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".

[EX Q]: Paragraph: The major biochemical and thermodynamic features of nucelocapsid protein of SARS coronavirus (SARS _ NP) were characterized by use of non-denatured gel electrophoresis, size-exclusion chromatographic and surface plasmon resonance (SPR) techniques. The results showed that SARS _ NP existed in vitro as oligomer, more probably dimer, as the basic functional unit. This protein shows its maximum conformational stability near pH 9.0, and it seems that its oligomer dissociation and protein unfolding occur simultaneously. Thermal-induced unfolding for SARS _ NP was totally irreversible. Both the thermal and chemical denaturant-induced denaturation analyses showed that oligomeric SARS _ NP unfolds and refolds through a two-state model, and the electrostatic interactions among the charge groups of SARS _ NP made a significant contribution to its conformational stability. D Abbreviations: SARS _ CoV, severe acute respiratory syndrome coronavirus; SARS _ NP, nucleocapsid protein of SARS; SPR, surface plasmon resonance; GuHCl, guanidine hydrochloride; CD, circular dichroism; T m and C m , transition midpoints of thermal and chemical denaturations; IPTG, isopropyl-h-d-thiogalasctopyranoside; N and U, native and unfolded states. 
 Title: In vitro biochemical and thermodynamic characterization of nucleocapsid protein of SARS
[EX A]: False

[EX Q]: Paragraph: Severe acute respiratory syndrome coronavirus (SARS-CoV) envelope (E) protein is a viroporin involved in virulence. E protein ion channel (IC) activity is specifically correlated with enhanced pulmonary damage, edema accumulation and death. IL-1β driven proinflammation is associated with those pathological signatures, however its link to IC activity remains unknown. In this report, we demonstrate that SARS-CoV E protein forms protein-lipid channels in ERGIC/Golgi membranes that are permeable to calcium ions, a highly relevant feature never reported before. Calcium ions together with pH modulated E protein pore charge and selectivity. Interestingly, E protein IC activity boosted the activation of the NLRP3 inflammasome, leading to IL-1β overproduction. Calcium transport through the E protein IC was the main trigger of this process. These findings strikingly link SARS-CoV E protein IC induced ionic disturbances at the cell level to immunopathological consequences and disease worsening in the infected organism. 
 Title: Severe acute respiratory syndrome coronavirus E protein transports calcium ions and activates the NLRP3 inflammasome
[EX A]: False

[EX Q]: Paragraph: B . A. Summers and M . J . G . Appel . Growth of canine distemper virus in cultured astrocytes : relationship to in vivo persistence and disease . Microbial Pathogenesis 1990 ; 8 : 71-82 . Canine distemper virus (CDV) causes an encephalomyelitis in dogs which varies with the viral strain . The CDV Cornell A75-17 strain produces a delayed, subacute to chronic, demyelinating CNS disease . In contrast, the Snyder Hill (CDV-SH) strain-associated neurological disease is more acute in onset, is usually non-demyelinating and primarily produces lesions in the gray matter . In these studies we describe the effects of these two virulent and one avirulent CDV strain, Rockborn (CDV-RO), on astrocytes in dissociated canine brain cell cultures . In multiple replicate experiments, astrocytes were infected most rapidly by CDV-RO [100% of astrocytes were infected by 14 days post-inoculation (p .i .)] . This strain caused severe cytopathic effect (CPE) and cytolysis . CDV-SH similarly produced a rapid infection of the astrocytes . In contrast . CDV A75-17 infected less than 25% of the astrocyte population during the first 28 days p .i . (±7 days) ; after 28 days p .i ., a rapid rise in astrocyte infection occurred . Both virulent viruses caused astrocytic syncytial formation but did not cause cytolysis of the astrocyte population as was observed with the attenuated virus . Titers of infectious virus, released into the supernatant fluid, reflected the degree of astrocyte infection . Virus released by the cultures late in CDV A75-17 infection showed enhanced ability to infect newly derived astrocytes ; in contrast, brain cell passaged CDV-SH did not show increased growth in these cells . These results show that (1) there is a difference in growth rate, CPE and capacity for adaptation of three different CDV strains in astrocytes in vitro, and (2) some aspects of the disease (such as persistence in white matter) produced by the virulent strains in vivo may be related to the course of astrocyte infection observed in vitro . 
 Title: Growth of canine distemper virus in cultured astrocytes : relationship to in vivo persistence and disease
[EX A]:
True