Importance Approximately 125 million people worldwide have psoriasis. Patients with psoriasis experience substantial morbidity and increased rates of inflammatory arthritis, cardiometabolic diseases, and mental health disorders. Observations Plaque psoriasis is the most common variant of psoriasis. The most rapid advancements addressing plaque psoriasis have been in its pathogenesis, genetics, comorbidities, and biologic treatments. Plaque psoriasis is associated with a number of comorbidities including psoriatic arthritis, cardiometabolic diseases, and depression. For patients with mild psoriasis, topical agents remain the mainstay of treatment, and they include topical corticosteroids, vitamin D analogues, calcineurin inhibitors, and keratolytics. The American Academy of Dermatology-National Psoriasis Foundation guidelines recommend biologics as an option for first-line treatment of moderate to severe plaque psoriasis because of their efficacy in treating it and acceptable safety profiles. Specifically, inhibitors to tumor necrosis factor α (TNF-α) include etanercept, adalimumab, certolizumab, and infliximab. Other biologics inhibit cytokines such as the p40 subunit of the cytokines IL-12 and IL-13 (ustekinumab), IL-17 (secukinumab, ixekizumab, bimekizumab, and brodalumab), and the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab, and mirikizumab). Biologics that inhibit TNF-α, p40IL-12/23, and IL-17 are also approved for the treatment of psoriatic arthritis. Oral treatments include traditional agents such as methotrexate, acitretin, cyclosporine, and the advanced small molecule apremilast, which is a phosphodiesterase 4 inhibitor. The most commonly prescribed light therapy used to treat plaque psoriasis is narrowband UV-B phototherapy. Conclusions and Relevance Psoriasis is an inflammatory skin disease that is associated with multiple comorbidities and substantially diminishes patients’ quality of life. Topical therapies remain the cornerstone for treating mild psoriasis. Therapeutic advancements for moderate to severe plaque psoriasis include biologics that inhibit TNF-α, p40IL-12/23, IL-17, and p19IL-23, as well as an oral phosphodiesterase 4 inhibitor.

Pathophysiology, Clinical Presentation, and Treatment of Psoriasis: A Review

In the past decade, significant progress has been made in complex disease research across multiple omics layers from genome, transcriptome and proteome to metabolome. There is an increasing awareness of the importance of biological interconnections, and much success has been achieved using systems biology approaches. However, because of the typical focus on one single omics layer at a time, existing systems biology findings explain only a modest portion of complex disease. Recent advances in multi-omics data collection and sharing present us new opportunities for studying complex diseases in a more comprehensive fashion, and yet simultaneously create new challenges considering the unprecedented data dimensionality and diversity. Here, our goal is to review extant and emerging network approaches that can be applied across multiple biological layers to facilitate a more comprehensive and integrative multilayered omics analysis of complex diseases.

/pdf/network-approaches-to-systems-biology-analysis-of-complex-4hix66d8o2.pdf

Network approaches to systems biology analysis of complex disease: integrative methods for multi-omics data.

Network approaches to systems biology analysis of complex disease: integrative methods for multi-omics data

During the last two to three decades our understanding of the immunobiology of periodontal disease has increased exponentially, both with respect to the microbial agents triggering the disease process and the molecular mechanisms of the host engagement maintaining homeostasis or leading to collateral tissue damage. These foundational scientific findings have laid the groundwork for translating cell phenotype, receptor engagement, intracellular signaling pathways and effector functions into a 'picture' of the periodontium as the host responds to the 'danger signals' of the microbial ecology to maintain homeostasis or succumb to a disease process. These findings implicate the chronicity of the local response in attempting to manage the microbial challenge, creating a 'Double Indemnity' in some patients that does not 'insure' health for the periodontium. As importantly, in reflecting the title of this volume of Periodontology 2000, this review attempts to inform the community of how the science of periodontal immunology gestated, how continual probing of the biology of the disease has led to an evolution in our knowledge base and how more recent studies in the postgenomic era are revolutionizing our understanding of disease initiation, progression and resolution. Thus, there has been substantial progress in our understanding of the molecular mechanisms of host-bacteria interactions that result in the clinical presentation and outcomes of destructive periodontitis. The science has embarked from observations of variations in responses related to disease expression with a focus for utilization of the responses in diagnosis and therapeutic outcomes, to current investigations using cutting-edge fundamental biological processes to attempt to model the initiation and progression of soft- and hard-tissue destruction of the periodontium. As importantly, the next era in the immunobiology of periodontal disease will need to engage more sophisticated experimental designs for clinical studies to enable robust translation of basic biologic processes that are in action early in the transition from health to disease, those which stimulate microenvironmental changes that select for a more pathogenic microbial ecology and those that represent a rebalancing of the complex host responses and a resolution of inflammatory tissue destruction.

