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9. Supplementary Fig. from Coronarin D, a labdane diterpene, inhibits both constitutive and inducible nuclear factor-κB pathway activation, leading to potentiation of apoptosis, inhibition of invasion, and suppression of osteoclastogenesis

Author

Kunnumakkara, Ajaikumar B., primary, Ichikawa, Haruyo, primary, Anand, Preetha, primary, Mohankumar, Chiramel J., primary, Hema, Padmanabhan S., primary, Nair, Mangalam S., primary, and Aggarwal, Bharat B., primary

Published
2023
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10. Supplementary Fig. from Coronarin D, a labdane diterpene, inhibits both constitutive and inducible nuclear factor-κB pathway activation, leading to potentiation of apoptosis, inhibition of invasion, and suppression of osteoclastogenesis

Author

Bharat B. Aggarwal, Mangalam S. Nair, Padmanabhan S. Hema, Chiramel J. Mohankumar, Preetha Anand, Haruyo Ichikawa, and Ajaikumar B. Kunnumakkara

Abstract

Supplementary Fig. from Coronarin D, a labdane diterpene, inhibits both constitutive and inducible nuclear factor-κB pathway activation, leading to potentiation of apoptosis, inhibition of invasion, and suppression of osteoclastogenesis

Published
2023
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11. Data from Coronarin D, a labdane diterpene, inhibits both constitutive and inducible nuclear factor-κB pathway activation, leading to potentiation of apoptosis, inhibition of invasion, and suppression of osteoclastogenesis

Author

Bharat B. Aggarwal, Mangalam S. Nair, Padmanabhan S. Hema, Chiramel J. Mohankumar, Preetha Anand, Haruyo Ichikawa, and Ajaikumar B. Kunnumakkara

Abstract

Compounds isolated from members of the Zingiberaceae family are traditionally used as a medicine against inflammatory diseases, but little is known about the mechanism. Here, we report the isolation and structural identification of coronarin D [E-labda-8(17),12-diene-15-ol], a labdane-type diterpene, from Hedychium coronarium and delineate its mechanism of action. Because the transcription factor nuclear factor-κB (NF-κB) is a key mediator of inflammation, apoptosis, invasion, and osteoclastogenesis, we investigated the effect of coronarin D on NF-κB activation pathway, NF-κB-regulated gene products, and NF-κB-regulated cellular responses. The coronarin D inhibited NF-κB activation induced by different inflammatory stimuli and carcinogens. This labdane also suppressed constitutive NF-κB activity in different cell lines and inhibited IκBα kinase activation, thus leading to the suppression of IκBα phosphorylation, degradation, p65 nuclear translocation, and reporter gene transcription. Coronarin D also inhibited the NF-κB-regulated gene products involved in cell survival (inhibitor of apoptosis protein 1, Bcl-2, survivin, and tumor necrosis factor receptor-associated factor-2), proliferation (c-myc, cyclin D1, and cyclooxygenase-2), invasion (matrix metalloproteinase-9), and angiogenesis (vascular endothelial growth factor). Suppression of these gene products by the diterpene enhanced apoptosis induced by TNF and chemotherapeutic agents, suppressed TNF-induced cellular invasion, and abrogated receptor activator of NF-κB ligand-induced osteoclastogenesis. Coronarin D was found to be more potent than its analogue coronarin D acid. Overall, our results show that coronarin D inhibited NF-κB activation pathway, which leads to inhibition of inflammation, invasion, and osteoclastogenesis, as well as potentiation of apoptosis. [Mol Cancer Ther 2008;7(10):3306–17]

Published
2023
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12. Data from Nimbolide, a Limonoid Triterpene, Inhibits Growth of Human Colorectal Cancer Xenografts by Suppressing the Proinflammatory Microenvironment

Author

Bharat B. Aggarwal, Yin-Yuan Mo, Mangalam S. Nair, Dhanya R. Sethumadhavan, Sahdeo Prasad, and Subash C. Gupta

Abstract

Purpose: Extensive research over the past decade has revealed that the proinflammatory microenvironment plays a critical role in the development of colorectal cancer. Whether nimbolide, a limonoid triterpene, can inhibit the growth of colorectal cancer was investigated in the present study.Experimental Design: The effect of nimbolide on proliferation of colorectal cancer cell lines was examined by MTT assay, apoptosis by caspase activation and poly-ADP ribose polymerase cleavage, NF-κB activation by DNA-binding assay, and protein expression by Western blotting. The effect of nimbolide on the tumor growth in vivo was examined in colorectal cancer xenografts in a nude mouse model.Results: Nimbolide inhibited proliferation, induced apoptosis, and suppressed NF-κB activation and NF-κB–regulated tumorigenic proteins in colorectal cancer cells. The suppression of NF-κB activation by nimbolide was caused by sequential inhibition of IκB kinase (IKK) activation, IκBα phosphorylation, and p65 nuclear translocation. Furthermore, the effect of nimbolide on IKK activity was found to be direct. In vivo, nimbolide (at 5 and 20 mg/kg body weight), injected intraperitoneally after tumor inoculation, significantly decreased the volume of colorectal cancer xenografts. The limonoid-treated xenografts exhibited significant downregulation in the expression of proteins involved in tumor cell survival (Bcl-2, Bcl-xL, c-IAP-1, survivin, and Mcl-1), proliferation (c-Myc and cyclin D1), invasion (MMP-9, ICAM-1), metastasis (CXCR4), and angiogenesis (VEGF). The limonoid was found to be bioavailable in the blood plasma and tumor tissues of treated mice.Conclusions: Our studies provide evidence that nimbolide can suppress the growth of human colorectal cancer through modulation of the proinflammatory microenvironment. Clin Cancer Res; 19(16); 4465–76. ©2013 AACR.

