Mathematical Modelling of a First Order Transducer

First chapter lays the ground work for this research paper. The problem is posed immediately, enabling the reader to gain a better appreciation of the material that follows. The next article explains the thought process that motivated this problem. This is followed by reviewing the available. literature in the field and on which the author has relied quite extensively. The chapter concludes by explaining the more common terminology which will be used frequently throughout the dissertation. Given a configuration of linear, passive network elements, termed filter, how faithful a reproduction of the input process is the process at the output of a first order transducer? Or, in other words, how much information is lost in a filter? This problem arises due to the necessity of using a filter in a system --- either for reasons of convenience or by force of circumstances. The paper attempts to model a transducer mathematically and to express the input and output processes statistically. In order to-do so, a meaningful measure of error should be chosen and defined. The error measure chosen is the Mean-Integral. Square Error (MISER). A very good approximation of the situation is the existence of the signal for a long period of time with respect to the time constants of the filter. The problem then lends itself to what is known as steady state analysis. This work is restricted to analyzing the pattern given a random Stationary Gaussian Markoff (SGM) process. An expression to calculate the MISER will be developed and a method to computerize the same will be indicated. However, actual numerical computations will be deferred. The expression for MISER will establish a relationship between the location of a pole and/or zero and the magnitude of MISER. The use of the SGM process as the input, enables one to describe output process in a concise manner. It also enables the results of this study to be compared with the results of others in related fields who have used the SGM process as a signal source

The Development of the Laws and Constitution of Cameroon.

The Federal Republic of Cameroon which came into existence on October 1, 1961, is made up of former Southern Cameroons which was administered by the British Government as an integral part of her Colony of Nigeria, and the Republic of Cameroon - a former trust territory under French Administration. Thus West Cameroon (i.e. former Southern Cameroons) was endowed with a legal system akin to that of Nigeria, and therefore of Great Britain, and East Cameroon (i.e. the former Republic of Cameroon) was endowed with the French legal system. This thesis, the first of its kind, attempts to trace the development of the laws and constitution of Cameroon within the framework not only of these two major foreign legal systems, but also of the indigenous systems. The work is divided into three Parts comprising of twelve chapters. Part I, comprising only of Chapter I, deals with a general historical and ethnographic survey of Cameroon. An attempt has been made, particularly in connection with the historical introduction, to piece together the various treaties and agreements which gave Cameroon her present boundaries. Part II comprises of Chapters II - IV. Chapter II deals with the administration, by the French and British Governments, within the framework of the Mandate and Trusteeship systems, of their respective parts of Cameroon. Attention is also paid to the political and constitutional developments leading to independence and reunification. These include the United Nations conducted plebiscites in the Cameroons and the Cameroons: case at the International Court of Justice which arose therefrom. Chapter III is devoted to an analysis of the Federal and Federated State constitutions while Chapter IV deals with the courts and legal profession in Cameroon. Part III comprises Chapters V - XII, each of which deals with a specific subject. Thus Chapter V traces the Sources of Law in Cameroon while Chapter VI deals with Procedure and Evidence. The five others deal respectively with Criminal Law, Civil Law (i.e. Contract and Tort), Commercial Law, Land Law and Family Law. Chapter XII deals briefly with the attempts, few as they are, which have been made to integrate the law. In each of the chapters in this part, we have tried to deal with both the French and English law on each topic, the aim being to point out where they are different and to make suggestions for dealing with such differences. Although these suggestions have sometimes come out either in favour of French or English law where either system was thought better, we have not ceased to emphasize the tremendous advantage in being able to produce new laws based on the best from both systems

Dysfunctional Crohn's Disease-Associated NOD2 Polymorphisms Cannot be Reliably Predicted on the Basis of RIPK2 Binding or Membrane Association.

Polymorphisms in NOD2 represent the single greatest genetic risk factor for the development of Crohn's disease. Three different non-synonomous NOD2 polymorphisms - R702W, G908R, and L1007fsincC - account for roughly 80% of all NOD2-associated cases of Crohn's disease and are reported to result in a loss of receptor function in response to muramyl dipeptide (MDP) stimulation. Loss of NOD2 signaling can result from a failure to detect ligand; alterations in cellular localization; and changes in protein interactions, such as an inability to interact with the downstream adaptor protein RIPK2. Using an overexpression system, we analyzed ~50 NOD2 polymorphisms reportedly connected to Crohn's disease to determine if they also displayed loss of function and if this could be related to alterations in protein localization and/or association with RIPK2. Just under half the polymorphisms displayed a significant reduction in signaling capacity following ligand stimulation, with nine of them showing near complete ablation. Only two polymorphisms, R38M and R138Q, lost the ability to interact with RIPK2. However, both these polymorphisms still associated with cellular membranes. In contrast, L248R, W355stop, L550V, N825K, L1007fsinC, L1007P, and R1019stop still bound RIPK2, but showed impaired membrane association and were unable to signal in response to MDP. This highlights the complex contributions of NOD2 polymorphisms to Crohn's disease and reiterates the importance of both RIPK2 binding and membrane association in NOD2 signaling. Simply ascertaining whether or not NOD2 polymorphisms bind RIPK2 or associate with cellular membranes is not sufficient for determining their signaling competency.The authors would like to thank Joe Boyle for helpful discussion. This work was funded by a Wellcome Trust CDF (WT085090MA) to TPM and the Medical Research Council (U105960399). RP was a BBSRC doctoral training student.This is the final version of the article. It first appeared from Frontiers via http://dx.doi.org/10.3389/fimmu.2015.0052

