Do literature research and literature review, determine the topic, and make a proposal report

Such as the molecular mechanism of anti-infective immunity

The molecular mechanism is networked, multi-level, and multivariate: the correspondence of the two systems of infection and immunity, the low-level correspondence of their decomposition matrix, and the overall intrinsity of their decomposition are our observations. Pen | fun | pavilion www. ｂｉｑｕｇｅ。 ｉｎｆｏ

Etiological level: Viruses, bacteria, and autoregulatory systems are decoupled at different levels

Symptom level: fever, cough, edema......

Signal regulation layer: receptor-ligand binding, cytokines, PRR, TLR, MHC

Specifically, corneal infection, ulcer perforation, blindness

The essence of the pathology is ulcer necrosis, which is a coupling point that can be caused by multiple causes, which can also lead to other concomitant changes

Treatment: Symptomatic to the cause, which is essentially the intrinsic correspondence of the network, so that the overall cycle returns to normal

Scientific question: Mechanism of immunopathological damage? (knowing the intrinsic features, and looking for the network in turn, can know that this is multimodal)

Multi-level decomposition, as in Fourier analysis: multi-stage products of bacteria and so on in the body, such as antibiotics, LPS, DNA, flagellins, shifts of position, changes in the coordination of their own mechanisms, receptor interfaces and operations

Working assumptions: various pathways (TLR, PRR, TOLL), linear combinations, matrix operations (changes in the probabilistic network between pathways)

For example, if TREM-1 and TLRS co-activate the TRF6 signaling pathway, the coupling of relatively independent pathways will inevitably cause certain probability changes, which can be equivalent to the operation of logical pathways

The formation of feedback is a manifestation of the convergence radius of the sublayer

Research: statistics of data, validation of experiments

The formation and combination of different modules to form larger modules. According to the median value theorem, we are confident that the network corresponds to the real world at a certain level. Important definition, i.e., delineation of thresholds

The basis for the project, the significance of the research, the research objectives, the research content, the research plan, the technical route, the working basis, and the working conditions

Meta-analysis, such as the transcriptional regulation of the BH3-only protein BIM (passive element) by SP1 (enduring element) during neuronal apoptosis (background conditions), which is a multi-concept connection, different objects for different conditions, this is a multi-dimensional space. It is considered as a connection of wave functions. The distribution of probabilities is an eigen, a Markov chain and a process, which is analogue and approximate like calculus

Myeloid cell-induced receptors (TREMs) are newly discovered receptors on the surface of cell membranes, and endotoxin stimulation and infection can induce TREM-1 to amplify inflammatory responses. So is TREM-1 involved in purulent keratitis and induces corneal ulcer necrosis? (hypothetical, single-level decomposition, incomplete) The pre-experimental results showed that the expression of TREM-1 in the cornea was significantly up-regulated after corneal infection, and was closely related to the pathological changes of corneal ulcer perforation. So, what is the mechanism by which TREM-1 induces corneal perforation blindness? Further experiments have shown that TREM-1 amplifies the corneal inflammatory response by synergizing with the Toll-like receptor (TLR) and activating the TRAF6 signaling pathway. Therefore, we put forward for the first time the hypothesis of "TREM-1 induces corneal ulcer perforation and blindness" (the valuable hypothesis is the intrinsic relationship connection): that is, corneal infection leads to the upregulation of TREM-1 expression, activates the DAP12/TRAF6 signaling pathway, and synergizes with the TLR signaling pathway to stimulate inflammatory cells to produce and release a large number of toxic products, dissolve and destroy corneal tissue, resulting in corneal purulent ulceration and blinding. This project aims to reveal the pathological damage mechanism of TREM-1-induced corneal blindness through in vitro experiments and animal experiments, and provide a theoretical basis for finding new therapeutic targets and developing new measures for the prevention and treatment of corneal blindness. (To directly derive important intrinsics, apply them directly)

Do research and acknowledge other people's work and intelligence

【Research Objectives】

1. To elucidate how TREM-1 induces and excessively amplifies corneal inflammatory response at the in vivo level, to obtain reliable evidence that TREM-1 directly induces corneal blindness, and to reveal the immunopathological damage mechanism of TREM-1 amplification and regulation of corneal inflammatory response leading to corneal blindness. At the same time, to determine whether TREM-1 can be used as one of the indicators of efficacy and prognosis of purulent keratitis. (The effect of the assessment is related to its distance from the eigen, and the eigenvalue is the best)

2. To explore the signal transduction mechanism of TREM-1 amplification and exacerbation of hyperinflammatory response, and to reveal the new mechanism of TREM-1 and TLR synergistically activating the TRAF6 signaling pathway, triggering and amplifying the inflammatory response, and leading to corneal ulcer blindness, so as to provide a theoretical basis for further establishing TREM-1 as a new target for the treatment of corneal blindness and developing new prevention and treatment measures. (Determination of the intrinsic nature of the network)

Research content (closely related to the research objectives)

1. To determine the relationship between TREM-1 and blindness caused by corneal purulent ulcers. (Identifying relationships at different levels)

2. Analyze how TREM-1 induces and amplifies corneal inflammation and leads to corneal ulcer perforation and blindness.

3. In-depth study of the signal transduction mechanisms of TREM-1 induced and over-amplified inflammatory responses. (Intrinsic network diffusion)

4. Further elucidate the molecular mechanism of action of TREM-1 activation and recruitment of TRAF6. (Formation of new relationships)

Finding evidence, research is a process of argumentation

Multi-level coupling (coupling of multiple equilibriums), periodic oscillations, and final probability distributions

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