Published
2023
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13. Supplementary Figure 1 from Nimbolide, a Limonoid Triterpene, Inhibits Growth of Human Colorectal Cancer Xenografts by Suppressing the Proinflammatory Microenvironment

Author

Bharat B. Aggarwal, Yin-Yuan Mo, Mangalam S. Nair, Dhanya R. Sethumadhavan, Sahdeo Prasad, and Subash C. Gupta

Abstract

PDF file - 130K, Nimbolide is bioavailable in the plasma and colorectal tumor tissues of nude mice. A, HPLC chromatogram of pure nimbolide. B, HPLC chromatogram of nimbolide in plasma. C, HPLC chromatogram of nimbolide in tumor tissues.

Published
2023
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16. Chemical constituents from Chonemorpha fragrans roots and antibacterial activity studies of sarcorucinine D

Author

Mangalam S. Nair, S. R. Dhanya, Vandana Sankar, and B. S. Dileep Kumar

Subjects
Naringenin, 010405 organic chemistry, Organic Chemistry, Plant Science, Aromadendrin, 01 natural sciences, Biochemistry, Protocatechuic acid, 0104 chemical sciences, Analytical Chemistry, Ferulic acid, 010404 medicinal & biomolecular chemistry, chemistry.chemical_compound, chemistry, Vanillic acid, Food science, Antibacterial activity, Matairesinol, Chonemorpha fragrans
Abstract

Nine non-alkaloid constituents viz., sitostenone (1), β-sitosterol (2), naringenin (3), aromadendrin (4), matairesinol (5), vanillic acid (6), ferulic acid (7), protocatechuic acid (8) and sitoster...

Published
2021
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17. Chemical constituents from

Author

S R, Dhanya, Mangalam S, Nair, B S, Dileep Kumar, and Vandana, Sankar

Subjects
Apocynaceae, Plant Roots, Anti-Bacterial Agents, Drugs, Chinese Herbal
Abstract

Nine non-alkaloid constituents viz., sitostenone (

Published
2022

24. Chemical constituents from Chonemorpha fragrans roots and antibacterial activity studies of sarcorucinine D.

Author

Dhanya, S. R., Nair, Mangalam S., Dileep Kumar, B. S., and Sankar, Vandana

Subjects
ANTIBACTERIAL agents, FERULIC acid, ALKALOIDS
Abstract

Nine non-alkaloid constituents viz., sitostenone (1), β-sitosterol (2), naringenin (3), aromadendrin (4), matairesinol (5), vanillic acid (6), ferulic acid (7), protocatechuic acid (8) and sitosterol-3-O-β-D-glucopyranoside (9) were isolated from the acetone extract as well as five alkaloids viz., japindine (10), sarcorucinine D (11), dictyophlebin (12), chonemorphine (13) and N-formylchonemorphine (14) were isolated from the ethanol extract of Chonemorpha fragrans roots. Except β-sitosterol, all other non-alkaloid compounds and the alkaloid sarcorucinine D are being reported for the first time from C. fragrans. From the MIC and MBC values, it has been found that sarcorucinine D shows most promising antibacterial activity. Quantification of antibacterial activity as well as killing curve determinations were performed in order to confirm the efficacy of the compound. The cytotoxic activity studies revealed that it is nontoxic up to 100 µM concentration. [ABSTRACT FROM AUTHOR]

Published
2022
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26. Epoxyazadiradione Purified from the Azadirachta indica Seed Induced Mitochondrial Apoptosis and Inhibition of NFκB Nuclear Translocation in Human Cervical Cancer Cells

Author

R. Saranga, Mangalam S. Nair, B.S. Sasidhar, G. Shilpa, Sulochana Priya, J. Renjitha, Francis K. Sajin, and Beena Joy

Subjects
0301 basic medicine, Pharmacology, Caspase-9, Cisplatin, biology, Cell growth, Cytochrome c, Azadirachta, biology.organism_classification, Molecular biology, HeLa, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Biochemistry, Downregulation and upregulation, Apoptosis, 030220 oncology & carcinogenesis, biology.protein, medicine, medicine.drug
Abstract

Epoxyazadiradione (EAD) is an important limonoid present in Neem (Azadirachta indica) plant. In the present study, we have purified EAD from Neem seed and studied its anticancer potential in human cervical cancer (HeLa) cells. Cell proliferation inhibition studies indicated that the GI50 value of EAD is 7.5 ± 0.0092 μM in HeLa cells, whereas up to 50 μM concentrations EAD did not affect the growth of normal H9C2 cells. The control drug cisplatin inhibited the growth of both HeLa and H9C2 cells with a GI50 value of 2.92 ± 1.192 and 4.22 ± 1.568 μM, respectively. Nuclear DNA fragmentation, cell membrane blebbing, phosphatidylserine translocation, upregulation of Bax, caspase 3 activity and poly (ADP ribose) polymerase cleavage and downregulation of BCl2 in HeLa cells on treatment with EAD indicated the apoptotic cell death. Increase in caspase 9 activity and release of active cytochrome c to the cytoplasm on treatment with EAD confirmed that the apoptosis was mediated through the mitochondrial pathway. Epoxyazadiradione also inhibited the nuclear translocation of nuclear factor κB in HeLa cells. Thus, our studies demonstrated EAD as a potent and safe chemotherapeutic agent when compared with the standard drug cisplatin that is toxic to both cancer and normal cells equally. Copyright © 2017 John Wiley & Sons, Ltd.

Published
2017
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27. Molecular mechanisms of anticancer activity of deoxyelephantopin in cancer cells

Author

Mangalam S. Nair, Farha Arakkaveettil Kabeer, Dhanya Sethumadhavan Rajalekshmi, and Remani Prathapan

Subjects
0301 basic medicine, autophagy, deoxyelephantopin, Activator (genetics), Kinase, Elephantopus scaber, apoptosis, Biology, lcsh:RZ409.7-999, Molecular biology, Urokinase receptor, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Complementary and alternative medicine, Apoptosis, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, Original Article, ER stress, Cytotoxicity, lcsh:Miscellaneous systems and treatments, Protein kinase B, PI3K/AKT/mTOR pathway
Abstract

