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Two popular machine learning methods are Support Vector Machines (SVM) and k-Nearest Neighbour (KNN). KNN Algorithms simply store datasets throughout the training phase, and when new data is received, it is classified into a category that is quite similar to the new data. SVM is a supervised machine technique that may be used for both classification and regression. Though we also state regression problems, categorization is the best fit. The SVM algorithm's goal is to find a hyperplane in an N-dimensional space that distinguishes between data points. Used for categorising images, The KNN and SVM each have strengths and disadvantages. When classifying an image, the SVM creates a hyperplane, dividing the input space into classes and classifying the image based on that hyperplane.

Increasing evidence in substantiating the roles of endoplasmic reticulum stress, oxidative stress, and inflammatory responses and their interplay is evident in various diseases. However, an in-depth mechanistic understanding of the crosstalk between the intracellular stress signaling pathways and inflammatory responses and their participation in disease progression has not yet been explored. Progress has been made in our understanding of the cross talk and integrated stress signaling network between endoplasmic reticulum stress and oxidative stress towards the pathogenesis of diabetic nephropathy. In this present study, we studied the crosstalk between the endoplasmic reticulum stress and oxidative stress by understanding the role of protein disulfide isomerase and endoplasmic reticulum oxidase 1α, a key player in redox protein folding in the endoplasmic reticulum. We had recruited a total of 90 subjects and divided into three groups (control (n = 30), type 2 diabetes mellitus (n = 30), and diabetic nephropathy (n = 30)). We found that endoplasmic reticulum stress markers, activating transcription factor 6, inositol-requiring enzyme 1α, protein kinase RNA-like endoplasmic reticulum kinase, C/EBP homologous protein, and glucose-regulated protein-78; oxidative stress markers, thioredoxin-interacting protein and cytochrome b-245 light chain; and the crosstalk markers, protein disulfide isomerase and endoplasmic reticulum oxidase-1α, were progressively elevated in type 2 diabetes mellitus and diabetic nephropathy subjects. The association between the crosstalk markers showed a positive correlation with endoplasmic reticulum stress and oxidative stress markers. Further, the interplay between endoplasmic reticulum stress and oxidative stress was investigated in vitro using a human leukemic monocytic cell line under a hyperglycemic environment and examined the expression of protein disulfide isomerase and endoplasmic reticulum oxidase-1α. DCFH-DA assay and flow cytometry were performed to detect the production of free radicals. Further, phosphorylation of eIF2α in high glucose–exposed cells was studied using western blot. In conclusion, our results shed light on the crosstalk between endoplasmic reticulum stress and oxidative stress and significantly contribute to the onset and progression of diabetic nephropathy and therefore represent the major therapeutic targets for alleviating micro- and macrovascular complications associated with this metabolic disturbance. [Figure: see text] SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12192-020-01176-z.

Lipopolysaccharide (LPS) induces apoptosis in murine macrophages through the autocrine secretion of tumor necrosis factor (TNF)-α and nitric oxide (NO). LPS-induced inflammation in murine macrophages is associated with hydrogen sulfide (H2S) production. In this present study, we reported the novel role of H2S in LPS-induced apoptosis and its underlying molecular mechanism specifically at late phases in murine macrophage cells. Stimulation of RAW 264.7 macrophages with LPS resulted in a time- and dose-dependent induction of apoptosis. We observed that the LPS-induced early apoptosis (associated with TNF-α secretion) in macrophages was not inhibited in the presence of H2S inhibitor (DL-propargylglycine), whereas early apoptosis was absent in the presence of TNF receptor antibody. Interestingly, LPS-induced late apoptosis paralleled with H2S production was reduced in the presence of H2S inhibitor but not with TNF receptor antibody. The late apoptotic events mediated by H2S and not the TNF-α induced early apoptosis correlated significantly with the induction of p53 and Bax expression in LPS-induced macrophages. Thus, it is possible that RAW 264.7 murine macrophages treated with LPS mediated early apoptosis through TNF-α and the late apoptotic events through the production of H2S.

