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: Cryptosporidiosis is one of the most common zoonosis worldwide, causing intestinal infection to both humans and livestock. The purpose of this study was to assess whether the level of anti-C. parvum IgG antibodies transferred through colostrum from dams to newborn calves impacts the susceptibility to cryptosporidiosis. A number of 50 dams and their healthy newborns were included in the study. Colostrum samples were collected within 12 h after birth and anti-C. parvum IgG antibody levels were determined by single radial immunodiffusion. The health condition of the newborns was daily monitored, and fecal samples were collected at first diarrheic episode of a calf. In all dams, the anti-C. parvum IgG antibody concentration in colostrum varied between 570 and 4070 mg/dl; in dams who gave birth to calves with diarrhea and were C. parvum-positive, the antibody concentration in colostrum varied between 680 and 3680 mg/dl (Table 1 ). The point-biserial correlation showed a negative correlation between the levels of anti-C. parvum antibodies and manifestation of clinical cryptosporidiosis (r=-0.425). Our findings highlight the importance of IgG levels in colostrum received by neonatal calves during their first day of life for prevention of C. parvum infection.

A: Importance of colostrum IgG antibodies level for prevention of infection with Cryptosporidium parvum in neonatal dairy calves
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Q: ORF la of lactate dehydrogenase-elevating virus, strain P (LDV-P), encodes a protein of 2206 amino acids. Eisenberg hydrophobic moment analysis of the protein predicted the presence of eleven transmembrane segments in the C-terminal half of the molecule (amino acids 980-1852) that flank the serine protease domain, cDNAs encoding ORF la protein segments encompassing transmembrane segments 5 to 11 and its amphipathic C-terminal end as well as the N-terminal 80 amino acids of the downstream ORF lb protein were transcribed and the transcripts in vitro translated in the absence and presence of microsomal membranes. The synthesis of the protein products with putative transmembrane segments was enhanced by the presence of the microsomal membranes and the proteins became membrane associated. When synthesized in the absence of membranes they were recovered in the supernatant upon ultracentrifugation of the translation reaction mixtures, whereas they were recovered in the membrane pellet when synthesized in the presence of membranes. Furthermore, the latter proteins were not released from the membranes by disruption of the membrane vesicles in carbonate buffer, pH 11.5, and large portions of the proteins were resistant to digestion by trypsin, chymotrypsin and proteinase K. No N-glycosylation was observed and only little, if any, processing of the protein by the putative serine protease. The results indicate that the C-terminal half of the ORF la protein represents a non-glycosylated integral membrane protein. Potential modes of synthesis and function of the protein are discussed. In addition, the results showed that the synthesis of the ORF la protein was generally terminated at its termination codon, but that read-through into the ORF lb gene occurred with low frequency.

A: Membrane association of the C-terminal half of the open reading frame la protein of lactate dehydrogenase-elevating virus Brief Report
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Q: Multiple sclerosis (MS) frequently starts near the lateral ventricles, which are lined by subventricular zone (SVZ) progenitor cells that can migrate to lesions and contribute to repair. Since MS-induced inflammation may decrease SVZ proliferation and thus limit repair, we studied the role of galectin-3 (Gal-3), a pro-inflammatory protein. Gal-3 expression was increased in periventricular regions of human MS in post-mortem brain samples and was also upregulated in periventricular regions in a murine MS model, Theiler's murine encephalomyelitis virus (TMEV) infection. Whereas TMEV increased SVZ chemokine (CCL2, CCL5, CCL8 and CXCL10) expression in wild type (WT) mice, this was inhibited in Gal-3 −/− mice. Though numerous CD45+ immune cells entered the SVZ of WT mice after TMEV infection, their numbers were significantly diminished in Gal-3 −/− mice. TMEV also reduced neuroblast and proliferative SVZ cell numbers in WT mice but this was restored in Gal-3 −/− mice and was correlated with increased numbers of doublecortin+ neuroblasts in the corpus callosum. In summary, our data showed that loss of Gal-3 blocked chemokine expression, reduced immune cell migration into the SVZ, reestablished SVZ proliferation and increased the number of progenitors in the corpus callosum. These results suggest Gal-3 plays a central role in modulating the SVZ neurogenic niche's response to this model of MS.

A:
Loss of galectin-3 decreases the number of immune cells in the subventricular zone and restores proliferation in a viral model of multiple sclerosis Graphical Abstract HHS Public Access
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