Background: Deoxyelephantopin (DOE) is a natural bioactive sesquiterpene lactone from Elephantopus scaber, a traditionally relevant herb in Chinese and Indian medicine. It has shown promising anticancer effects against a broad spectrum of cancers. Methods: We examined the effect of DOE on growth, autophagy, apoptosis, cell cycle progression, metastasis, and various molecular signaling pathways in cancer cells, and endeavored to decipher the molecular mechanisms underlying its effect. The cytotoxicity of DOE was examined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) and colony formation assays. The antimetastatic potential of DOE was identified by wound closure, as well as invasion and migration assays. The expression of mRNAs and proteins related to cytotoxicity in cancer cells induced by DOE was investigated using reverse transcription-polymerase chain reaction, flow cytometry, and Western blot analysis. Results: DOE showed significant cytotoxicity and induced apoptosis in cancer cells. DOE promoted the autophagy of HCT 116 and K562 cells. DOE arrested cell cycle progression in the G2/M phase. DOE treatment caused activation of caspase-8, -9, -3 and -7, reactive oxygen species production, and cleavage of cleavage of poly-ADP-ribose polymerase (PARP), the markers of apoptosis. Moreover, apoptosis induction was associated with mitochondrial permeability and endoplasmic reticulum stress. Treatment of cancer cells with DOE inhibited mitogen-activated protein kinases, nuclear factor-kappa B, phosphatidylinositol 3-kinase (PI3K/Akt), and β-catenin signaling. Furthermore, treatment of DOE increased the expression of p53, phospho-Jun amino-terminal kinases (p-JNK), and p-p38 and decreased the expression of phospho-signal transducer and activator of transcription 3 (p-STAT3) and phospho-mammalian target of rapamycin (p-mTOR) in cancer cells. DOE downregulated matrix metalloproteinase (MMP-2) and MMP-9, urokinase-type plasminogen activator (uPA), and urokinase-type plasminogen activator receptor (uPAR) mRNA levels in cancer cells. Conclusion: These findings concluded that DOE may be useful as a chemotherapeutic agent against cancer. Keywords: apoptosis, autophagy, deoxyelephantopin, Elephantopus scaber, ER stress

Published
2017
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28. Metal-Free trans -Aziridination of Zerumbone: Synthesis and Biological Evaluation of Aziridine Derivatives of Zerumbone

Author

Kokkuvayil Vasu Radhakrishnan, P. Nisha, Jayaram Saranya, Thekke V. Baiju, Mangalam S. Nair, T. R. Reshmitha, Greeshma Gopalan, Murugan Thulasi Meenu, and B. P. Dhanya

Subjects
chemistry.chemical_compound, Metal free, 010405 organic chemistry, Chemistry, Organic Chemistry, Organic chemistry, Physical and Theoretical Chemistry, Aziridine, 010402 general chemistry, 01 natural sciences, 0104 chemical sciences, Biological evaluation
Abstract

Herein, we describe a metal-free, iodosobenzenediacetate mediated trans-aziridination of zerumbone by the direct use of sulphonamides. The preliminary in vitro-screening showed better anti-proliferative and anti-diabetic activity compared to parent compound zerumbone.

Published
2017
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29. Epidemiology of injuries from fire, heat and hot substances: global, regional and national morbidity and mortality estimates from the Global Burden of Disease 2017 study

Author

James, SL, Lucchesi, LR, Bisignano, C, Castle, CD, Dingels, Z, Fox, JT, Hamilton, EB, Henry, NJ, McCracken, D, Roberts, NLS, Sylte, DO, Ahmadi, A, Ahmed, MB, Alahdab, F, Alipour, V, Andualem, Z, Antonio, CAT, Arabloo, J, Badiye, AD, Bagherzadeh, M, Banstola, A, Baernighausen, TW, Barzegar, A, Bayati, M, Bhaumik, S, Bijani, A, Bukhman, G, Carvalho, F, Crowe, CS, Dalal, K, Daryani, A, Nasab, MD, Hoa, TD, Huyen, PD, Endries, AY, Fernandes, E, Filip, I, Fischer, F, Fukumoto, T, Gebremedhin, KBB, Gebremeskel, GG, Gilani, SA, Haagsma, JA, Hamidi, S, Hostiuc, S, Househ, M, Igumbor, EU, Ilesanmi, OS, Irvani, SSN, Jayatilleke, AU, Kahsay, A, Kapoor, N, Kasaeian, A, Khader, YS, Khalil, IA, Khan, EA, Khazaee-Pool, M, Kokubo, Y, Lopez, AD, Madadin, M, Majdan, M, Maled, V, Malekzadeh, R, Manafi, N, Manafi, A, Mangalam, S, Massenburg, BB, Meles, HG, Menezes, RG, Meretoja, TJ, Miazgowski, B, Miller, TR, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Morrison, SD, Negoi, I, Trang, HN, Son, HN, Cuong, TN, Nixon, MR, Olagunju, AT, Olagunju, TO, Padubidri, JR, Polinder, S, Rabiee, N, Rabiee, M, Radfar, A, Rahimi-Movaghar, V, Rawaf, S, Rawaf, DL, Rezapour, A, Rickard, J, Roro, EM, Roy, N, Safari-Faramani, R, Salamati, P, Samy, AM, Satpathy, M, Sawhney, M, Schwebel, DC, Senthilkumaran, S, Sepanlou, SG, Shigematsu, M, Soheili, A, Stokes, MA, Tohidinik, HR, Bach, XT, Valdez, PR, Wijeratne, T, Yisma, E, Zaidi, Z, Zamani, M, Zhang, Z-J, Hay, S, Mokdad, AH, James, SL, Lucchesi, LR, Bisignano, C, Castle, CD, Dingels, Z, Fox, JT, Hamilton, EB, Henry, NJ, McCracken, D, Roberts, NLS, Sylte, DO, Ahmadi, A, Ahmed, MB, Alahdab, F, Alipour, V, Andualem, Z, Antonio, CAT, Arabloo, J, Badiye, AD, Bagherzadeh, M, Banstola, A, Baernighausen, TW, Barzegar, A, Bayati, M, Bhaumik, S, Bijani, A, Bukhman, G, Carvalho, F, Crowe, CS, Dalal, K, Daryani, A, Nasab, MD, Hoa, TD, Huyen, PD, Endries, AY, Fernandes, E, Filip, I, Fischer, F, Fukumoto, T, Gebremedhin, KBB, Gebremeskel, GG, Gilani, SA, Haagsma, JA, Hamidi, S, Hostiuc, S, Househ, M, Igumbor, EU, Ilesanmi, OS, Irvani, SSN, Jayatilleke, AU, Kahsay, A, Kapoor, N, Kasaeian, A, Khader, YS, Khalil, IA, Khan, EA, Khazaee-Pool, M, Kokubo, Y, Lopez, AD, Madadin, M, Majdan, M, Maled, V, Malekzadeh, R, Manafi, N, Manafi, A, Mangalam, S, Massenburg, BB, Meles, HG, Menezes, RG, Meretoja, TJ, Miazgowski, B, Miller, TR, Mohammadian-Hafshejani, A, Mohammadpourhodki, R, Morrison, SD, Negoi, I, Trang, HN, Son, HN, Cuong, TN, Nixon, MR, Olagunju, AT, Olagunju, TO, Padubidri, JR, Polinder, S, Rabiee, N, Rabiee, M, Radfar, A, Rahimi-Movaghar, V, Rawaf, S, Rawaf, DL, Rezapour, A, Rickard, J, Roro, EM, Roy, N, Safari-Faramani, R, Salamati, P, Samy, AM, Satpathy, M, Sawhney, M, Schwebel, DC, Senthilkumaran, S, Sepanlou, SG, Shigematsu, M, Soheili, A, Stokes, MA, Tohidinik, HR, Bach, XT, Valdez, PR, Wijeratne, T, Yisma, E, Zaidi, Z, Zamani, M, Zhang, Z-J, Hay, S, and Mokdad, AH

