Animal models for the study of primary and secondary hypertension in humans.

This is the final version of the article. It first appeared from Spandidos Publications via http://dx.doi.org/10.3892/br.2016.784Hypertension is a significant cause of morbidity and mortality worldwide. It is defined as systolic and diastolic blood pressures (SBP/DBP) >140 and 90 mmHg, respectively. Individuals with an SBP between 120 and 139, or DBP between 80 and 89 mmHg, are said to exhibit pre-hypertension. Hypertension can have primary or secondary causes. Primary or essential hypertension is a multifactorial disease caused by interacting environmental and polygenic factors. Secondary causes are renovascular hypertension, renal disease, endocrine disorders and other medical conditions. The aim of the present review article was to examine the different animal models that have been generated for studying the molecular and physiological mechanisms underlying hypertension. Their advantages, disadvantages and limitations will be discussed.Biotechnology and Biological Sciences Research Council (Doctoral Training Award), Economic and Social Research Counci

Animal models of atherosclerosis.

Atherosclerosis is a significant cause of morbidity and mortality globally. Many animal models have been developed to study atherosclerosis, and permit experimental conditions, diet and environmental risk factors to be carefully controlled. Pathophysiological changes can be produced using genetic or pharmacological means to study the harmful consequences of different interventions. Experiments using such models have elucidated its molecular and pathophysiological mechanisms, and provided platforms for pharmacological development. Different models have their own advantages and disadvantages, and can be used to answer different research questions. In the present review article, different species of atherosclerosis models are outlined, with discussions on the practicality of their use for experimentation.GT was supported by a BBSRC Doctoral Training Award and thanks the Croucher Foundation of Hong Kong for the generous support of his clinical assistant professorship. YC is supported by the ESRC

Wireless Power Transmission on Biomedical Applications

Wireless power transmission (WPT) can provide an alternative for wireless power in implantable medical devices (IMDs). The WPT in implantable medical devices will involve many emerging biomedical topics, such as implantable pacemakers, optogenetic devices, and bio-impedance sensors. To this end, this chapter comprehensively reviews the recent WPT studies for those mentioned above emerging biomedical applications. The specific key components are carried out for those applications. Besides, the operation principle and system design are presented. In conclusion, this chapter’s significance can help evolve reliable implantable device development in the future

Electromagnetic Compatibility Issues in Medical Devices

Electromagnetic compatibility (EMC) in biomedical applications is a significant issue related to the user’s life safety, especially in implantable medical devices. Cardiovascular diseases and neurodegenerative disorders are the main chronic disease worldwide that rely on implantable treatment devices such as cardiac pacemakers and vagus nerve stimulators. Both devices must have high EMC to avoid electromagnetic interference-induced health risks, even death during the treatment. Thus, it is important to understand how EMI can affect implantable devices and proactively protect devices from electromagnetic interference, providing reliable and safe implantable device therapy. To this end, this chapter comprehensively introduces the clinical issues and provides EMC requirements for the implantable device such as a cardiac pacemaker and vagus nerve stimulator. The significance of this chapter is to present the EMC important issues in medical engineering that can help to evolve reliable and secure implantable device development in the future

Animal models of atherosclerosis.

Atherosclerosis is a significant cause of morbidity and mortality globally. Many animal models have been developed to study atherosclerosis, and permit experimental conditions, diet and environmental risk factors to be carefully controlled. Pathophysiological changes can be produced using genetic or pharmacological means to study the harmful consequences of different interventions. Experiments using such models have elucidated its molecular and pathophysiological mechanisms, and provided platforms for pharmacological development. Different models have their own advantages and disadvantages, and can be used to answer different research questions. In the present review article, different species of atherosclerosis models are outlined, with discussions on the practicality of their use for experimentation.GT was supported by a BBSRC Doctoral Training Award and thanks the Croucher Foundation of Hong Kong for the generous support of his clinical assistant professorship. YC is supported by the ESRC

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

A 9 bp cis-element in the promoters of class I small heat shock protein genes on chromosome 3 in rice mediates L-azetidine-2-carboxylic acid and heat shock responses

In rice, the class I small heat shock protein (sHSP-CI) genes were found to be selectively induced by L-azetidine-2-carboxylic acid (AZC) on chromosome 3 but not chromosome 1. Here it is shown that a novel cis-responsive element contributed to the differential regulation. By serial deletion and computational analysis, a 9 bp putative AZC-responsive element (AZRE), GTCCTGGAC, located between nucleotides –186 and –178 relative to the transcription initiation site of Oshsp17.3 was revealed. Deletion of this putative AZRE from the promoter abolished its ability to be induced by AZC. Moreover, electrophoretic mobility shift assay (EMSA) revealed that the AZRE interacted specifically with nuclear proteins from AZC-treated rice seedlings. Two AZRE–protein complexes were detected by EMSA, one of which could be competed out by a canonical heat shock element (HSE). Deletion of the AZRE also affected the HS response. Furthermore, transient co-expression of the heat shock factor OsHsfA4b with the AZRE in the promoter of Oshsp17.3 was effective. The requirement for the putative AZRE for AZC and HS responses in transgenic Arabidopsis was also shown. Thus, AZRE represents an alternative form of heat HSE, and its interaction with canonical HSEs through heat shock factors may be required to respond to HS and AZC

Differences in cardiovascular outcomes between men and women with acute pancreatitis

INTROduCTION The risk of cardiovascular disease increases in patients with acute pancreatitis (AP). However, it remains unknown whether this increase varies between sexes. ObjECTIvEs Our aim was to assess sex differences in cardiovascular outcomes in AP patients during long‑term follow‑up. PATIENTs ANd mEThOds The participants were recruited from the United Kingdom Biobank, which is a population‑based cohort study consisting of 502 368 individuals aged 40–69 years old. Cardiovascular outcomes were defined as major cardiovascular and cerebrovascular adverse events (MACCEs), en‑ compassing all‑cause death, myocardial infarction, and stroke. We compared sex difference in MACCE incidence using incidence rate per 1000 person‑years. The association between sex and MACCE risk was assessed using the Cox proportional hazards models and win ratio method, adjusted for demographic, lifestyle, metabolic factors, and medication use. REsuLTs A total of 1371 participants with AP were included, 42.5% were men. Over the median (interquartile range) follow‑up of 13.9 (13–14.7) years, 226 MACCEs occurred. The incidence rate of MACCE was 16.44 for men and 9.8 for women. The multivariate Cox regression analysis indicated a higher risk of MACCEs in men than in women (hazard ratio [HR], 1.8; 95% CI, 1.36–2.38). Adjusted HR for all‑cause mortality, myocardial infarction, and stroke were 1.49, 2.75, and 1.67, respectively. The adjusted win ratio by inverse probability of treatment weighting was 0.55 (P <0.001), suggesting a worse outcome in men. CONCLusIONs Men experienced more adverse cardiovascular outcomes than women in long follow‑up after AP, suggesting a need for sex‑specific management strategies in AP patients