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 Input:
In this paper, a modified susceptible infected susceptible (SIS) epidemic model is proposed on community structure networks considering birth and death of node. For the existence of node's death would change the topology of global network, the characteristic of network with death rate is discussed. Then we study the epidemiology behavior based on the mean-field theory and derive the relationships between epidemic threshold and other parameters, such as modularity coefficient, birth rate and death rates (caused by disease or other reasons). In addition, the stability of endemic equilibrium is analyzed. Theoretical analysis and simulations show that the epidemic threshold increases with the increase of two kinds of death rates, while it decreases with the increase of the modularity coefficient and network size.

Ex Output:
The Journal of China Universities of Posts and Telecommunications Modeling and analysis of epidemic spreading on community network with node's birth and death


Ex Input:
This paper describes the development and evaluation of in situ hybridization (ISH) for the detection of rhinovirus in cells obtained from nasal washings of volunteers infected with human rhinovirus 14 (HRV-14). Twenty-five (66%) and 27 (71%) of 38 volunteers inoculated with HRV-14 had evidence of infection by virus isolation and ISH, respectively, on at least one of 4 days investigated after virus challenge. In contrast, only 14 of 38 (37%) volunteers had significant antibody rises as detected by the neutralization test. Of the 38 volunteers inoculated with HRV-14, only 13 (34%) had symptoms of colds. Of these, 12 (92%) and 10 (77%) were positive by virus isolation or ISH, respectively, on at least one day. Six (46%) had significant antibody rises by neu~ization. Similarly, of the 38 volunteers ch~lenged, 22 (58%) were asymptomatic and of these 10 (45.5%) and 12 (54.5%) were positive by virus isolation and ISH, respectively, on at least one day. Only 8 (36.4%) of these asymptomatic volunteers showed significant antibody rises by neutralization. There were significant associations between the detection of rhinoviruses by ISH and virus isolation on the third day (PcO.025) after virus challenge in the group as a whole and in the symptomatic group. These rest&s show that generally rhinovirus detection by ISH compares well with virus isolation and both tests are clearly more sensitive than the neutralization test in detecting evidence of infection. It is concluded that ISH is an interesting new technique that may play an important role in the study of rhinovirus infection and pathogenesis.

Ex Output:
115-l 26 Correspondence to: W. Al-Nakib, 30 Berkshire Road


Ex Input:
In the presence of IL-6, transforming growth factor (TGF)-β1 induces differentiation of T helper (Th) 17 cells in mice. Interleukin (IL)-23, a heterodimeric cytokine composed of IL-23p19 and IL-12/23p40 subunits, stimulates the growth and expansion of Th17 cells, and has been implicated in psoriasis pathogenesis. To study the associations between TGF-β1, the IL-23/Th17 inflammatory pathway, and psoriasis, we investigated inflammatory skin disease in transgenic mice that constitutively overexpress human TGF-β1 in basal keratinocytes (K5.hTGF-β1 transgenic mice); these mice had previously been reported as having a psoriasis-like disease. K5.hTGF-β1 transgenic mice had high levels of TGF-β1 mRNA and protein in both skin and serum. Levels of cytokines involved in IL-23/Th17-mediated inflammation were not elevated in lesional skin compared with those in non-lesional and wild-type skin. It is noteworthy that IL-4 and IgE were markedly elevated in inflamed skin and serum, respectively, of transgenic mice. Monoclonal antibodies (mAbs) specifically directed against IL-23p19 or IL-12/23p40 had no clinical effect on established inflammatory skin disease in K5.hTGF-β1 transgenic mice, whereas the same mAbs were able to block the development of murine experimental autoimmune encephalomyelitis, an IL-23/Th17mediated disease. In summary, the IL-23/Th17 inflammatory pathway is not responsible for the maintenance of inflammatory skin disease in K5.hTGF-β1 transgenic mice.

Ex Output:

Inflammatory Skin Disease in K5.hTGF-β1 Transgenic Mice Is Not Dependent on the IL-23/Th17 Inflammatory Pathway