Abstract

BACKGROUND: Past research has shown how fires, heat and hot substances are important causes of health loss globally. Detailed estimates of the morbidity and mortality from these injuries could help drive preventative measures and improved access to care. METHODS: We used the Global Burden of Disease 2017 framework to produce three main results. First, we produced results on incidence, prevalence, years lived with disability, deaths, years of life lost and disability-adjusted life years from 1990 to 2017 for 195 countries and territories. Second, we analysed these results to measure mortality-to-incidence ratios by location. Third, we reported the measures above in terms of the cause of fire, heat and hot substances and the types of bodily injuries that result. RESULTS: Globally, there were 8 991 468 (7 481 218 to 10 740 897) new fire, heat and hot substance injuries in 2017 with 120 632 (101 630 to 129 383) deaths. At the global level, the age-standardised mortality caused by fire, heat and hot substances significantly declined from 1990 to 2017, but regionally there was variability in age-standardised incidence with some regions experiencing an increase (eg, Southern Latin America) and others experiencing a significant decrease (eg, High-income North America). CONCLUSIONS: The incidence and mortality of injuries that result from fire, heat and hot substances affect every region of the world but are most concentrated in middle and lower income areas. More resources should be invested in measuring these injuries as well as in improving infrastructure, advancing safety measures and ensuring access to care.

Published
2020

30. Anticancer activity studies of cubebin isolated from Piper cubeba and its synthetic derivatives

Author

Dhanya S. Rajalekshmi, Sunil Varughese, Mangalam S. Nair, Arya R. Madhusoodhanan, Arun K. Bahulayan, Nisha Prakasan, Farha Arakkaveettil Kabeer, and Remani Prathapan

Subjects
Models, Molecular, food.ingredient, Stereochemistry, Clinical Biochemistry, Pharmaceutical Science, Apoptosis, 01 natural sciences, Biochemistry, Lignans, chemistry.chemical_compound, food, Cell Line, Tumor, Neoplasms, Amide, Drug Discovery, Piper cubeba, Humans, MTT assay, Molecular Biology, chemistry.chemical_classification, Piper, biology, 010405 organic chemistry, Organic Chemistry, biology.organism_classification, Antineoplastic Agents, Phytogenic, In vitro, 0104 chemical sciences, 010404 medicinal & biomolecular chemistry, chemistry, Cell culture, Seeds, Molecular Medicine, Lactone
Abstract

(-)-Cubebin, isolated from the seeds of Piper cubeba, and its five different types of derivatives (a total of 17), with varying functionalities, were tested for their in vitro anticancer activity against six human cancer cell lines (A549, K562, SiHa, KB, HCT116 and HT29) using MTT assay. Cubebin as well as its derivatives containing lactone and amide groups showed significant anticancer activity. In some of the tested cell lines, the amide derivatives showed higher activity. Morphological analysis indicated that these compounds act through apoptosis mediated pathway of cell death and we expect that these results will pave new paths in the development of novel anticancer agents by the derivatization of (-)-cubebin.

Published
2016
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32. Discovery of Natural Product Derived Labdane Appended Triazoles as Potent Pancreatic Lipase Inhibitors

Author

Sasidhar B. Somappa, Venkata Rao D. Krishna Rao, Raghu K. Gopalan, Mangalam S. Nair, Shyni G. Leela, Praveen K. Valmiki, Renjitha Jalaja, Chettiyan Thodi F. Salfeena, and Kizhakkan T. Ashitha

Subjects
Natural product, 010405 organic chemistry, Organic Chemistry, Fatty liver, Pharmacology, medicine.disease, 01 natural sciences, Biochemistry, 0104 chemical sciences, Labdane, Hep G2, 010404 medicinal & biomolecular chemistry, Orlistat, chemistry.chemical_compound, chemistry, Drug Discovery, medicine, Cytotoxicity, IC50, Dyslipidemia, medicine.drug
Abstract

[Image: see text] Obesity contributes to the genesis of many metabolic disorders including dyslipidemia, coronary heart disease (CHD), nonalcoholic fatty liver, type 2 diabetes, etc. Pancreatic lipase plays a vital role in food fat digestion and absorption. Therefore, to control obesity, inhibition of pancreatic lipase is the active therapy. Thus, novel natural product derived labdane appended triazoles with pancreatic lipase inhibition potential were designed and synthesized. Among these hybrids, 6b and 6f exhibited excellent inhibitory activity (IC(50) 0.75 ± 0.02 μM and 0.77 ± 0.01 μM), slightly better than that of the positive control Orlistat (IC(50) 0.8 ± 0.03 μM). Compounds 6c, 6e, and 6g–j inhibited the PL comparable to that of positive control. Interestingly none of the compounds showed cytotoxicity (Hep G2) in the concentration range from 0.5 to 100 μM. Overall results reveal the potential of labdane appended triazoles as antiobesity agents.