Background and Objectives Morinda citrifolia (Noni), an important traditional medicinal plant still used in patients with bone fractures or dislocation to promote connective tissue repair and to reduce inflammation. However, the effects of Noni on bone metabolism and whether it influences the osteogenic differentiation is yet to be clarified. In this study, we investigated the effect of Morinda citrifolia (Noni) juice on the proliferation rate of rat bone marrow derived mesenchymal stem cells (BMSC) and the osteoblastic differentiation as shown by alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2) and osteocalcin (OCN) mRNA expression in vitro. Methods and Results Treatment with 200 μg/ml Noni juice enhanced the proliferation rate of the BMSC and also upregulated the osteogenic differentiation marker genes ALP and OCN, and Runx2 measured by RTPCR. Consistent with these results collagen scaffolds implanted in vivo, which were loaded with BMSC pre-exposed to Noni, showed increased bone density measured by computed tomography and histological analysis revealed neo-angiogenesis for bone formation. Conclusions These results suggest that Noni stimulates osteoblastogenesis and can be used as adjuvant natural medicine for bone diseases such as osteoporosis.

Aims The aim of this study was to investigate the effect of yoga intervention on the biochemical, oxidative stress markers and inflammatory markers and sleep quality among subjects with type 2 diabetes. Methods Subjects with type 2 diabetes attending a tertiary care centre for diabetes during Feb 2017 to Oct 2019 in Chennai, India were randomly assigned to two different groups. Group1(non-Yoga) (n = 150) was advised on simple physical exercises whereas group2(Yoga) (n = 150) was trained and advised to do yogasanas with static loosening exercises for 50 min for 5 days in a week. Both the groups were followed up for a period of 3 months. Anthropometric, biochemical, oxidative stress markers, inflammatory markers and sleep quality were assessed at baseline and after follow up. Results There was a significant reduction in BMI, blood glucose levels, HbA1c, lipid levels, IL6, TNFα and TBARS in Yoga group as compared to non-Yoga group. There was marked improvement in the levels of Adiponectin, PTGIS and sleep quality among subjects practising yogasanas. Conclusion Regular practice of yogasanas improved glycaemic control, oxidative stress, inflammatory response and sleep quality among subjects with type 2 diabetes. Hence, Yogasanas can be used as an adjuvant therapy for managing type 2 diabetes.

Oxidant imbalance is a key feature in the pathogenesis and progression of chronic obstructive airway diseases (COADs) like asthma and chronic obstructive pulmonary disease (COPD). Proinflammatory reaction and oxidative stress complement each other in COAD pathogenesis. Genetic predisposition, like variations and altered regulation of antioxidant genes as well as their transcriptional control mechanisms, may also render susceptibility to COADs. Dietary supplementation particularly of nonenzymatic antioxidants such as vitamin E and C are suggested as plausible preventive measures for COAD development. Thiols, and antioxidant mimetics like spin traps are also being explored as potential therapeutic options for COADs. This chapter discusses the association of disrupted redox homeostasis in asthma and COPD, various exogenous and endogenous sources of reactive oxygen species that contribute to oxidative stress development in COAD, antioxidant defense system of the lung, biochemical mechanisms of oxidative stress mediated damage, and the antioxidant based preventive as well as therapeutic modalities that are currently being explored to treat COADs.