Pattern recognition receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Pattern Recognition Receptors (PRRs, [89]) (nomenclature as agreed by NC-IUPHAR sub-committee on Pattern Recognition Receptors, [17]) participate in the innate immune response to microbial agents, the stimulation of which leads to activation of intracellular enzymes and regulation of gene transcription. PRRs express multiple leucine-rich regions to bind a range of microbially-derived ligands, termed PAMPs or pathogen-associated molecular patterns or endogenous ligands, termed DAMPS or damage-associated molecular patterns. These include peptides, carbohydrates, peptidoglycans, lipoproteins, lipopolysaccharides, and nucleic acids. PRRs include both cell-surface and intracellular proteins. PRRs may be divided into signalling-associated members, identified here, and endocytic members, the function of which appears to be to recognise particular microbial motifs for subsequent cell attachment, internalisation and destruction. Some are involved in inflammasome formation, and modulation of IL-1β cleavage and secretion, and others in the initiation of the type I interferon response. PRRs included in the Guide To PHARMACOLOGY are:Catalytic PRRs (see links below this overview)Toll-like receptors (TLRs)Nucleotide-binding oligomerization domain, leucine-rich repeat containing receptors (NLRs, also known as NOD (Nucleotide oligomerisation domain)-like receptors)RIG-I-like receptors (RLRs)Caspase 4 and caspase 5 Non-catalytic PRRsAbsent in melanoma (AIM)-like receptors (ALRs)C-type lectin-like receptors (CLRs)Other pattern recognition receptorsAdvanced glycosylation end-product specific receptor (RAGE

Caspase-8 functions as a key mediator of inflammation and pro-IL-1β processing via both canonical and non-canonical pathways.

Caspase-8 is an apical component of cell death pathways. Activated caspase-8 can drive classical caspase-dependent apoptosis and actively inhibits cell death mediated by RIPK3-driven necroptosis. Genetic deletion of Casp8 results in embryonic lethality as a result of uncontrolled necroptosis. This lethality can be rescued by simultaneous deletion of Ripk3. Recently, caspase-8 has been additionally connected to inflammatory pathways within the cell. In particular, caspase-8 has been shown to be crucially involved in the induction of pro-IL-1β synthesis and processing via both non-canonical and canonical pathways. In this review, we bring together current knowledge regarding the role of caspase-8 in cellular inflammation with a particular emphasis on the interplay between caspase-8 and the classical and non-canonical inflammasomes.The authors received financial support of the Wellcome Trust (TPM; WT085090MA) and the Biotechnology and Biological Sciences Research Council (CEB; BB/K006436/1).This is the accepted manuscript. The final version is available from Wiley at http://onlinelibrary.wiley.com/doi/10.1111/imr.12284/abstract

Pattern recognition receptors in GtoPdb v.2021.3

Pattern Recognition Receptors (PRRs, [104]) (nomenclature as agreed by NC-IUPHAR sub-committee on Pattern Recognition Receptors, [18]) participate in the innate immune response to microbial agents, the stimulation of which leads to activation of intracellular enzymes and regulation of gene transcription. PRRs express multiple leucine-rich regions to bind a range of microbially-derived ligands, termed PAMPs or pathogen-associated molecular patterns or endogenous ligands, termed DAMPS or damage-associated molecular patterns. These include peptides, carbohydrates, peptidoglycans, lipoproteins, lipopolysaccharides, and nucleic acids. PRRs include both cell-surface and intracellular proteins. PRRs may be divided into signalling-associated members, identified here, and endocytic members, the function of which appears to be to recognise particular microbial motifs for subsequent cell attachment, internalisation and destruction. Some are involved in inflammasome formation, and modulation of IL-1β cleavage and secretion, and others in the initiation of the type I interferon response. PRRs included in the Guide To PHARMACOLOGY are:Catalytic PRRs (see links below this overview)Toll-like receptors (TLRs)Nucleotide-binding oligomerization domain, leucine-rich repeat containing receptors (NLRs, also known as NOD (Nucleotide oligomerisation domain)-like receptors)RIG-I-like receptors (RLRs)Caspase 4 and caspase 5 Non-catalytic PRRsAbsent in melanoma (AIM)-like receptors (ALRs)C-type lectin-like receptors (CLRs)Other pattern recognition receptorsAdvanced glycosylation end-product specific receptor (RAGE

Pattern recognition receptors in GtoPdb v.2023.1

Pattern Recognition Receptors (PRRs, [110]) (nomenclature as agreed by NC-IUPHAR sub-committee on Pattern Recognition Receptors, [20]) participate in the innate immune response to microbial agents, the stimulation of which leads to activation of intracellular enzymes and regulation of gene transcription. PRRs express multiple leucine-rich regions to bind a range of microbially-derived ligands, termed PAMPs or pathogen-associated molecular patterns or endogenous ligands, termed DAMPS or damage-associated molecular patterns. These include peptides, carbohydrates, peptidoglycans, lipoproteins, lipopolysaccharides, and nucleic acids. PRRs include both cell-surface and intracellular proteins. PRRs may be divided into signalling-associated members, identified here, and endocytic members, the function of which appears to be to recognise particular microbial motifs for subsequent cell attachment, internalisation and destruction. Some are involved in inflammasome formation, and modulation of IL-1β cleavage and secretion, and others in the initiation of the type I interferon response. PRRs included in the Guide To PHARMACOLOGY are:Catalytic PRRs (see links below this overview)Toll-like receptors (TLRs)Nucleotide-binding oligomerization domain, leucine-rich repeat containing receptors (NLRs, also known as NOD (Nucleotide oligomerisation domain)-like receptors)RIG-I-like receptors (RLRs)Caspase 4 and caspase 5 Non-catalytic PRRsAbsent in melanoma (AIM)-like receptors (ALRs)C-type lectin-like receptors (CLRs)Other pattern recognition receptorsAdvanced glycosylation end-product specific receptor (RAGE