AIM Agent for Uremic Toxin Reduction in Felids With Severe Renal Failure
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Solution Overview
Problem
There is no effective method to suppress the progression of uremia in Felids suffering from severe renal failure, as the binding mechanism of apoptosis inhibitor of macrophage (AIM) with IgM pentamers is very strong, leading to insufficient clearance of dead cell debris and eventual renal function decline.
Innovation Solution
Administering apoptosis inhibitor of macrophage (AIM), an AIM fragment, or a nucleic acid encoding AIM to Felids with severe renal failure, defined by specific blood indoxyl sulfate and inorganic phosphorus concentrations, to reduce uremic toxin levels without improving renal function.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Object-affected harmful factors
If AIM is administered to Felids with severe renal failure, then the concentration of uremic toxins in the blood is reduced, but renal function cannot be recovered
Solution Approach 1:
The invention extracts and addresses the specific problem of uremic toxin accumulation in Felids with severe renal failure. By administering AIM, the patent targets and removes harmful uremic toxins from the blood without making unrealistic claims about recovering renal function, thus resolving the contradiction between toxin reduction and functional recovery.
Solution Approach 2:
The invention converts the harmful accumulation of uremic toxins into a treatable condition by using AIM to specifically target and clear these toxins. The strong binding between AIM and IgM pentamers, which initially seemed to cause insufficient clearance, is leveraged to achieve effective toxin removal despite the strong binding characteristic.
2Ease of operation
If the binding between AIM and IgM pentamers is very strong, then AIM is highly internalized by phagocytes, but dead cell debris is not cleared sufficiently in Felids
Solution Approach 1:
The invention introduces exogenous AIM as an intermediary substance to compensate for the insufficient endogenous AIM-IgM interaction in Felids. By administering external AIM, the patent bypasses the natural binding limitation and provides sufficient AIM to achieve both high internalization and effective clearance of dead cell debris.
Solution Approach 2:
The invention changes the quantity parameter of AIM in the system by administering exogenous AIM. This increases the overall concentration of AIM available for binding with IgM pentamers and for clearance functions, overcoming the insufficient natural production and binding in Felids.
3Object-affected harmful factors
If dead cell debris accumulates in renal tissue, then renal function declines, but administering AIM does not improve renal function in severe renal failure
Solution Approach 1:
The invention extracts and removes dead cell debris from renal tissue through AIM-mediated clearance mechanisms. By administering AIM, the patent enables the removal of accumulated debris without promising unrealistic renal function recovery, thus addressing the harmful accumulation while being realistic about functional outcomes.
Solution Approach 2:
The invention converts the harmful accumulation of dead cell debris into a removable condition by using AIM to target and clear these substances. The strong binding characteristics of AIM are utilized to effectively bind and remove debris, transforming the harmful accumulation into a treatable state.
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
The concentration of uremic toxins in the blood is reduced, thereby suppressing the deterioration of uremia and prolonging the life of Felids with severe renal failure.
Implementation Method 1
a unique positively-charged amino-acid cluster is present at the carboxyl terminus within the third SRCR domain. This cluster forms charge-based interactions with dead cells that are strongly negatively charged due to the high-level exposure of phosphatidylserine on their surface
Implementation Method 2
This association highly enhances the engulfment of dead cells by phagocytes, as AIM is highly internalized by phagocytes via multiple scavenger receptors
Data Source
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AI summary
The present invention provides an agent for suppressing deterioration of uremia in Felids suffering from severe renal failure, which contains an apoptosis inhibitor of macrophage (AIM), an AIM fragment having a biological activity of AIM, or a nucleic acid encoding the AIM or AIM fragment.