Periodontal disease immunology: 'double indemnity' in protecting the host.

Clinical significance and immunobiology of IL-21 in autoimmunity

Genome-wide interaction-based association (GWIBA) analysis has the potential to identify novel susceptibility loci. These interaction effects could be missed with the prevailing approaches in genome-wide association studies (GWAS). However, no convincing loci have been discovered exclusively from GWIBA methods, and the intensive computation involved is a major barrier for application. Here, we developed a fast, multi-thread/parallel program named ‘‘pair-wise interaction-based association mapping’’ (PIAM) for exhaustive two-locus searches. With this program, we performed a complete GWIBA analysis on seven diseases with stringent control for false positives, and we validated the results for three of these diseases. We identified one pair-wise interaction between a previously identified locus, C1orf106, and one new locus, TEC, that was specific for Crohn’s disease, with a Bonferroni corrected P,0.05 (P=0.039). This interaction was replicated with a pair of proxy linked loci (P=0.013) on an independent dataset. Five other interactions had corrected P,0.5. We identified the allelic effect of a locus close to SLC7A13 for coronary artery disease. This was replicated with a linked locus on an independent dataset (P=1.09610 27 ). Through a local validation analysis that evaluated association signals, rather than locus-based associations, we found that several other regions showed association/interaction signals with nominal P,0.05. In conclusion, this study demonstrated that the GWIBA approach was successful for identifying novel loci, and the results provide new insights into the genetic architecture of common diseases. In addition, our PIAM program was capable of handling very large GWAS datasets that are likely to be produced in the future.

/pdf/genome-wide-interaction-based-association-analysis-1wc7juvxeb.pdf

Genome-Wide Interaction-Based Association Analysis Identified Multiple New Susceptibility Loci for Common Diseases

Background
Copy number variations (CNV) are important causal genetic variations for human disease; however, the lack of a statistical model has impeded the systematic testing of CNVs associated with disease in large-scale cohort

/pdf/novel-association-strategy-with-copy-number-variation-for-2eyfwbru05.pdf

Novel association strategy with copy number variation for identifying new risk Loci of human diseases.

In this paper, a framework of opportunistic beamforming for multiuser MIMO downlink employing rateless codes is considered. By exploiting the benefits of a combination of opportunistic beamforming and rateless codes, the system performance is obviously improved while guaranteeing QoS requirement, such as maximum average delay. It is proved that, in order to satisfying delay constraint, the maximum number of admissible users is bounded. With the purpose of achieving a balance between throughput and feedback, a novel concept of netput is introduced accordingly. Through maximizing the netput, the optimal feedback threshold in terms of the number of user, the maximum delay constraint, transmit power and the arrival rate of user data at the base station (BS) is derived. Moreover, the impact of feedback delay on the netput is investigated in detail and the corresponding feedback threshold is given. Finally, our theoretical claims are validated by the numerical results.

Opportunistic Beamforming for Multiuser MIMO Downlink Employing Rateless Codes with Delay Constraint

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Genome-Wide Interaction-Based Association Analysis Identified Multiple New Susceptibility Loci for Common Diseases

Novel association strategy with copy number variation for identifying new risk Loci of human diseases.

Opportunistic Beamforming for Multiuser MIMO Downlink Employing Rateless Codes with Delay Constraint