In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Ex Input:
Scorpions are well known for their dangerous stings that can result in severe consequences for human beings, including death. Neurotoxins present in their venoms are responsible for their toxicity. Due to their medical relevance, toxins have been the driving force in the scorpion natural compounds research field. On the other hand, for thousands of years, scorpions and their venoms have been applied in traditional medicine, mainly in Asia and Africa. With the remarkable growth in the number of characterized scorpion venom components, several drug candidates have been found with the potential to tackle many of the emerging global medical threats. Scorpions have become a valuable source of biologically active molecules, from novel antibiotics to potential anticancer therapeutics. Other venom components have drawn attention as useful scaffolds for the development of drugs. This review summarizes the most promising candidates for drug development that have been isolated from scorpion venoms.

Ex Output:
Scorpion venom components as potential candidates for drug development


Ex Input:
The presence of immunoglobulin oligoclonal bands in the cerebrospinal fluid of Multiple Sclerosis (MS) patients supports the hypothesis of an infectious etiology, although the antigenic targets remain elusive. Neurotropic mouse hepatitis virus (MHV) infection in mice provides a useful tool for studying mechanisms of demyelination in a virus-induced experimental model of MS. This study uses Affymetrix microarray analysis to compare differential spinal cord mRNA levels between mice infected with demyelinating and non-demyelinating strains of MHV to identify host immune genes expressed in this demyelinating disease model. The study reveals that during the acute stage of infection, both strains induce inflammatory innate immune response genes, whereas upregulation of several immunoglobulin genes during chronic stage infection is unique to infection with the demyelinating strain. Results suggest that the demyelinating strain induced an innate-immune response during acute infection that may promote switching of Ig isotype genes during chronic infection, potentially playing a role in antibody-mediated progressive demyelination even after viral clearance.

Ex Output:
Demyelinating strain of mouse hepatitis virus infection bridging innate and adaptive immune response in the induction of demyelination


Ex Input:
Interactions between the immune system and the central nervous system (CNS) constitute the most complex and interactive regulatory network in mammals. The high degree of specialization of cell types that comprise the CNS, and their intricate communication, controls both cognitive and vital functions. Disruption of the communication network and poor CNS regenerative properties make this organ vulnerable to microbial as well as physical injury. Although it is known that host responses must be strictly regulated to preserve CNS function and to minimize the incidence of autoimmunity, the factors regulating CNS immune and repair responses are not well understood. In addition to the absence of a dedicated lymphatic drainage system, CNS cells express few, if any, molecules encoded by the major histocompatibility complex (MHC) 1-3 . Therefore, in the quiescent CNS there is little endogenous antigen presentation or potential to activate T cells. Although the underlying basis for this limited immunological activity is not completely understood, interactions between both neurons and the glial population represented by microglia, astrocytes and oligodendrocytes (BOX 1), as well as constitutive secretion of neurotrophins and transforming growth factor-β, might contribute to this quiescent resting state 1,4-7 . The limited expression of adhesion molecules by endothelial cells of the blood-brain barrier (BBB) and the presence of tight junctions between these cells also limit or prevent large molecules, such as antibodies, and T cells from entering the CNS 2,8 . Despite this, a few activated/memory CD4 + and CD8 + T cells randomly patrol the CNS in the absence of 'danger' signals, and either exit or die in situ in the absence of antigen recognition 2,8 . Abstract | Several viruses infect the mammalian central nervous system (CNS), some with devastating consequences, others resulting in chronic or persistent infections associated with little or no overt pathology. Coronavirus infection of the murine CNS illustrates the contributions of both the innate immune response and specific host effector mechanisms that control virus replication in distinct CNS cell types. Despite T-cell-mediated control of acute virus infection, host regulatory mechanisms, probably designed to protect CNS integrity, contribute to the failure to eliminate virus. Distinct from cytolytic effector mechanisms expressed during acute infection, non-lytic humoral immunity prevails in suppressing infectious virus during persistence.

Ex Output:

Neurotrophins Coronavirus infection of the central nervous system: host-virus stand-off