Table S1. List of the genes screened for association to higher Chronic Obstructive Pulmonary Disease (COPD) susceptibility. Table S2. Summary of the transcript (Gene Paint; mouse embryo) and protein (Human Protein Atlas) expression domains of the significantly associated chronic obstructive pulmonary disease (COPD) genes. Table S3. Analysis of lung transcript expression of the associated 20 genes in chronic obstructive pulmonary disease (COPD) and/ or emphysematous lung tissues using available datasets [GSE: 29133, 22,148, 1650, 47,460 and 54,837] in Genome Expression Omnibus (GEO) database. ↓: Decreased ↑: Increased ✓: significantly altered. Table S4. Analysis of l transcript expression of the associated 20 genes in mouse cigarette smoke exposed lungs using available datasets [GSE: 8790, 7310, 17,737, and 6205] in Genome Expression Omnibus (GEO) database. ↓: Decreased ↑: Increased ✓: significantly altered. Table S5. The difference in minor allele frequencies of the associated single nucleotide polymorphisms (SNPs) between Korean population and global population indicates the influence of ethnicity on the findings. The Korean population data was accessed from the KoreanDB: http://152.99.75.168/KRGDB/menuPages/firstInfo.jsp and http://152.99.75.168/KRGDB/browser/mainBrowser.jsp Global SNP data(dbSNP database): https://www.ncbi.nlm.nih.gov/SNP/ . Figure S1. Analysis of protein domain and functional sites in the “A Disintegrin and metallopeptidase domain 19” (ADAM19). Figure S2. Transcript (Gene Paint; mouse embryo) and protein expression (Human Protein atlas; normal lung) domain of holliday junction recognition protein (HJURP). Figure S3. Transcript (Gene Paint; mouse embryo) and protein expression (Human Protein atlas; normal lung) domain of microspherule protein 1 (MCRS1). Figure S4. Protein expression (Human Protein atlas; normal lung) domain of toll like receptor 8 (TLR8). Figure S5. Gene-set enrichment analysis for the associated 20 genes for (A) cellular component enrichment (B) biological process enrichment (C) molecular function enrichment (D) diseases enrichment using Enrichr interactive enrichment analysis tool [71]. (PDF 1296 kb)

Rationale. Exposure to biomass smoke (BMS) has been implicated in chronic obstructive pulmonary disease (COPD). About 3 billion people worldwide use biomass fuel for cooking and heating. Women in rural communities of low- and lower-middle-income countries are disproportionately exposed to massive amounts of BMS during active cooking hours (4–6 h/day). Therefore, BMS exposure is considered as a risk factor for COPD in the same order of magnitude as tobacco smoke. In rural India, due to cultural reasons, women are the primary cook of the family and are mostly nonsmokers. Thus, BMS-induced COPD is predominant among rural Indian women. However, BMS-COPD remains a relatively unexplored health problem globally. Therefore, we investigated the serum chemokine and cytokine signatures of BMS-COPD and tobacco smoke-induced COPD (TS-COPD) patients compared to their control in a rural South Indian population for this field study. Methods. Concentrations of 40 serum chemokines and cytokines were measured using a multiplexed immunoassay. The study cohort consisted of BMS-COPD (female; n=29) and BMS-exposed subjects without COPD (BMS-CONTROL; female; n=24). For comparison, data from TS-COPD patients (male, n=23) and tobacco smokers without COPD (TS-CONTROL; male, n=22) were investigated. Subjects were matched for age, sex, and biomass exposure. Tobacco consumption was slightly higher in TS-COPD subjects compared to TS-CONTROL. BMS-exposed and TS-exposed subjects (currently exposed) were from the same locality with similar dwelling habits and socioeconomic status. A validated structured questionnaire-based survey and spirometry was performed. An additional control group with no tobacco and BMS exposure (TS-BMS-CONTROL; n=15) was included. Statistical significance was set at p≤0.01. Results. Serum median concentrations (pg/ml) of CCL15 [8799.35; 5977.22], CCL27 [1409.14; 1024.99], and CXCL13 [37.14; 26.03] were significantly higher in BMS-CONTROL compared to BMS-COPD subjects. Nine analytes exhibited higher concentrations in TS-CONTROL compared to TS-COPD subjects. Comparison of chemokine and cytokine concentrations among BMS-COPD versus TS-COPD and BMS-CONTROL versus TS-CONTROL subjects also revealed distinct molecular signatures. Conclusion. Our data identifies CCL27 and CXCL13 as putative, plausibly homeostatic/protective biomarkers for BMS-COPD within the investigated population that warrants validation in larger and multiple cohorts. The findings further indicate exposure-specific systemic response of chemokines and cytokines.

