rPPG-MAE: Self-supervised Pre-training with Masked Autoencoders for Remote Physiological Measurement

Remote photoplethysmography (rPPG) is an important technique for perceiving human vital signs, which has received extensive attention. For a long time, researchers have focused on supervised methods that rely on large amounts of labeled data. These methods are limited by the requirement for large amounts of data and the difficulty of acquiring ground truth physiological signals. To address these issues, several self-supervised methods based on contrastive learning have been proposed. However, they focus on the contrastive learning between samples, which neglect the inherent self-similar prior in physiological signals and seem to have a limited ability to cope with noisy. In this paper, a linear self-supervised reconstruction task was designed for extracting the inherent self-similar prior in physiological signals. Besides, a specific noise-insensitive strategy was explored for reducing the interference of motion and illumination. The proposed framework in this paper, namely rPPG-MAE, demonstrates excellent performance even on the challenging VIPL-HR dataset. We also evaluate the proposed method on two public datasets, namely PURE and UBFC-rPPG. The results show that our method not only outperforms existing self-supervised methods but also exceeds the state-of-the-art (SOTA) supervised methods. One important observation is that the quality of the dataset seems more important than the size in self-supervised pre-training of rPPG. The source code is released at https://github.com/linuxsino/rPPG-MAE

U1RNP/lncRNA/Transcription Cycle Axis Promotes Tumorigenesis of Hepatocellular Carcinoma

As a component of the spliceosome, U1 small nuclear ribonucleoproteins (U1RNPs) play critical roles in RNA splicing, and recent studies have shown that U1RNPs could recruit long non-coding RNAs (lncRNAs) to chromatin which are involved in cancer development. However, the interplay of U1 snRNP, lncRNAs and downstream genes and signaling pathways are insufficiently understood in hepatocellular carcinoma (HCC). The expression of U1RNPs was found to be significantly higher in tumors than normal tissues in liver hepatocellular carcinomas of The Cancer Genome Atlas (TCGA-LIHC) dataset. LncRNAs with potential U1-binding sites (termed U1-lncRNAs) were found to be mostly located in the nucleus and their expression was higher in tumor than in normal tissues Bioinformatic analysis indicated that U1-lncRNAs worked with RNA-binding proteins and regulated the transcription cycle in HCC. A U1-lncRNA risk model was constructed using a TCGA dataset, and the AUCs of this risk model to predict 1-, 3- and 5-year overall survival were 0.82, 0.84 and 0.8, respectively. Furthermore, silencing of the small nuclear ribonucleoprotein D2 polypeptide (SNRPD2) resulted in impaired proliferation, G1/M cell cycle arrest and downregulation of transcription-cycle-related genes in HCC cell lines. Taken together, these results indicate that U1RNPs interact with lncRNAs and promote the transcription cycle process in HCC, which suggests that these could be novel biomarkers in the clinical management of HCC

Inhibition of Epac2 Attenuates Neural Cell Apoptosis and Improves Neurological Deficits in a Rat Model of Traumatic Brain Injury

Traumatic brain injury (TBI) is a major cause of mortality and disability worldwide. TBI-induced neuronal apoptosis is one of the main contributors to the secondary injury process. The aim of this study is to investigate the involvement of Exchange protein directly activated by cAMP 2 (Epac2) on TBI. We found that the expression level of Epac2 surrounding the injured area of brain in rats of TBI model was significantly increased at 12 h after TBI. The role of Epac2 in TBI was further explored by using a selective Epac2 antagonist ESI-05 to decrease the Epac2 expression. We discovered that inhibition of Epac2 could improve the neurological impairment and attenuate brain edema following TBI. The Epac2 inhibition effectively reduced neuronal cell death and P38 MAPK signaling pathway may be involved in this process. Our results suggest that inhibition of Epac2 may be a potential therapy for TBI by reducing the neural cell death, alleviating brain edema and improving neurologic deficits

Triple combination of HAIC-FO plus tyrosine kinase inhibitors and immune checkpoint inhibitors for advanced hepatocellular carcinoma: A systematic review and meta-analysis.

