Additional file 3: of Effectiveness of government strategies for financial protection against costs of hospitalization Care in India

Average Out-of-pocket expenditure (OOPE) per hospitalization episode (the mean, in Rs.) across various socio-economic categories by type of insurance coverage. This table was calculated by the authors using the NSS 71st Round unit level data. This table shows OOPE across different equity indicators (sex, residence and social group). (XLSX 9 kb

Additional file 8: of Effectiveness of government strategies for financial protection against costs of hospitalization Care in India

Factors affecting likelihood of hospitalization in India. This table was calculated by the authors using the NSS 71st Round unit level data. It is based on a logistic regression and shows factors affecting hospitalization in India. (XLSX 9 kb

Additional file 4: of Effectiveness of government strategies for financial protection against costs of hospitalization Care in India

Major source of finance for expenses incurred during hospitalization. This table was calculated by the authors using the NSS 71st Round unit level data. This table shows major sources of financing for households to meet their healthcare expenditure. (XLSX 10 kb

Additional file 1: of Effectiveness of government strategies for financial protection against costs of hospitalization Care in India

Different public funded health insurance (PFHI) programmes in India. This table shows the different PFHIs in India, including eligible beneficiaries, packages of services, sources of funding and covered population. This was obtained from different states’ websites and the World Bank Report, 2012. (XLSX 10 kb

Classification of samples with intact <i>E2</i> gene into those harbouring pure episomal and concomitant (episomal+integrated) viral genomes based on <i>E7</i> C_T/<i>E4</i> C_T derived from APOT-coupled-quantitative-RT-PCR assay.

<p>Concomitant refers to the presence of both episomal and integrated viral genomes.</p

Linear regression analyses.

<p>(<b>A</b>) Correlation of <i>E7</i> C_T/<i>ACTB</i> C_T with viral load (natural log values) in CaCx cases with episomal (purely episomal and concomitant) viral genomes; (<b>B</b>) Correlation of <i>E7</i> C_T/<i>ACTB</i> C_T with viral load (natural log values) in CaCx cases with integrated viral genomes; (<b>C</b>) Correlation of <i>E2</i> C_T/<i>ACTB</i> C_T with viral load (natural log values) with respect to <i>E2</i> gene in CaCx cases with episomal (purely episomal and concomitant) viral genomes.</p

APOT-coupled-quantitative-RT-PCR assay.

<p>(<b>A</b>) Representative gel electrophoresis showing P2 - (dT)17-P3 products. Lane 1: sample showing presence of 1050 bp band-size indicating episomal viral genome. Presence of other band-sizes indicates concomitant status; Lanes 2, 3, 4, 6: absence of band-size 1050 bp indicates integrated status of these samples. Lane 5: 100 bp ladder (Roche)<b>.</b> (<b>B</b>) TaqMan-based quantitative RT-PCR amplification plots of <i>E7</i> and <i>E4</i> cDNA. <i>E7</i> is transcribed in both episomal (pure or concomitant) and integrated cases, but <i>E4</i> is transcribed in only episomal cases. (<b>C</b>) Agarose gel electrophoresis of PCR products of <i>GAPDH</i> cDNA (primers span exon-exon junction). Lane 1: negative control; Lane 2: CaSki cell line DNA (negative control); Lanes 3–7: sample cDNAs showing specific band size of 106 bp; Lanes 3 and 7 show episomal (pure or concomitant) samples T323 and T329, respectively, while, Lanes 4–6 show purely integrated samples T327, T326 and T328, respectively; Lane 8: <i>Hae</i> III digested ?x174 DNA marker (Promega). (<b>D</b>) Agarose gel electrophoresis of PCR products of <i>TP53</i> cDNA (primers span introns). Lane 1–6, 8, 9: sample cDNA not showing specific band size of 448 bp; Lanes 1, 2, 4, 6 and 9 show purely integrated samples T326, T327, T345, T344 and T328, respectively, while, lanes 3, 5 and 8 show episomal (pure or concomitant) samples T329, T323 and T339, respectively; Lane 10: CaSki cell line DNA (positive control); Lane 11: sample DNA (positive control); Lane 12: water (negative control); Lane 7: <i>Hae</i> III digested ?x174 DNA marker (Promega).</p

A Quest for miRNA Bio-Marker: A Track Back Approach from Gingivo Buccal Cancer to Two Different Types of Precancers

<div><p>Deregulation of miRNA expression may contribute to tumorigenesis and other patho-physiology associated with cancer. Using TLDA, expression of 762 miRNAs was checked in 18 pairs of gingivo buccal cancer-adjacent control tissues. Expression of significantly deregulated miRNAs was further validated in cancer and examined in two types of precancer (leukoplakia and lichen planus) tissues by primer-specific TaqMan assays. Biological implications of these miRNAs were assessed bioinformatically. Expression of <i>hsa-miR-1293, hsa-miR-31, hsa-miR-31*</i> and <i>hsa-miR-7</i> were significantly up-regulated and those of <i>hsa-miR-206, hsa-miR-204</i> and <i>hsa-miR-133a</i> were significantly down-regulated in all cancer samples. Expression of only <i>hsa-miR</i>-31 was significantly up-regulated in leukoplakia but none in lichen planus samples. Analysis of expression heterogeneity divided 18 cancer samples into clusters of 13 and 5 samples and revealed that expression of 30 miRNAs (including the above-mentioned 7 miRNAs), was significantly deregulated in the cluster of 13 samples. From database mining and pathway analysis it was observed that these miRNAs can significantly target many of the genes present in different cancer related pathways such as “proteoglycans in cancer”, <i>PI3K-AKT</i> etc. which play important roles in expression of different molecular features of cancer. Expression of <i>hsa-miR-31</i> was significantly up-regulated in both cancer and leukoplakia tissues and, thus, may be one of the molecular markers of leukoplakia which may progress to gingivo-buccal cancer.</p></div

Methylation analysis.

<p>(<b>A</b>) Bar diagram comparing percentage of samples methylated at different CpGs within the LCR of HPV16 genome between <i>E2</i>-intact and <i>E2</i>-disrupted samples. (<b>B</b>) Diagrammatic representation of the mentioned CpG positions within the LCR: 7862 – Viral replication origin; 31 – SpI binding site; 37 and 43 – E2BS II; 52 and 58 – E2BS I.</p

Samples with purely integrated viral genomes grouped into 4 clusters after <i>k</i>-means clustering analysis.

<p>Cluster 1: low viral load and low <i>E7</i> expression; Cluster 2: high viral load and low <i>E7</i> expression; Cluster 3: moderate viral load and moderate <i>E7</i> expression; Cluster 4: low to moderate viral load and high <i>E7</i> expression.</p