Rationale: Biomass (BM) smoke induced household air pollution (HAP) is a risk factor for COPD. Crude estimates suggest about 30 million COPD patients in India. Although tobacco smoke (TS) is the predominant COPD risk factor world-wide, in India, despite male to female smoking ratio being 10:1, the corresponding COPD ratio is 1.5:1. This is mainly attributed to high BM-HAP exposure among poor rural women who are also the primary cook of the family. It is plausible that the underlying molecular patho-mechanisms of BM-COPD and TS-COPD may also be different. Therefore in this study we investigated the serum cytokine signature of BM-COPD and TS-COPD patients in a South Indian (Mysuru) population. Methods: All procedures were approved by the institutional ethical committee (JSSMC/IEC/13/4048/2016-2017) of JSS Medical College and Hospital, India. COPD was diagnosed according to the GOLD 2012 guidelines. Serum cytokine profiles of 27 subjects: TS-COPD (n=13, male); asymptomatic smokers (n=4, male); BM-COPD (n=5, female); BM exposed without COPD (n=5, female) were assessed using the 40-plex inflammatory marker panel (Biorad: #171AK99MR2). Results: CCL27, CXCL2, CCL23 and CXCL16 were increased among TS-COPD cases compared to asymptomatic smokers (p Conclusion: Our preliminary data indicates specific serum cytokine signature among TS-COPD and BM-COPD patients that warrants further investigation in larger cohort. Acknowledgement: DBT-India BT/PR12987/INF/22/205/2015

Background Failure to attain peak lung function by early adulthood is a risk factor for chronic lung diseases. Previously, we reported that C3H/HeJ mice have about twice total lung capacity (TLC) compared to JF1/MsJ mice. We identified seven lung function quantitative trait loci (QTL: Lfnq1-Lfnq7) in backcross/intercross mice derived from these inbred strains. We further demonstrated, superoxide dismutase 3, extracellular (Sod3), Kit oncogene (Kit) and secreted phosphoprotein 1 (Spp1) located on these Lfnqs as lung function determinants. Emanating from the concept of early origin of lung disease, we sought to identify novel candidate genes for pulmonary function by investigating lung transcriptome in C3H/HeJ and JF1/MsJ mice at the completion of embryonic development, bulk alveolar formation and maturity. Methods Design-based stereological analysis was performed to study lung structure in C3H/HeJ and JF1/MsJ mice. Microarray was used for lung transcriptomic analysis [embryonic day 18, postnatal days 28, 70]. Quantitative real time polymerase chain reaction (qRT-PCR), western blot and immunohistochemical analysis were used to confirm selected differences. Results Stereological analysis revealed decreased alveolar number density, elastin to collagen ratio and increased mean alveolar volume in C3H/HeJ mice compared to JF1/MsJ. Gene ontology term “extracellular region” was enriched among the decreased JF1/MsJ transcripts. Candidate genes identified using the expression-QTL strategy include: ATP-binding cassette, sub-family G (WHITE), member 1 (Abcg1), formyl peptide receptor 1 (Fpr1), gamma-aminobutyric acid (GABA) B receptor, 1 (Gabbr1); histocompatibility 2 genes: class II antigen E beta (H2-Eb1), D region locus 1 (H2-D1), and Q region locus 4 (H2-Q4); leucine rich repeat containing 6 (testis) (Lrrc6), radial spoke head 1 homolog (Rsph1), and surfactant associated 2 (Sfta2). Noteworthy genes selected as candidates for their consistent expression include: Wnt inhibitor factor 1 (Wif1), follistatin (Fst), chitinase-like 1 (Chil1), and Chil3. Conclusions Comparison of late embryonic, adolescent and adult lung transcript profiles between mouse strains with extreme TLCs lead to the identification of candidate genes for pulmonary function that has not been reported earlier. Further mechanistic investigations are warranted to elucidate their mode of action in determining lung function. Electronic supplementary material The online version of this article (doi:10.1186/s12931-017-0629-3) contains supplementary material, which is available to authorized users.

