Detailed Instructions: 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.
Problem: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.
Solution:
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