FD and FO in various stages of HCC development. Bisulfite sequencing for p16 and RASSF1A promoter was performed. The promoter region of p16 gene was hypermethylated at 7th and that of RASSF1A was hypomethylated at 10th CpG in cirrhotic category in FD rats. Hyper and hypomethylation at 10th and 24th CpG respectively in RASSF1A promoter was observed in HCC category in both FD and FO groups. Edralbrutinib All TSGs showed differential expression at transcript and protein level. Increased expression of DPT, RASSF1A, SOCS1 and decreased expression of RUNX3 could be playing role in HCC development in FD rats. Reduced expression of RUNX3, RASSF1A and SOCS1 in HCC category was demonstrated in FO rats. Thus, the studied TSGs are differentially expressed with dietary folate modulations during the development of HCC in DEN-treated rat model and the promoter methylation might be a contributing mechanism under these conditions.

Vogt-Koyanagi-Harada (VKH) disease is a rare autoimmune disease. The autoimmune response in VKH disease is against the melanin-producing cells; therefore, in affected individuals melanocyte-containing organs manifest disease symptoms including eyes, ears, skin and nervous system. VKH is a multifactorial disease, and the precise cause of the VKH disease is unknown. Studies have suggested that both environmental and genetic factors are responsible for the VKH disease. In this review, the authors have collected all the available literature on the genetics of VKH to their knowledge and discussed the role of genetic variants in causing VKH disease.

An extensive literature search was performed in order to review all the published studies regarding VKH clinical phenotyping and genetic variants in VKH disease. Medline, PubMed, Cochrane library, and Scopus was searched using combination of keywords.

It was found that variants in HLA genes, IL-12b, TNFSF4, and miR-20-5p genes are significantly associated with VKH; however, variants in genes ATG10, TNIP1 and CLEC16A did not achieve significant genome-wide association threshold. Moreover, polymorphisms in TNIP1 and CLEC16A play a protective role against VKH.

The authors conclude that increased sample size and a more homogeneous VKH patient population may reveal a significant association of variants in ATG10, TNIP1 and CLEC16A genes with VKH disease.

The authors conclude that increased sample size and a more homogeneous VKH patient population may reveal a significant association of variants in ATG10, TNIP1 and CLEC16A genes with VKH disease.