Background and Objectives Morinda citrifolia (Noni), an important traditional medicinal plant still used in patients with bone fractures or dislocation to promote connective tissue repair and to reduce inflammation. However, the effects of Noni on bone metabolism and whether it influences the osteogenic differentiation is yet to be clarified. In this study, we investigated the effect of Morinda citrifolia (Noni) juice on the proliferation rate of rat bone marrow derived mesenchymal stem cells (BMSC) and the osteoblastic differentiation as shown by alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2) and osteocalcin (OCN) mRNA expression in vitro. Methods and Results Treatment with 200 μg/ml Noni juice enhanced the proliferation rate of the BMSC and also upregulated the osteogenic differentiation marker genes ALP and OCN, and Runx2 measured by RTPCR. Consistent with these results collagen scaffolds implanted in vivo, which were loaded with BMSC pre-exposed to Noni, showed increased bone density measured by computed tomography and histological analysis revealed neo-angiogenesis for bone formation. Conclusions These results suggest that Noni stimulates osteoblastogenesis and can be used as adjuvant natural medicine for bone diseases such as osteoporosis.

This study was conducted to assess the anti-inflammatory effect of a novel synthesized phenanthridine alkaloid (PHE-4i) and to examine the possible involvement of hydrogen sulfide (H2S) in anti-inflammatory mechanism. The synthesized phenanthridine derivative PHE-4i (2, 5, and 10 mg/kg) was administered intraperitoneally to rats. One hour following treatment, inflammation was induced by intraplantar injection of carrageenan (1 %), in the hind paw. Paw volume as the index of inflammation was measured before and after carrageenan injection. Neutrophil sequestration into the hind paw was quantified by measuring tissue myeloperoxidase (MPO) activity and was compared for the inhibition of H2S production. Pretreatment with PHE-4i significantly reduced carrageenan-induced hind paw weight, MPO activity, leukocyte infiltration, and H2S production in a dose-dependent manner (p

Purpose To document transcriptional activation (expression) of key aflatoxin biosynthetic pathway genes in corneal isolates of Aspergillus flavus. Methods The expression of certain regulatory (aflatoxin regulatory [aflR] and aflatoxin J [aflJ]) and structural (polyketide synthase acetate [pksA] and norsolonic acid-1 [nor-1]) genes in four corneal A. flavus isolates was evaluated by reverse transcription PCR. The aflatoxin-producing potential of each strain was determined by thin-layer chromatography and quantified by spectrophotometry. Four environmental isolates were used for comparison. The mean expression levels of these genes were compared in the corneal and environmental A. flavus isolates. In addition, the mean expression levels were also correlated with the aflatoxin production levels. Results All isolates expressed aflJ, nor-1, and pksA, while all but one expressed aflR. Overall, significantly higher mean expression levels occurred in aflatoxigenic than in non-aflatoxigenic corneal isolates. A significant positive correlation was noted between the mean expression level of aflR and the quantum of aflatoxin production by the corneal isolates. Essentially similar patterns of expression of these genes were noted in four environmental A. flavus isolates used for comparison. Conclusions For the first time, isolates of A. flavus from human keratitis patients have been shown to express regulatory and structural aflatoxin biosynthetic pathway genes. Further studies are needed to clarify the precise influence of the corneal microenvironment on expression of these genes and aflatoxin production by A. flavus infecting the cornea.