Published
2018

33. Anti-cancer activities of Bharangin against breast cancer: Evidence for the role of NF-κB and lncRNAs

Author

Vipin Rai, Sumit Singh Verma, Mangalam S. Nair, Subash C. Gupta, K. Sajin Francis, and Nikee Awasthee

Subjects
0301 basic medicine, Cell signaling, Biophysics, Poly (ADP-Ribose) Polymerase-1, Apoptosis, Breast Neoplasms, Biochemistry, Causes of cancer, 03 medical and health sciences, chemistry.chemical_compound, Breast cancer, Cell Line, Tumor, medicine, Humans, DAPI, skin and connective tissue diseases, Molecular Biology, Transcription factor, Cell Proliferation, Flavonoids, Chemistry, NF-kappa B, NF-κB, medicine.disease, Antineoplastic Agents, Phytogenic, 030104 developmental biology, Cell culture, Cancer research, Female, RNA, Long Noncoding, Signal Transduction
Abstract

Breast cancer remains one of the leading causes of cancer related deaths in women worldwide. Bharangin is a diterpenoid quinonemethide that has demonstrated therapeutic potential against leukemia, lymphoma, and multiple myeloma cells. Whether this diterpenoid exhibit activities against breast cancer cells and the underlying mechanism is largely unknown. Herein, we provide evidence that bharangin suppresses the proliferation of MCF-7, MDA-MB-231, MDA-MB-453, MDA-MB-468 and T-47D breast cancer cells. As examined by AO/PI staining, DAPI staining, sub-G1 analysis, phosphatidylserine externalization, caspase activation, DNA laddering, and poly-ADP ribose polymerase cleavage, the diterpenoid induced apoptosis in breast cancer cells. The growth inhibitory effect of bharangin on breast cancer cells was further confirmed from colony-formation assay. Furthermore, the cancer cell migration was also suppressed by the diterpenoid. Mechanistically, bharangin was found to modulate multiple cancer related cell signalling pathways in breast cancer cells. Bharangin suppressed the expression of cell survival and invasive proteins, and induced Bax and mitochondrial depolarization in breast cancer cells. The diterpenoid also suppressed the activation of pro-inflammatory transcription factor, nuclear factor (NF)-κB induced by okadaic acid. Finally, the diterpenoid induced the expression of tumor suppressor lncRNAs (MEG-3, GAS-5), while down-regulating oncogenic H19 expression. Overall, these results suggest that bharangin exhibits anti-carcinogenic, anti-proliferative and anti-inflammatory activities against breast cancer cells. The modulation of lncRNA expression and inhibition of NF-κB activation by bharangin may contribute to its anti-carcinogenic activities.

Published
2018

34. Phytochemical investigation on Myristica fragrans stem bark

Author

Beena James, Mangalam S. Nair, Sajin K. Francis, and Sunil Varughese

Subjects
Phytochemicals, India, Plant Science, Dioxoles, Anisoles, 01 natural sciences, Biochemistry, Lignans, Analytical Chemistry, Myristicaceae, Myristica, chemistry.chemical_compound, Furans, Benzofurans, Sri Lanka, Lignan, Stem bark, biology, Traditional medicine, Molecular Structure, 010405 organic chemistry, Spectrum Analysis, Organic Chemistry, Elemicin, Nutmeg, biology.organism_classification, 0104 chemical sciences, 010404 medicinal & biomolecular chemistry, chemistry, Phytochemical, Indonesia, visual_art, visual_art.visual_art_medium, Plant Bark, Myristica fragrans, Bark
Abstract

Myristica fragrans Houtt., the source of very important spice 'nutmeg' used world over is native to India, Indonesia, Sri Lanka, South Africa and Southeast Asia. Phytochemical investigation of M. fragrans stem bark led to the isolation of bis-aryl dimethyl tetrahydrofuran lignans, such as grandisin [(7S,8S,7'S,8'S)-3,3',4,4',5,5'-hexamethoxy-7,7',8,8'-lignan] and (7S,8S,7'R,8'R)-3,3',4,4',5,5'-hexamethoxy-7,7',8,8'-lignan along with important lignans and neolignans, licarinA, licarin B, odoratisol A, (2S, 3R)-7-methoxy-3-methyl-5-((E)-prop-1-enyl)-2-(5-methoxy,3,4-methylenedioxyphenyl)-2,3-dihydrobenzofuran, elemicin, fragransin B1, raphidecursinol B, erythro-(7S,8R)-Δ8'-4,7-dihydroxy-3,5,3'-trimethoxy-8-O-4'-neolignan, erythro-(7S,8R)-Δ8'-7-hydroxy-3,4,3',5'-tetramethoxy-8-O-4'-neolignan, surinamensin.and β-sitosterol. Structures of the 12 compounds isolated were unambiguously identified by various spectroscopic methods. The former two compounds were isolated from M. fragrans for the first time. Furthermore, the X-ray crystal structure of odoratisol A is reported in this paper for the first time.

