In this paper, we aim to establish a new mathematical model that relates pulse wave velocity (PWV) to blood pressure (BP) for continuous and noninvasive BP measurement. For the first time, we derive an ordinary differential equation (ODE) expressing the fundamental relation between BP, elastic modulus G and PWV. The general solution of this ODE is the mathematical BP-PWV model. In our model, the elastic modulus G is included in model parameters, unlike the existing theoretical models. This enables us to express the BP-PWV relationship for subjects of different ages and genders. A family of BP-PWV functions for specific age and gender groups can be obtained using statistical methods based on clinical trial data, which serve as the calibrated benchmark models for continuous and noninvasive BP measurement. To illustrate the modeling methodology, we construct benchmark models for people aged 19 and 60 and apply them to continuous diastolic blood pressure (DBP) measurement without individual calibration. The results of clinical tests meet the test standard in ANSI/AAMI SP10, which attests the feasibility of the modeling methodology.

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These results suggest that RJH-E inhibits the development of AD-like skin lesions in NC/Nga mice by suppressing the T-helper 2 cell response. Our results indicate that RJH treatment could provide an effective alternative therapy for the management of AD.

There is keen interest in continuous and noninvasive blood pressure (BP) measurement. However, many technologies have a shortcoming of complex mechanical structure. In our study, two arterial pulses are acquired by photoplethysmography (PPG) at ear and toe in order to explore a new method of measuring BP by pulse wave velocity (PWV). We previously validated and reported a BP-PWV mathematical model with measurements from humans with no evidence of cardiovascular disease, but were only able to determine PWV related to diastolic blood pressure (DBP). In this paper, we propose methods of identifying pulse transmit time (PTT) in low, normal and high systolic blood pressure (SBP) conditions. By averaging the PTT's of incident wave and reflected wave for non-systematic error reduction, we obtain a PWV that is suitable for estimating SBP. SBP and DBP are estimated by two separate PWV's based on the previously calibrated models. Experimental measurements are conducted on 26 subjects (age 19 ± 1 and 60 ± 1) with no evidence of cardiovascular disease. The measurement errors (Mean Deviation = 2.16 mmHg (SBP) and 1.49 mmHg (DBP); Standard Deviation = 6.23 mmHg (SBP) and 6.51 mmHg (DBP)) satisfy the accuracy criteria of Association for the Advancement of Medical Instrumentation. The results verify that SBP and DBP can be estimated by one mathematical model with the same model parameters and two separate PWV's.

The underlying molecular mechanisms of how dysregulated microRNAs (miRNAs) cause neurodegeneration after traumatic brain injury (TBI) remain elusive. Here we analyzed the biological roles of approximately 600 genes - we previously found these dysregulated in dying and surviving rat hippocampal neurons - that are targeted by ten TBI-altered miRNAs. Bioinformatic analysis suggests that neurodegeneration results from a global miRNA-mediated suppression of genes essential for maintaining proteostasis; many are hub genes - involved in RNA processing, cytoskeletal metabolism, intracellular trafficking, cell cycle progression, repair/maintenance, bioenergetics and cell-cell signaling - whose disrupted expression is linked to human disease. Notably, dysregulation of these essential genes would significantly impair synaptic function and functional brain connectivity. In surviving neurons, upregulated miRNA target genes are co-regulated members of prosurvival pathways associated with cellular regeneration, neural plasticity, and development. This study captures the diversity of miRNA-regulated genes that may be essential for cell repair and survival responses after TBI.