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.

[EX 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.
[EX A]: Importance of colostrum IgG antibodies level for prevention of infection with Cryptosporidium parvum in neonatal dairy calves

[EX Q]: The lengthy duration of multidrug therapy needed to cure tuberculosis (TB) poses significant challenges for global control of the disease. Moreover, chronic inflammation associated with TB leads to pulmonary damage that can remain even after successful cure. Thus, there is a great need for the development of effective shorter drug regimens to improve clinical outcome and strengthen TB control. Host-directed therapy (HDT) is emerging as a novel adjunctive strategy to enhance the efficacy and shorten the duration of TB treatment. Previously, we showed that the administration of CC-3052, a phosphodiesterase-4 inhibitor (PDE4i), reduced the host inflammatory response during Mycobacterium tuberculosis (Mtb) infection and improved the antimicrobial efficacy of isoniazid (INH) in both the mouse and rabbit models. In the present study, we evaluated the pharmacokinetics and explored the mechanism underlying the efficacy of a more potent PDE4i, CC-11050, as adjunct to INH treatment in a mouse model of pulmonary Mtb infection. Genome-wide lung transcriptome analysis confirmed the dampening of inflammation and associated network genes that we previously reported with CC-3052. Consistent with the reduction in inflammation, a significant improvement in Mtb control and pathology was observed in the lungs of mice treated with CC-11050 plus INH, compared to INH alone. This important confirmatory study will be used to help design upcoming human clinical trials with CC-11050 as an HDT for TB treatment.
[EX A]: Pharmacologic inhibition of host Phosphodiesterase-4 improves isoniazid-Mediated clearance of Mycobacterium tuberculosis

[EX Q]: To examine data in support of the viral hypothesis of atopic disease. Data Sources: We retrieved review articles and original research from MEDLINE, OVID, and PubMed (1950-June 2009) that addressed our topic of interest, using the terms respiratory virus, asthma, IgE, atopy, and viral-induced wheeze. Study Selection: Articles were selected for their relevance to viruses and their role in asthma. Much of the data in support of the viral role in asthma focuses on rhinovirus and respiratory syncytial virus. Epidemiologic studies have used factors such as day-care and family size as surrogates for infection in studies that support and negate the role of viruses in the development of asthma. A large volume of literature supports the theory that virus exacerbates preexisting asthma by setting off the inflammatory cascade. No mechanistic studies fully explain how viral infections can translate or exacerbate atopic disease. We provide information from our mouse model that suggests that dendritic cells, IgE, and FcRI are critical to the induction of atopy. Studies of patients taking antiviral agents (eg, ribavirin or palvizumab) support the notion that interfering with respiratory viral infections may decrease the development of atopy. Conclusions: Many studies suggest strongly that viral infections may predispose patients to the development of asthma and other atopic diseases. Further, mechanistic studies are necessary to allow for the development of targeted therapeutics to prevent the translation of viral into atopic disease.
[EX A]:
The role of viruses in the development and exacerbation of atopic disease