Published
2018

36. Licarin B from Myristica fragrans improves insulin sensitivity via PPARγ and activation of GLUT4 in the IRS-1/PI3K/AKT pathway in 3T3-L1 adipocytes

Author

G. L. Shyni, Sajin K. Francis, Kavitha Sasidharan, Arya A. Das, Kozhiparambil Gopalan Raghu, and Mangalam S. Nair

Subjects
0301 basic medicine, chemistry.chemical_classification, biology, General Chemical Engineering, Peroxisome proliferator-activated receptor, General Chemistry, medicine.disease, Cell biology, 03 medical and health sciences, Insulin receptor, 030104 developmental biology, Insulin resistance, chemistry, Biochemistry, Adipogenesis, biology.protein, medicine, Adiponectin secretion, Rosiglitazone, GLUT4, PI3K/AKT/mTOR pathway, medicine.drug
Abstract

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors regulating lipid and glucose metabolism. The objective of the present study is to characterize the cellular effect of Licarin B (LB), a neolignan isolated from Myristica fragrans on the PPARγ and insulin signaling pathways in 3T3-L1 preadipocytes. The molecular mechanism of action of LB on PPARγ and insulin signaling pathways were studied using in vitro and in silico methods. Functional activation of PPARγ in vitro was confirmed by 3T3-L1 preadipocyte differentiation, regulation of target genes and protein expression. LB caused triglyceride accumulation during adipogenesis but significantly less compared to rosiglitazone (RG), a PPARγ full agonist. In in vitro time-resolved fluorescence resonance energy transfer-based competitive binding assay, LB showed an IC50 value of 2.4 μM whereas for RG and GW9662 it was 57.96 nM and 18.68 nM respectively. Virtual screening of LB with PPARγ showed hydrophobic interactions with a binding energy of −9.36 kcal mol−1. Interestingly enough LB improved insulin sensitivity by up regulating the GLUT4 expression and translocation via IRS-1/PI3K/AKT pathway, enhanced adiponectin secretion and modulated mRNA expression profile of PPARγ target genes C/EBPα, IRS-2, and LPL significantly compared to RG. This scientifically validate LB as a promising bioactive for insulin resistance and associated complications through its partial PPARγ activity.

Published
2016
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38. Epidemiology of injuries from fire, heat and hot substances: Global, regional and national morbidity and mortality estimates from the Global Burden of Disease 2017 study

