In this task, you are given a paragraph (from a research paper) and your task is to classify each sentence of the paragraph (assume n sentence) into the following categories: Background, Purpose, Method, Finding/Contribution, or Other. Return the output in this format: 1 - category of sentence 1, 2 - category of sentence 2, ..., n - category of sentence n; where each number indicates the order of the sentence. The categories can be identified using the following questions: 
 Background: - Why is this problem important? - What relevant works have been done before? - What did the previous works miss? - What are the high-level research questions? - How might this help other researchers?
 Purpose: - What specific things do the researchers want to do? - What specific knowledge do the researchers want to know? - What specific hypothesis do the researchers want to test?
 Method: - How did the researchers do it or find it out? - What are the procedures and steps of this research?
 Finding/Contribution: - What did the researchers find out? Did the proposed methods work? - Did things behave as the researchers expected?
Other: put every text fragment that does not fit into any of the categories above here. Put a sentence here if its not in English, is not part of the article, contains numbers and dates, is a caption of a figure or a table, is a formatting error, or you are not sure about it.

[Q]: Acute otitis media (AOM) is an inflammatory response to microbes in the middle ear, sometimes associated with rupture of the tympanic membrane. Human leukocytes produce different patterns of inflammatory mediators in vitro when stimulated with Gram-positive and Gram-negative bacteria, respectively. Here, we investigated the cytokine and prostaglandin E 2 (PGE 2 ) responses in middle ear fluids (MEFs) from children with spontaneously perforated AOM, and related the mediator levels to the presence of pathogens detected by culture (live) or PCR (live or dead). Furthermore, the in vivo cytokine pattern was compared with that induced in leukocytes stimulated by dead bacteria in vitro. MEFs with culturable pathogenic bacteria contained more interleukin (IL)-1b (median: 110 lg/L vs. <7.5 lg/L), tumour necrosis factor (TNF) (6.3 lg/L vs. <2.5 lg/L), IL-8 (410 lg/L vs. 38 lg/L) and IL-10 (0.48 lg/L vs. <0.30 lg/L) than culture-negative fluids, irrespective of PCR findings. IL-6 and PGE 2 were equally abundant (69-110 lg/L) in effusions with live, dead or undetectable bacteria. Cytokine levels were unrelated to bacterial species and to the presence or absence of virus. Similar levels of TNF and IL-6 as found in the MEFs were obtained by in vitro stimulation of leukocytes, whereas 11 times more IL-1b and 3.5 times more IL-8 were produced in vivo, and 22 times more IL-10 was produced in vitro. Vigorous production of proinflammatory cytokines accompanies AOM with membrane rupture, regardless of the causative agent, but the production seems to cease rapidly once the bacteria are killed and fragmented. IL-6 and PGE 2 , however, remain after bacterial disintegration, and may play a role in the resolution phase.
[A]: 1 - background, 2 - background, 3 - background, 4 - purpose, 5 - purpose, 6 - method, 7 - finding, 8 - finding, 9 - finding, 10 - finding, 11 - finding, 12 - finding, 13 - finding, 14 - finding, 15 - finding, 16 - finding, 17 - finding, 18 - finding, 19 - finding


[Q]: We evaluated if interventions aimed at air travellers can delay establishment of a SARS-CoV-2 outbreak in a previously unaffected country. Methods: For countries with no sustained SARS-CoV-2 transmission and with no shared border with affected regions we simulated arriving infected air travellers. We assessed the effectiveness of syndromic screening at departure and/or arrival & traveller sensitisation to the COVID-2019-like symptoms with the aim to trigger rapid self-isolation and reporting on symptom onset to enable contact tracing. We assumed that syndromic screening would reduce the number of infected arrivals and that traveller sensitisation reduce the average number of secondary cases. We report the minimal expected delay achievable in 50% (75% & 97.5%) of simulations. In the simulations we account for uncertainty in the number of secondary cases in the absence of air traveller targeted interventions and the arrival times of infected cases and also present sensitivity analyses on arrival rates of infected travellers and the effectiveness of traveller sensitisation. Results: Under baseline assumptions exit and entry screening combined with traveller sensitisation can delay a local SARS-CoV-2 outbreak by at least 83 (75% of simulations: at least 36, 97.5% 8) days while there is no more than 1 infected traveller per week. The benefit of entry screening is small if exit screening is effective: the combination of only exit screening and traveller sensitisation can delay an outbreak by at least 76 (75%: 33, 97.5%: 7) days. With increasing rates of infected travellers, less effective sensitisation or without screening these delays shrink rapidly to a week or less. Conclusion: Syndromic screening and traveller sensitisation in combination could delay outbreaks in yet unaffected countries and support local containment efforts, but only if infected traveller numbers are very low.
[A]: 1 - background, 2 - method, 3 - method, 4 - method, 5 - finding, 6 - method, 7 - finding, 8 - finding, 9 - finding, 10 - finding, 11 - finding, 12 - finding


[Q]: Human bocavirus (HBoV) was recently discovered in children with respiratory distress and/or diarrhea. To our knowledge, no previous study has reported the existence of bocavirus in Saudi Arabia. Swabs samples from 80 children with respiratory tract infections were examined for the presence of HBoV. Real-time polymerase chain reaction was used as a sensitive method to detect the HBoV. Direct gene sequencing was used to determine the genotype of the detected virus isolates. HBoV was detected in 22.5% of the examined patients. The NP1 partial gene sequence from all patients showed that the circulated strains were related to HBoV-1 genotype. Most of HBoV infected patients showed evidence of mixed coinfection with other viral pathogens. The current study clearly demonstrated that genetically conserved HBoV1 circulates in Saudi Arabia. Interestingly, most of the HBoV1 infected cases were associated with high rates of co-infections with other viruses.
[A]:
1 - background, 2 - background, 3 - background, 4 - background, 5 - background, 6 - finding, 7 - finding, 8 - finding, 9 - finding, 10 - finding