BackgroundThe triple combination of hepatic arterial infusion chemotherapy (HAIC) with fluorouracil, leucovorin, and oxaliplatin (FOLFOX) plus tyrosine kinase inhibitor (TKI) and immune checkpoint inhibitors (ICIs) is expected to have a synergistic anticancer effect in HCC. We conducted this meta-analysis to evaluate the efficacy and safety of the triple combination treatment in advanced HCC patients.MethodsPubMed, Embase, Cochrane Library, Web of Science databases were systematically searched for relevant studies from the inception of each database to May 10, 2023. All articles focusing the triple combination treatment of HAIC-FO plus TKI and ICIs for advanced HCC were eligible. The meta-analysis was conducted following the PRISMA guidelines. The risk of bias was assessed using the Joanna Briggs Institute (JBI) for case series and Newcastle-Ottawa Scale (NOS) for cohort studies. The primary outcomes were overall survival (OS), progression-free survival (PFS), objective response rate (ORR) and disease control rate (DCR). The secondary results were adverse events. Further meta-analysis of control studies demonstrated the superiority of the triple combination modality to TKI plus ICIs, and TKI alone.ResultsNine articles (four cohort studies and five one-arm studies) involving 777 advanced HCC patients were included in this meta-analysis. In terms of survival analysis, the pooled median PFS was 11 months (95% CI: 10.1-12.0 months) with low heterogeneity (I2 = 0%, p = 0.97). With regard to tumor response, the pooled ORR and DCR was 61.6% (I2=0%, p = 0.71) and 87.9% (I2 = 13%, p = 0.33) with low heterogeneity, respectively. As compared with TKIs plus ICIs, and TKIs alone, the triple combination thrapy was associated with improved median OS (HR=0.51, 95%CI 0.41-0.62) with low heterogeneity across studies (I2 = 0%, p = 0.47), median PFS (HR=0.51, 95%CI 0.41-0.64) with low heterogeneity across studies (I2 = 0%, p = 0.41), ORR (RR = 0.56, 95% CI: 0.42-0.74) with high heterogeneity across studies (I2 = 69%, p = 0.02), and DCR (RR = 0.38, 95%CI 0.27-0.54) with low heterogeneity across studies (I2 = 14%, p = 0.32). The most common 3/4 AEs were elevated ALT and AST, thrombocytopenia, hypertension, nausea and vomiting in this meta-analysis.ConclusionsThe triple combination therapy of HAIC-FO plus TKI and ICIs showed promising efficacy and safety in patients with advanced HCC.RegistrationThe protocol was registered with PROSPERO (ID:CRD42023424281)

P268S in NOD2 associates with susceptibility to Parkinson's disease in Chinese population

Fujian Province Natural Science Foundation Association of glucocerebrosidase gene mutations; Parkinson's disease in Chinese Han patients [2009D001]; Fujian Province Health Department Youth Research Projects Association of glutamate transporter gene and patients; Parkinson's disease [2009-2-72]; Fujian Province Science and Technology Department Key Project of The Screening of Susceptibility Gene in Parkinson's Disease; Platform Establishment of Molecular Diagnosis [2012D062]Background: The cause of almost all cases of Parkinson's disease (PD) remains unknown. Recent years have seen an explosion in the rate of discovery of genetic defects linked to PD. Different racial and geographical populations may have different distributions of genetic variants. Methods: In the current study, we screened the following genetic variants, including some rare mutations and single nucleotide polymorphisms (SNPs), in a pedigree and cases-controls. To best of our knowledge, we first screened these variants known to be associated with neurodegeneration disease, E46K (rs104893875) in SNCA, A1442P in LRRK2, IVS9 in PARK2, A350V in SLC41A1, P268S (rs2066842), R702W (rs2066844), G908R (rs2066845), 1007fs (rs2066847) in NOD2 and G2385R (rs34778348) in LRRK2 from southern China population. Genotyping was performed by jointly using primers overlapping polymerase chain reaction (PCR) site-directed mutagenesis, restriction fragment length polymorphism (RFLP), and capillary electrophoresis (CE). Results: We didn't discover above 9 variants in the family members of the pedigree. Furthermore, of 237 patients with sporadic Parkinson's disease and 190 controls, no heterozygosity or homozygosity were found from E46K, A1442P, A350V, R702W, G908R, or 1007fs but heterozygosity onto G2385R, IVS9, and P268S. No significant difference between cases and controls was found in both allele frequency (P = 0.572) and genotype frequency (P = 0.348) of IVS9. However, significant differences in genotype frequency (P = 0.009) of G2385R were consistent with prior observation. Eight patients with Parkinson's disease (2 women and 6 men are over the age of 50 years at onset of PD) carried the P268S heterozygous variation in NOD2. There was no heterozygosity or homozygosity of P268S in the controls. Genotype frequency of P268S (P = 0.0450) had significant differences. Conclusions: Our results suggested that the P268S variant in NOD2 might be a risk factor for susceptibility to sporadic Parkinson's disease in Chinese populations. It also implied that the inflammatory response may play a role in PD