Author

James, S.L. (Spencer L.), Lucchesi, L.R. (Lydia R.), Bisignano, C. (Catherine), Castle, C.D. (Chris D.), Dingels, Z.V. (Zachary V.), Fox, J.T. (Jack T.), Hamilton, E.B. (Erin B.), Henry, N.J. (Nathaniel J.), McCracken, D. (Darrah), Roberts, N.L.S. (Nicholas L.S.), Sylte, D.O. (Dillon O.), Ahmadi, A. (Alireza), Ahmed, M.B. (Muktar Beshir), Alahdab, F. (Fares), Alipour, V. (Vahid), Andualem, Z. (Zewudu), Antonio, C.A.T. (Carl Abelardo T), Arabloo, J. (Jalal), Badiye, A.D. (Ashish D.), Bagherzadeh, M. (Mojtaba), Banstola, A. (Amrit), Bärnighausen, T. (Till), Barzegar, A. (Akbar), Bayati, M. (Mohsen), Bhaumik, S. (Soumyadeep), Bijani, A. (Ali), Bukhman, G. (Gene), Carvalho, F. (Félix), Crowe, C.S. (Christopher Stephen), Dalal, K. (Koustuv), Daryani, A. (Ahmad), Nasab, M.D. (Mostafa Dianati), Do, H.T. (Hoa Thi), Do, H.P. (Huyen Phuc), Endries, A.Y. (Aman Yesuf), Fernandes, E. (Eduarda), Filip, I. (Irina), Fischer, F. (Florian), Fukumoto, T. (Takeshi), Gebremedhin, K.B.B. (Ketema Bizuwork Bizuwork), Gebremeskel, G.G. (Gebreamlak Gebremedhn), Gilani, S.A. (Syed Amir), Haagsma, J.A. (Juanita), Hamidi, S. (Samer), Hostiuc, S. (Sorin), Househ, M. (Mowafa), Igumbor, E.U. (Ehimario U.), Ilesanmi, O.S. (Olayinka Stephen), Irvani, S.S.N. (Seyed Sina Naghibi), Jayatilleke, A.U. (Achala Upendra), Kahsay, A. (Amaha), Kapoor, N. (Neeti), Kasaeian, A. (Amir), Khader, Y.S. (Yousef Saleh), Khalil, I.A. (Ibrahim A.), Khan, E.A. (Ejaz Ahmad), Khazaee-Pool, M. (Maryam), Kokubo, Y. (Yoshihiro), Lopez, A.D. (Alan D), Madadin, M. (Mohammed), Majdan, M. (Marek), Maled, V. (Venkatesh), Malekzadeh, R. (Reza), Manafi, N. (Navid), Manafi, A. (Ali), Mangalam, S. (Srikanth), Massenburg, B.B. (Benjamin Ballard), Meles, H.G. (Hagazi Gebre), Menezes, R.G. (Ritesh G.), Meretoja, T.J. (Tuomo J.), Miazgowski, B. (Bartosz), Miller, T.R. (Ted R), Mohammadian-Hafshejani, A. (Abdollah), Mohammadpourhodki, R. (Reza), Morrison, S.D. (Shane Douglas), Negoi, I. (Ionut), Nguyen, T.H. (Trang Huyen), Nguyen, S.H. (Son Hoang), Nguyen, C.T. (Cuong Tat), Nixon, M.R. (Molly R.), Olagunju, A.T. (Andrew T.), Olagunju, T.O. (Tinuke O.), Padubidri, J.R. (Jagadish Rao), Polinder, S. (Suzanne), Rabiee, N. (Navid), Rabiee, M. (Mohammad), Radfar, A. (Amir), Rahimi-Movaghar, V. (Vafa), Rawaf, S. (Salman), Rawaf, D.L. (David Laith), Rezapour, A. (Aziz), Rickard, J. (Jennifer), Roro, E.M. (Elias Merdassa), Roy, N. (Nadine) van, Safari-Faramani, R. (Roya), Salamati, P. (Payman), Samy, A.M. (Abdallah M.), Satpathy, M. (Maheswar), Sawhney, M. (Monika), Schwebel, D.C. (David C), Senthilkumaran, S. (Subramanian), Sepanlou, S.G. (Sadaf G), Shigematsu, M. (Mika), Soheili, A. (Amin), Stokes, M.A. (Mark A.), Tohidinik, H.R. (Hamid Reza), Tran, B.X. (Bach Xuan), Valdez, P.R. (Pascual R.), Wijeratne, T. (Tissa), Yisma, E. (Engida), Zaidi, Z. (Zoubida), Zamani, M. (Mohammad), Zhang, Z.-J. (Zhi-Jiang), Hay, S.I. (Simon), Mokdad, A.H. (Ali H.), James, S.L. (Spencer L.), Lucchesi, L.R. (Lydia R.), Bisignano, C. (Catherine), Castle, C.D. (Chris D.), Dingels, Z.V. (Zachary V.), Fox, J.T. (Jack T.), Hamilton, E.B. (Erin B.), Henry, N.J. (Nathaniel J.), McCracken, D. (Darrah), Roberts, N.L.S. (Nicholas L.S.), Sylte, D.O. (Dillon O.), Ahmadi, A. (Alireza), Ahmed, M.B. (Muktar Beshir), Alahdab, F. (Fares), Alipour, V. (Vahid), Andualem, Z. (Zewudu), Antonio, C.A.T. (Carl Abelardo T), Arabloo, J. (Jalal), Badiye, A.D. (Ashish D.), Bagherzadeh, M. (Mojtaba), Banstola, A. (Amrit), Bärnighausen, T. (Till), Barzegar, A. (Akbar), Bayati, M. (Mohsen), Bhaumik, S. (Soumyadeep), Bijani, A. (Ali), Bukhman, G. (Gene), Carvalho, F. (Félix), Crowe, C.S. (Christopher Stephen), Dalal, K. (Koustuv), Daryani, A. (Ahmad), Nasab, M.D. (Mostafa Dianati), Do, H.T. (Hoa Thi), Do, H.P. (Huyen Phuc), Endries, A.Y. (Aman Yesuf), Fernandes, E. (Eduarda), Filip, I. (Irina), Fischer, F. (Florian), Fukumoto, T. (Takeshi), Gebremedhin, K.B.B. (Ketema Bizuwork Bizuwork), Gebremeskel, G.G. (Gebreamlak Gebremedhn), Gilani, S.A. (Syed Amir), Haagsma, J.A. (Juanita), Hamidi, S. (Samer), Hostiuc, S. (Sorin), Househ, M. (Mowafa), Igumbor, E.U. (Ehimario U.), Ilesanmi, O.S. (Olayinka Stephen), Irvani, S.S.N. (Seyed Sina Naghibi), Jayatilleke, A.U. (Achala Upendra), Kahsay, A. (Amaha), Kapoor, N. (Neeti), Kasaeian, A. (Amir), Khader, Y.S. (Yousef Saleh), Khalil, I.A. (Ibrahim A.), Khan, E.A. (Ejaz Ahmad), Khazaee-Pool, M. (Maryam), Kokubo, Y. (Yoshihiro), Lopez, A.D. (Alan D), Madadin, M. (Mohammed), Majdan, M. (Marek), Maled, V. (Venkatesh), Malekzadeh, R. (Reza), Manafi, N. (Navid), Manafi, A. (Ali), Mangalam, S. (Srikanth), Massenburg, B.B. (Benjamin Ballard), Meles, H.G. (Hagazi Gebre), Menezes, R.G. (Ritesh G.), Meretoja, T.J. (Tuomo J.), Miazgowski, B. (Bartosz), Miller, T.R. (Ted R), Mohammadian-Hafshejani, A. (Abdollah), Mohammadpourhodki, R. (Reza), Morrison, S.D. (Shane Douglas), Negoi, I. (Ionut), Nguyen, T.H. (Trang Huyen), Nguyen, S.H. (Son Hoang), Nguyen, C.T. (Cuong Tat), Nixon, M.R. (Molly R.), Olagunju, A.T. (Andrew T.), Olagunju, T.O. (Tinuke O.), Padubidri, J.R. (Jagadish Rao), Polinder, S. (Suzanne), Rabiee, N. (Navid), Rabiee, M. (Mohammad), Radfar, A. (Amir), Rahimi-Movaghar, V. (Vafa), Rawaf, S. (Salman), Rawaf, D.L. (David Laith), Rezapour, A. (Aziz), Rickard, J. (Jennifer), Roro, E.M. (Elias Merdassa), Roy, N. (Nadine) van, Safari-Faramani, R. (Roya), Salamati, P. (Payman), Samy, A.M. (Abdallah M.), Satpathy, M. (Maheswar), Sawhney, M. (Monika), Schwebel, D.C. (David C), Senthilkumaran, S. (Subramanian), Sepanlou, S.G. (Sadaf G), Shigematsu, M. (Mika), Soheili, A. (Amin), Stokes, M.A. (Mark A.), Tohidinik, H.R. (Hamid Reza), Tran, B.X. (Bach Xuan), Valdez, P.R. (Pascual R.), Wijeratne, T. (Tissa), Yisma, E. (Engida), Zaidi, Z. (Zoubida), Zamani, M. (Mohammad), Zhang, Z.-J. (Zhi-Jiang), Hay, S.I. (Simon), and Mokdad, A.H. (Ali H.)

Abstract

Background: Past research has shown how fires, heat and hot substances are important causes of health loss globally. Detailed estimates of the morbidity and mortality from these injuries could help drive preventative measures and improved access to care. Methods: We used the Global Burden of Disease 2017 framework to produce three main results. First, we produced results on incidence, prevalence, years lived with disability, deaths, years of life lost and disability-adjusted life years from 1990 to 2017 for 195 countries and territories. Second, we analysed these results to measure mortality-to-incidence ratios by location. Third, we reported the measures above in terms of the cause of fire, heat and hot substances and the types of bodily injuries that result. Results: Globally, there were 8 991 468 (7 481 218 to 10 740 897) new fire, heat and hot substance injuries in 2017 with 120 632 (101 630 to 129 383) deaths. At the global level, the age-standardised mortality caused by fire, heat and hot substances significantly declined from 1990 to 2017, but regionally there was variability in age-standardised incidence with some regions experiencing an increase (eg, Southern Latin America) and others experiencing a significant decrease (eg, High-income North America). Conclusions: The incidence and mortality of injuries that result from fire, heat and hot substances affect every region of the world but are most concentrated in middle and lower income areas. More resources should be invested in measuring these injuries as well as in improving infrastructure, advancing safety measures and ensuring access to care.

