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Background: Converging data have suggested that monocytic inflammation and C-reactive protein (CRP) are biologically intertwined processes and are involved in diabetogenesis. This study aimed to investigate the association between systemic inflammation assessed by joint cumulative high-sensitivity C-reactive protein (CumCRP) and monocyte to high-density lipoprotein ratio (CumMHR) and incident type 2 diabetes (T2D) and their predictive value for T2D in a general population. Methods: A total of 40,813 nondiabetic participants from a prospective real-life cohort (Kailuan Study, China) were followed biennially from 2010/2011 until December 31, 2020. Multivariable Cox regression analyses were conducted to evaluate the adjusted hazard ratios (aHRs) of incident diabetes. Results: During a median follow-up of 7.98 (IQR: 5.74–8.87) years, 4848 T2D cases developed. CumMHR and CumCRP were alone or jointly associated with incident T2D after adjusting for potential confounders. Elevated CumMHR levels significantly increased the risk of incident diabetes in each CumCRP strata (P-interaction: 0.0278). Participants with concomitant elevations in CumMHR and CumCRP levels had the highest risk (aHR: 1.71, 95% CI 1.52–1.91) compared to both in the low strata. Notably, the coexposure-associated T2D risk was modified by age, sex, hypertension, dyslipidemia, and prediabetes status. C-statistics increased from 0.7377 to 0.7417 when CumMHR and CumCRP were added into the multivariable-adjusted model, with a net reclassification improvement (%) of 12.39 (9.39–15.37) (P < 0.0001). Conclusions: Cumulative hsCRP and MHR were both independently and jointly associated with an increased risk of T2D and their addition to established risk factors should improve risk prediction and reclassification of diabetes.

Type 2 diabetes (T2D) is a major health threat of our era and has become a health priority worldwide. Emerging evidence suggests that T2D is a main post-COVID-19 metabolic sequela, further exacerbating its epidemic. Inflammation and metabolic disorders are two hallmarks of T2D, and both have been shown to heighten the risk of incident diabetes. However, there are significant heterogeneities in the risks of incident diabetes with exposure to each of them. Notably, accumulated evidence suggests a closely intertwined biological process between them. It is unknown whether elevated inflammation could interact with metabolic disorders acting on diabetogenesis and explain the diabetic risk heterogeneity in metabolic disorders. Furthermore, different levels of inflammation have distinct sources. Low-grade systemic inflammation commonly results from metabolic disorders, whereas highgrade inflammation is indicative of an acute phase response, mainly initiated from acute infectious processes and acute stress. Currently, mainstream knowledge excludes highgrade inflammation for addressing the risk of cardiometabolic diseases and has seldom linked it to the pathophysiology of diabetes. Nonetheless, the alarmingly high incidence of T2D postacute SARS-CoV-2 infections has awakened a need to link infectious diseases to the development of T2D. This thesis aims to provide data-based epidemiological insights into the combined effect of different sources and levels of inflammation with a wide range of metabolic disorders on the development of diabetes and specifically considers the potential interactive effects between them. This thesis is composed of nine chapters: an overview of the thesis (Chapter 1); a comprehensive literature review (Chapter 2); six results chapters (Chapters 3–8); and a final chapter with a general discussion of the main findings and future directions (Chapter 9). The first chapter of the thesis includes an introduction and overview of the entire thesis. This is t

Live video streaming has grown dramatically in recent years. A key challenge is achieving high video quality of experience (QoE) in low-rate networks. To tackle this problem, recent streaming approaches strategically drop video frames, thus reducing the bandwidth required. However, these methods are usually designed for video on demand (VoD) services and perform poorly in live video streaming. In this paper, we design a new live video streaming approach, Reparo, which aims to improve users' QoE in low-rate networks. On the upload client side, Reparo discards video frames such that they are never encoded or transmitted. To decide which frames should be dropped, we design a real-time Video Frame Discarding (VFD) model, which strives to minimize the impact on video quality while maximizing bandwidth savings. To complement this, Reparo further proposes a modified adaptive bitrate algorithm and two encoding modes, targeting low-frame-rate encoding. On the server side, Reparo then recovers the dropped frames using a lightweight Video Frame Interpolation Deep Neural Network (VFI-DNN). Experimental results show that, compared with vanilla DASH, Reparo reaches an SSIM gain of 0.018, or reduces bandwidth consumption by 30.86%. With an average bandwidth of 0.974Mbps, it improves QoE by 18.13% on average compared to DASH. © 2023 ACM.

Deletion in the Xp22.31 region is increasingly suggested to be involved in the etiology of epilepsy. Little is known regarding the genomic and clinical delineations of X-linked epilepsy in the Chinese population or the sex-stratified difference in epilepsy characteristics associated with deletions in the Xp22.31 region. In this study, we reported two siblings with a 1.69 Mb maternally inherited microdeletion at Xp22.31 involving the genes VCX3A, HDHD1, STS, VCX, VCX2, and PNPLA4 presenting with easily controlled focal epilepsy and language delay with mild ichthyosis in a Chinese family with a traceable 4-generation history of skin ichthyosis. Both brain magnetic resonance imaging results were normal, while EEG revealed epileptic abnormalities. We further performed an exhaustive literature search, documenting 25 patients with epilepsy with gene defects in Xp22.31, and summarized the epilepsy heterogeneities between sexes. Males harboring the Xp22.31 deletion mainly manifested with child-onset, easily controlled focal epilepsy accompanied by X-linked ichthyosis; the deletions were mostly X-linked recessive, with copy number variants (CNVs) in the classic region of deletion (863.38 kb–2 Mb). In contrast, epilepsy in females tended to be earlier-onset, and relatively refractory, with pathogenic CNV sizes varying over a larger range (859 kb–56.36 Mb); the alterations were infrequently inherited and almost combined with additional CNVs. A candidate region encompassing STS, HDHD1, and MIR4767 was the likely pathogenic epilepsy-associated region. This study filled in the knowledge gap regarding the genomic and clinical delineations of X-linked recessive epilepsy in the Chinese population and extends the understanding of the sex-specific characteristics of Xp22.31 deletion in regard to epilepsy.