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.

[Q]: Background: Feline leishmaniosis caused by Leishmania infantum is considered a rare disease in endemic areas, whereas subclinical infections are common. Immune response plays a key role in driving the course of L. infantum infection in other host species; however, the feline cell-mediated immune response to L. infantum infection has not yet been investigated. The aim of this study was to determine the cell-mediated immune response specific to L. infantum by means of interferon (IFN)-γ release in whole blood assay from cats living in endemic areas (66 in Sicily and 113 in Catalonia) and to compare with antibody levels to L. infantum [enzyme-linked immunosorbent assay (ELISA) and immunofluorescence antibody test (IFAT)], blood parasite load and retroviral infections. Results: Most cats (n = 140) were L. infantum antibody negative and only 22% (n = 39) were positive. Only 9 and 2% of tested cats had a feline immunodeficency virus (FIV) infection or a feline leukemia virus (FeLV) infection, respectively. Thirty-two cats out of 179 (18%) produced IFN-γ after stimulation with L. infantum soluble antigen (LSA) while the majority of cats (93%) produced IFN-γ after stimulation with concanavalin A (ConA). Six LSA-IFN-γ-producer cats were seropositive (three to ELISA and five to IFAT) but they were polymerase chain reaction (PCR) negative, while only one cat was antibody-and PCR-positive. Significant positive correlations were found between IFN-γ concentrations after stimulation with LSA and ConA, and between serology and PCR testing. No association was found between FIV status and LSA or ConA-IFN-γ production. Combining PCR, serology and specific IFN-γ concentration results, we found that 36% of cats studied were exposed to L. infantum. As expected, cats from endemic areas produce IFN-γ after ex vivo blood stimulation with LSA and therefore are able to activate a cell-mediated adaptive immune response against the parasite that is variably associated with antibody or blood PCR positivity. The association of this assay to serological and molecular tests provides a better estimate of cat exposure to L. infantum.
[A]: Leishmania infantum-specific IFN-γ production in stimulated blood from cats living in areas where canine leishmaniosis is endemic


[Q]: This study investigates property securities bubbles and crashes by using a dynamic mathematical methodology developed from the previous research (Watanabe et al. 2007a, b [31,32]). The improved model is used to detect the bubble and crash periods in five international countries/cities (namely, . By this model definition, we are able to detect the beginning of each bubble period even before it bursts. Meanwhile, the empirical results show that most of property securities markets experienced bubble periods between 2003 and 2007, and crashes happened in Apr 2008 triggered by the Subprime Mortgage Crisis of US. In contrast, Japan suffered the shortest bubble period and no evidence has documented the existence of crash there.
[A]: Physica A A dynamic mathematical test of international property securities bubbles and crashes


[Q]: Precursor B acute lymphoblastic leukemias (pre-B ALLs) abnormally express a specific glycan structure, 9-O-acetylated sialic acid (9-O-Ac-Sia), on their cell surface, but glycoproteins that carry this modification have not been identified. Using three different lectins that specifically recognize this structure, we establish that nucleolin (NCL), a protein implicated in cancer, contains 9-O-Ac-Sia. Surprisingly, antibodies against the glycolipid 9-O-Ac-Sia GD3 also detected 9-O-Ac-Sia NCL. NCL is present on the surface of pre-B ALL cells as a sialoglycoprotein that is partly 9-O-acetylated and conversely, 9-O-Ac-Sia-containing structures other than NCL are present on these cells as well. Interestingly, NCL and the 9-O-Ac-Sia signal had less co-localization on normal pre-B cells. We also investigated regulation of NCL on the cell surface and found that sialidase treatment increased the percentage of cells positive for cell surface NCL, suggesting that sialylation of NCL promotes internalization. Treatment of pre-B ALL cells with the chemotherapy drug vincristine also increased the percentage of cells with surface NCL and correlated with increased 9-O-Ac-Sia expression. All tested leukemia cells including primary samples expressed NCL, suggesting it as a possible therapeutic target. We confirmed this by showing inhibition of cell proliferation in some pre-B ALLs by exposure to a NCLspecific aptamer AS1411. Precursor B-cell acute lymphoblastic leukemia (pre-B ALL) is the most prevalent malignancy of childhood 1 . Cell surface structures that selectively identify leukemia cells could be used for diagnosis or perhaps even treatment, and therefore previous studies reporting increased expression of a very specific glycan structure on pre-B ALL cells, consisting of sialic acid modified by 9-O-acetylation, are of significant interest in this context 2,3 . Sialic acids (Sias) belong to a family of 9-carbon carboxylated monosaccharides that most frequently are found as the terminal residues of glycoconjugates, which include glycoproteins and glycolipids. Sias are often highly expressed in cancer 4,5 , and, moreover, changes in sialylation promote cancer progression 6 . Sialic acids can carry further modifications, of which O-acetylation is the most common, and preferentially occurs at the hydroxyl group of carbon C9, yielding 9-O-Ac-Sia 7 . Sialic acids further modified by O-acetylation are expressed in a tissue and cell-specific manner on glycoproteins or glycolipids on normal cells, and those modified Sias can act as selective receptors for entry of some viruses 8 . However, abnormal expression of sialic acid-containing glycoconjugates and O-acetylated derivatives has also been noted to correlate with tumorigenesis. For example, the ganglioside GD2 is a tumor-specific marker for neuroblastoma, and antibodies against it are currently part of maintenance therapy for this pediatric malignancy 9 . Interestingly, the 9-O-acetylated form of GD2 may be a more specific treatment target than GD2 10 . The ganglioside GD3 and its 9-O-acetylated form (9-O-Ac-GD3, also called CD60b) are sialylated glycolipids expressed in glioblastomas 11 and melanomas 12 . In GD3 (Sia-α2,8-Sia-α2,3-Gal-β1,4-Glc-β1,1′-Cer), the terminal Sia is α2,8-linked and the O-acetylation only occurs on the terminal Sia residue. Published: xx xx xxxx OPEN www.nature.com/scientificreports/
[A]:
Pre-B acute lymphoblastic leukemia expresses cell surface nucleolin as a 9-O-acetylated sialoglycoprotein OPEN