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".

Example Input: Paragraph: The chemokine CXCL10 is produced during infection and inflammation to activate the chemokine receptor CXCR3, an important regulator of lymphocyte trafficking and activation. The goal of this study was to assess the contributions of CXCL10 to the pathogenesis of experimental septic shock in mice. Methods: Septic shock was induced by cecal ligation and puncture (CLP) in mice resuscitated with lactated Ringer's solution and, in some cases, the broad spectrum antibiotic Primaxin. Studies were performed in CXCL10 knockout mice and mice treated with anti-CXCL10 immunoglobulin G (IgG). Endpoints included leukocyte trafficking and activation, core body temperature, plasma cytokine concentrations, bacterial clearance and survival. Results: CXCL10 was present at high concentrations in plasma and peritoneal cavity during CLP-induced septic shock. Survival was significantly improved in CXCL10 knockout (CXCL10KO) mice and mice treated with anti-CXCL10 IgG compared to controls. CXCL10KO mice and mice treated with anti-CXCL10 IgG showed attenuated hypothermia, lower concentrations of interleukin-6 (IL-6) and macrophage inhibitory protein-2 (MIP-2) in plasma and lessened natural killer (NK) cell activation compared to control mice. Compared to control mice, bacterial burden in blood and lungs was lower in CXCL10-deficient mice but not in mice treated with anti-CXCL10 IgG. Treatment of mice with anti-CXCL10 IgG plus fluids and Primaxin at 2 or 6 hours after CLP significantly improved survival compared to mice treated with non-specific IgG under the same conditions. Conclusions: CXCL10 plays a role in the pathogenesis of CLP-induced septic shock and could serve as a therapeutic target during the acute phase of septic shock.
Title: The role of CXCL10 in the pathogenesis of experimental septic shock
Example Output: False

Example Input: Paragraph: In March 2003, a novel coronavirus was isolated from patients exhibiting atypical pneumonia and subsequently proven to be the causative agent of the disease now referred to as severe acute respiratory syndrome (SARS). The complete genome of the SARS coronavirus (SARS-CoV) has since been sequenced. The SARS-CoV nucleocapsid (SARS-CoV N) shares little homology with other members of the coronavirus family. To determine if the N protein is involved in the regulation of cellular signal transduction, an ELISA-based assay on transcription factors was used. We found that the amount of transcription factors binding to promoter sequences of c-Fos, ATF2, CREB-1, and FosB was increased by the expression of SARS-CoV N. Since these factors are related to AP-1 signal transduction pathway, we investigated whether the AP-1 pathway was activated by SARS-CoV N protein using the PathDetect system. The results demonstrated that the expression of N protein, not the membrane protein (M), activated AP-1 pathway. We also found that SARS-CoV N protein does not activate NF-jB pathway, demonstrating that activation of important cellular pathways by SAS-CoV N protein is selective. Thus our data for the first time indicate that SARS-CoV has encoded a strategy to regulate cellular signaling process.
Title: Activation of AP-1 signal transduction pathway by SARS coronavirus nucleocapsid protein
Example Output: True

Example Input: Paragraph: Dengue virus infections can cause hemorrhagic fever, shock, encephalitis, and even death. Worldwide, approximately 2.5 billion people live in dengue-infested regions with about 100 million new cases each year, although many of these infections are believed to be silent. There are four antigenically distinct serotypes of dengue virus; thus, immunity from one serotype will not cross-protect from infection with the other three. The difficulties that hamper vaccine development include requirements of the natural conformation of the envelope glycoprotein to induce neutralizing immune responses and the necessity of presenting antigens of all four serotypes. Currently, the only way to meet these requirements is to use a mixture of four serotypes of live attenuated dengue viruses, but safety remains a major problem. In this study, we have developed the basis for a tetravalent dengue vaccine using a novel complex adenovirus platform that is capable of expressing multiple antigens de novo. This dengue vaccine is constructed as a pair of vectors that each expresses the premembrane and envelope genes of two different dengue virus serotypes. Dengue fever is a widespread mosquito-borne illness affecting an estimated 100 million people worldwide each year (9). While a majority of dengue virus infections are asymptomatic and go unnoticed, the disease can occasionally present with symptoms, such as severe headache, retro-orbital pain, or joint and muscle pain. The most severe cases can lead to dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), manifesting as hemorrhage in multiple organs, including the central nervous system, as well as massive vascular damage, bleeding, and shock. Fatality rates for DHF and DSS can reach up to 15%, the majority of which are in the pediatric demographic (23, 24). Dengue viruses are members of the flavivirus family of viruses. All four serotypes (dengue virus [DEN] serotype 1 [DEN1] to DEN4) are identical in gene structure, consisting of three structural proteins, capsid (C), premembrane (prM), and envelope (E), and seven nonstructural proteins, NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5 (14). These genes are translated from the positive-stranded RNA genome as a single polyprotein that is cleaved into individual proteins by cellular and viral proteases. Despite the structural similarities, there is variation in the genetic sequences of each serotype mainly in the membrane glycoproteins (prM and E) that results in antigenic distinction and lack of cross protection among the serotypes. Furthermore, subsequent infection with an alternate serotype may enhance disease severity, contributing to the onset of DHF or DSS. One possibility for this disease enhancement is that (nonneutralizing) antibodies may be aiding in viral entry into host cells, thereby enhancing the infection. Alternatively, broadly reactive cytotoxic T-lymphocyte (CTL) responses to DEN antigens, in the absence of neutralizing responses, may accelerate the destruction of host cells. There is currently no licensed vaccine available for dengue virus infection. Because of the immune enhancement associated with subsequent DEN infections, a successful DEN vaccine must induce neutralizing responses against all four DEN serotypes simultaneously (tetravalent). The difficulties that hamper vaccine development include the preservation of the neutralizing epitopes of the native DEN glycoprotein antigens and the necessity to present antigens from all serotypes. If a dengue vaccine does not offer tetravalent protection, a vaccinated individual would be susceptible to development of DHF or DSS if infected by a serotype not targeted by the vaccine. A great amount of effort has focused on traditional approaches to dengue vaccine development; however, these approaches have yet to generate a licensed tetravalent dengue vaccine. For example, live attenuated DEN vaccines have shown protective immunity in animal models (3) but have been
Title: Two Complex, Adenovirus-Based Vaccines That Together Induce Immune Responses to All Four Dengue Virus Serotypes Downloaded from
Example Output:
False