Background: Studies provide compelling evidences for particulate matter (PM) associated cardiovascular health effects. Elderly individuals, particularly those with preexisting conditions like hypertension are regarded to be vulnerable. Experimental data are warranted to reveal the molecular pathomechanism of PM related cardiovascular impairments among aged/predisposed individuals. Thus we investigated the cardiovascular effects of ultrafine carbon particles (UfCP) on aged (12-13 months) spontaneously hypertensive rats (SHRs) and compared the findings with our pervious study on adult SHRs (6-7 months) to identify age related predisposition events in cardiovascular compromised elderly individuals. Methods: Aged SHRs were inhalation exposed to UfCP for 24 h (~180 μg/m3) followed by radio-telemetric assessment for blood pressure (BP) and heart rate (HR). Bronchoalveolar lavage (BAL) fluid cell differentials, interleukin 6 (IL-6) and other proinflammatory cytokines; serum C-reactive protein (CRP) and haptoglobin (HPT); and plasma fibrinogen were measured. Transcript levels of hemeoxygenase 1 (HO-1), endothelin 1 (ET1), endothelin receptors A, B (ETA, ETB), tissue factor (TF), and plasminogen activator inhibitor-1 (PAI-1) were measured in the lung and heart to assess oxidative stress, endothelial dysfunction and coagulation cascade. Result: UfCP exposed aged SHRs exhibited increased BP (4.4%) and HR (6.3%) on 1st recovery day paralleled by a 58% increase of neutrophils and 25% increase of IL-6 in the BAL fluid. Simultaneously higher CRP, HPT and fibrinogen levels in exposed SHRs indicate systemic inflammation. HO-1, ET1, ET-A, ET-B, TF and PAI-1 were induced by 1.5-2.0 folds in lungs of aged SHRs on 1st recovery day. However, in UfCP exposed adult SHRs these markers were up-regulated (2.5-6 fold) on 3rd recovery day in lung without detectable pulmonary/systemic inflammation. Conclusions: The UfCP induced pulmonary and systemic inflammation in aged SHRs is associated with oxidative stress, endothelial dysfunction and disturbed coagulatory hemostasis. UfCP exposure increased BP and HR in aged SHRs rats which was associated with lung inflammation, and increased expression of inflammatory, vasoconstriction and coagulation markers as well as systemic changes in biomarkers of thrombosis in aged SHRs. Our study provides further evidence for potential molecular mechanisms explaining the increased risk of particle mediated cardiac health effects in cardiovascular compromised elderly individuals.

Secreted phosphoprotein 1 (Spp1) is located within quantitative trait loci associated with lung function that was previously identified by contrasting C3H/HeJ and JF1/Msf mouse strains that have extremely divergent lung function. JF1/Msf mice with diminished lung function had reduced lung SPP1 transcript and protein during the peak stage of alveologenesis (postnatal day [P]14-P28) as compared with C3H/ HeJ mice. In addition to a previously identified genetic variant that altered runt-related transcription factor 2 (RUNX2) binding in the Spp1 promoter, we identified another promoter variant in a putative RUNX2 binding site that increased the DNA protein binding. SPP1 induced dose-dependent mouse lung epithelial-15 cell proliferation. Spp1(-/-) mice have decreased specific total lung capacity/body weight, higher specific compliance, and increased mean airspace chord length (Lm) compared with Spp1(+/+) mice. Microarray analysis revealed enriched gene ontogeny categories, with numerous genes associated with lung development and/or respiratory disease. Insulin-like growth factor 1, Hedgehog-interacting protein, winglessrelated mouse mammary tumor virus integration site 5A, and NOTCH1 transcripts decreased in the lung of P14 Spp1(-/-) mice as determined by quantitative RT-PCR analysis. SPP1 promotes pneumocyte growth, and mice lacking SPP1 have smaller, more compliant lungs with enlarged airspace (i.e., increased Lm). Microarray analysis suggests a dysregulation of key lung developmental transcripts in gene-targeted Spp1(-/-) mice, particularly during the peak phase of alveologenesis. In addition to its known roles in lung disease, this study supports SPP1 as a determinant of lung development in mice. Copyright � 2014 by the American Thoracic Society.

Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at embryonic day 18. Table S2. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at embryonic stage 18. Table S3. Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 28. Table S4. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 28. Table S5. Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 70. Table S6. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 70. Table S7. Transcripts showing consistent pattern of expression lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice across E18/ P28 stages. Table S8. Transcripts showing consistent pattern of expression lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice across P28/ P70 stages. Figure S1. Representative lung sections showing smaller alveoli in JF1/Msf (JF1) mice compared to C3H/HeJ (C3H) in both males and females. (DOCX 216Â kb)

Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at embryonic day 18. Table S2. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at embryonic stage 18. Table S3. Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 28. Table S4. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 28. Table S5. Increased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 70. Table S6. Decreased lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice at postnatal day 70. Table S7. Transcripts showing consistent pattern of expression lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice across E18/ P28 stages. Table S8. Transcripts showing consistent pattern of expression lung transcripts in JF1/MsJ (JF1) compared to C3H/HeJ (C3H) mice across P28/ P70 stages. Figure S1. Representative lung sections showing smaller alveoli in JF1/Msf (JF1) mice compared to C3H/HeJ (C3H) in both males and females. (DOCX 216Â kb)