In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Input: Consider Input: Paragraph: Spongiform degeneration is characterized by vacuolation in nervous tissue accompanied by neuronal death and gliosis. Although spongiform degeneration is a hallmark of prion diseases, this pathology is also present in the brains of patients suffering from Alzheimer's disease, diffuse Lewy body disease, human immunodeficiency virus (HIV) infection, and Canavan's spongiform leukodystrophy. The shared outcome of spongiform degeneration in these diverse diseases suggests that common cellular mechanisms must underlie the processes of spongiform change and neurodegeneration in the central nervous system. Immunohistochemical analysis of brain tissues reveals increased ubiquitin immunoreactivity in and around areas of spongiform change, suggesting the involvement of ubiquitin-proteasome system dysfunction in the pathogenesis of spongiform neurodegeneration. The link between aberrant ubiquitination and spongiform neurodegeneration has been strengthened by the discovery that a null mutation in the E3 ubiquitin-protein ligase mahogunin ring finger-1 (Mgrn1) causes an autosomal recessively inherited form of spongiform neurodegeneration in animals. Recent studies have begun to suggest that abnormal ubiquitination may alter intracellular signaling and cell functions via proteasome-dependent and proteasome-independent mechanisms, leading to spongiform degeneration and neuronal cell death. Further elucidation of the pathogenic pathways involved in spongiform neurodegeneration should facilitate the development of novel rational therapies for treating prion diseases, HIV infection, and other spongiform degenerative disorders. transmissible spongiform encephalopathy (TSE); retroviral infection; mahogunin ring finger-1 (Mgrn1); oxidative stress; autophagy; endocytic trafficking NIH Public Access 
 Title: The ubiquitin-proteasome system in spongiform degenerative disorders

Output: True


Input: Consider Input: Paragraph: Dendritic cells (DCs) are recognized as highly potent antigen-presenting cells that are able to stimulate cytotoxic T lymphocyte (CTL) responses with antitumor activity. Consequently, DCs have been explored as cellular vaccines in cancer immunotherapy. To that end, DCs are modified with tumor antigens to enable presentation of antigen-derived peptides to CTLs. In this review we discuss the use of viral vectors for in situ modification of DCs, focusing on their clinical applications as anticancer vaccines. Among the viral vectors discussed are those derived from viruses belonging to the families of the Poxviridae, Adenoviridae, Retroviridae, Togaviridae, Paramyxoviridae, and Rhabdoviridae. We will further shed light on how the combination of viral vector-based vaccination with T-cell supporting strategies will bring this strategy to the next level. Since their discovery in 1973, it was clear that dendritic cells (DCs) stood out above the immune cell pack (1, 2). They are morphologically distinct from all other immune cell types and are gifted with an unparalleled capacity to take up, process and present self and foreign antigens to both CD4 + and CD8 + T cells. DCs are critical intermediaries between the innate and adaptive immune systems, as they stimulate, regulate, and shape both immunity and tolerance in all its disguises. Ralph Steinmann, who discovered these cells, was awarded the Nobel Prize for Medicine in 2011, because the discovery of DCs changed medicine (3). Dendritic cells in both humans and mice represent a population of at least four different subtypes with distinct phenotypical and functional characteristics (4-7). These subsets are: plasmacytoid DCs (pDCs), two subsets of conventional DCs (cDC1 and cDC2), and inflammatory DCs. The latter represent a monocyte-derived subset that appears during inflammatory responses (Table 1) . Recently, additional types of human blood DCs, monocytes, and progenitors were revealed using single cell RNA-sequencing. The group of Prof. Nir Hacohen identified pDCs next to cDC progenitor-derived cDC1 (Clec9A + ) and two types of CD1c + cDC2, of which one can also be derived from CD14 + DCs. Furthermore they found a CD141 − CD1c − CD11c + DC subset derived from CD16 + monocytes and an AXL + Siglec6 + subset (8). Future research will have to unravel a possible murine representative for the human cDC2 and AXL + Siglec6 + DC subset. Also, Langerhans cells have been considered an important DC subset for vaccination as they are localized in the epidermis (HLA-DR + CD11c + CD1a + CD207 + ). However, recent evidence suggests that they are related to macrophages, another antigen-presenting cell (APC) type with potential antitumor activity (9). 
 Title: The Journey of in vivo Virus Engineered Dendritic Cells From Bench to Bedside: A Bumpy Road

Output: True


Input: Consider Input: Paragraph: Objective-To evaluate clinical manifestations, response to treatment, and outcome for Weimaraners with hypertrophic osteodystrophy (HOD). Design-Retrospective case series. Procedures-Medical records were reviewed for signalment, vaccination history, clinical signs, laboratory test results, response to treatment, and relapses. Radiographs were reviewed. Results-Clinical signs included pyrexia, lethargy, and ostealgia; signs involving the gastrointestinal, ocular, or cutaneous systems were detected. Of the 53 dogs, 28 (52.8%) had HOD-affected littermates. Dogs with HOD-affected littermates were more likely to relapse, compared with the likelihood of relapse for dogs with no HOD-affected littermates. All 53 dogs had been vaccinated 1 to 30 days before HOD onset; no difference was found between the number of dogs with a history of vaccination with a recombinant vaccine (n = 21) versus a nonrecombinant vaccine (32). Fifty (94.3%) dogs had radiographic lesions compatible with HOD at disease onset, and the other 3 (5.7%) had HOD lesions 48 to 72 hours after the onset of clinical signs. Twelve of 22 (54.5%) dogs treated with NSAIDs did not achieve remission by 7 days after initiation of treatment. All dogs treated initially with corticosteroids achieved remission within 8 to 48 hours. Of the 33 dogs that reached adulthood, 28 (84.8%) were healthy and 5 (15.2%) had episodes of pyrexia and malaise. Conclusions and Clinical Relevance-Treatment with corticosteroids was superior to treatment with NSAIDs in Weimaraners with HOD. It may be necessary to evaluate repeated radiographs to establish a diagnosis of HOD. Most HOD-affected Weimaraners had resolution of the condition with physeal closure. 
 Title: Clinical manifestations, response to treatment, and clinical outcome for Weimaraners with hypertrophic osteodystrophy: 53 cases (2009-2011) NIH Public Access


Output: True