Dear Receptor Polymorphisms for Hypertension Prediction
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Solution Overview
Problem
Current methods for identifying genetic markers for hypertension and managing angiogenesis are inadequate, with no reliable genetic marker for hypertension and unsatisfactory clinical results for inhibiting or stimulating angiogenesis.
Innovation Solution
Identification of mutations and polymorphisms in the Dual Endothelin-1/Angiotensin II Receptor (Dear) that enhance ET-1 binding, allowing for prediction of hypertension susceptibility and modulation of angiogenesis through Dear inhibitors or activators.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If separate receptors for ET-1 and AngII are used, then specific physiological responses are achieved, but the ability to predict hypertension susceptibility and modulate angiogenesis is insufficient
Solution Approach 1:
The patent combines the functions of ET-1 and AngII receptors into a single dual receptor (Dear) that can bind both ligands. This merging approach enables the receptor to mediate both vasoconstriction and angiogenesis pathways simultaneously, improving prediction accuracy for hypertension susceptibility while reducing system complexity compared to using separate receptors for each ligand.
Solution Approach 2:
The Dear receptor exhibits multi-functionality by serving as a binding target for both ET-1 and AngII, thereby integrating multiple physiological functions (blood pressure regulation and angiogenesis) into a single receptor system. This universality allows for more comprehensive diagnostic and therapeutic applications in hypertension and cancer-related conditions.
2Measurement precision
If current methods are used for identifying genetic markers, then some genetic information is obtained, but accurate prediction of hypertension and reliable angiogenesis modulation is not achieved
Solution Approach 1:
The patent uses polymorphisms in the Dear receptor as intermediary markers that link genetic information to clinical outcomes. These polymorphisms serve as measurable indicators that correlate with hypertension susceptibility and angiogenesis potential, enabling more accurate prediction and reliable clinical intervention strategies.
Solution Approach 2:
The invention focuses on detecting specific parameter changes in the Dear receptor sequence (polymorphisms at positions 44 and 74) that correlate with disease susceptibility. By measuring these specific genetic parameters, the patent achieves more precise identification of individuals at risk for hypertension and those who may respond to angiogenesis modulation therapies.
3Measurement precision
If Dear polymorphisms are detected, then hypertension susceptibility can be predicted, but the complexity of genetic analysis increases
Solution Approach 1:
The patent applies local quality analysis by focusing genetic screening on specific, predetermined positions (44 and 74) in the Dear receptor sequence where polymorphisms are most informative. This targeted approach maintains high prediction precision while minimizing the overall complexity of genetic analysis compared to whole-genome sequencing or analysis of multiple positions.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
Enables accurate prediction of hypertension and modulation of angiogenesis, providing effective diagnostic and therapeutic strategies for hypertension and cancer-related conditions.
Implementation Method 1
Functional analysis has shown that both ET-1 and AngII bind to Dear and induce coupling to a Ca2+ mobilizing transduction system
Data Source
AI summary
The present application is directed to the identification of mutations and/or polymorphisms in the Dual Endothelin-1/Angiotensin II Receptor (Dear) that indicate susceptibility to, or show current affliction with, hypertension. Additionally, the present invention discloses methods for the modulation of angiogenesis via the regulation of Dear.