Published
2019
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42. Measuring progress from 1990 to 2017 and projecting attainment to 2030 of the health-related Sustainable Development Goals for 195 countries and territories: a systematic analysis for the Global Burden of Disease Study 2017

Author

Lozano, R. Fullman, N. Abate, D. Abay, S.M. Abbafati, C. Abbasi, N. Abbastabar, H. Abd-Allah, F. Abdela, J. Abdelalim, A. Abdel-Rahman, O. Abdi, A. Abdollahpour, I. Abdulkader, R.S. Abebe, N.D. Abebe, Z. Abejie, A.N. Abera, S.F. Abil, O.Z. Aboyans, V. Abraha, H.N. Abrham, A.R. Abu-Raddad, L.J. Abu-Rmeileh, N.M. Abyu, G.Y. Accrombessi, M.M.K. Acharya, D. Acharya, P. Adamu, A.A. Adebayo, O.M. Adedeji, I.A. Adedoyin, R.A. Adekanmbi, V. Adetokunboh, O.O. Adhena, B.M. Adhikari, T.B. Adib, M.G. Adou, A.K. Adsuar, J.C. Afarideh, M. Afshari, M. Afshin, A. Agarwal, G. Aghayan, S.A. Agius, D. Agrawal, A. Agrawal, S. Ahmadi, A. Ahmadi, M. Ahmadieh, H. Ahmed, M.B. Ahmed, S. Akalu, T.Y. Akanda, A.S. Akbari, M.E. Akibu, M. Akinyemi, R.O. Akinyemiju, T. Akseer, N. Alahdab, F. Al-Aly, Z. Alam, K. Alam, T. Albujeer, A. Alebel, A. Alene, K.A. Al-Eyadhy, A. Alhabib, S. Ali, R. Alijanzadeh, M. Alizadeh-Navaei, R. Aljunid, S.M. Alkerwi, A. Alla, F. Allebeck, P. Allen, C.A. Almasi, A. Al-Maskari, F. Al-Mekhlafi, H.M. Alonso, J. Al-Raddadi, R.M. Alsharif, U. Altirkawi, K. Alvis-Guzman, N. Amare, A.T. Amenu, K. Amini, E. Ammar, W. Anber, N.H. Anderson, J.A. Andrei, C.L. Androudi, S. Animut, M.D. Anjomshoa, M. Ansari, H. Ansariadi, A. Ansha, M.G. Antonio, C.A.T. Anwari, P. Appiah, L.T. Aremu, O. Areri, H.A. Ärnlöv, J. Arora, M. Aryal, K.K. Asayesh, H. Asfaw, E.T. Asgedom, S.W. Asghar, R.J. Assadi, R. Ataro, Z. Atique, S. Atre, S.R. Atteraya, M.S. Ausloos, M. Avila-Burgos, L. Avokpaho, E.F.G.A. Awasthi, A. Quintanilla, B.P.A. Ayele, H.T. Ayele, Y. Ayer, R. Azarpazhooh, M.R. Azzopardi, P.S. Azzopardi-Muscat, N. Babalola, T.K. Babazadeh, A. Badali, H. Badawi, A. Balakrishnan, K. Bali, A.G. Banach, M. Banerjee, A. Banoub, J.A.M. Banstola, A. Barac, A. Barboza, M.A. Barker-Collo, S.L. Bärnighausen, T.W. Barrero, L.H. Barthelemy, C.M. Bassat, Q. Basu, A. Basu, S. Battista, R.J. Baune, B.T. Baynes, H.W. Bazargan-Hejazi, S. Bedi, N. Beghi, E. Behzadifar, M. Behzadifar, M. Béjot, Y. Bekele, B.B. Belachew, A.B. Belay, A.G. Belay, S.A. Belay, Y.A. Bell, M.L. Bello, A.K. Bennett, D.A. Bensenor, I.M. Benzian, H. Berhane, A. Berhe, A.K. Berman, A.E. Bernabe, E. Bernstein, R.S. Bertolacci, G.J. Beuran, M. Beyranvand, T. Bhala, N. Bhalla, A. Bhansali, A. Bhattarai, S. Bhaumik, S. Bhutta, Z.A. Biadgo, B. Biehl, M.H. Bijani, A. Bikbov, B. Bililign, N. Sayeed, M.S.B. Birlik, S.M. Birungi, C. Bisanzio, D. Biswas, T. Bitew, H. Bizuneh, H. Bjertness, E. Bobasa, E.M. Boufous, S. Bourne, R. Bozorgmehr, K. Bragazzi, N.L. Brainin, M. Brant, L.C. Brauer, M. Brazinova, A. Breitborde, N.J.K. Briant, P.S. Britton, G. Brugha, T. Bukhman, G. Busse, R. Butt, Z.A. Cahuana-Hurtado, L. Callender, C.S.K.H. Campos-Nonato, I.R. Rincon, J.C.C. Cano, J. Car, J. Car, M. Cárdenas, R. Carrero, J.J. Carter, A. Carvalho, F. Castañeda-Orjuela, C.A. Rivas, J.C. Castro, F. Causey, K. Çavlin, A. Cercy, K.M. Cerin, E. Chaiah, Y. Chalek, J. Chang, H.-Y. Chang, J.-C. Chattopadhyay, A. Chattu, V.K. Chaturvedi, P. Chiang, P.P.-C. Chin, K.L. Chisumpa, V.H. Chitheer, A. Choi, J.-Y.J. Chowdhury, R. Christensen, H. Christopher, D.J. Chung, S.-C. Cicuttini, F.M. Ciobanu, L.G. Cirillo, M. Claro, R.M. Claßen, T.K.D. Cohen, A.J. Collado-Mateo, D. Cooper, C. Cooper, L.T. Cornaby, L. Cortinovis, M. Costa, M. Cousin, E. Cromwell, E.A. Crowe, C.S. Cunningham, M. Daba, A.K. Dadi, A.F. Dandona, L. Dandona, R. Dang, A.K. Dargan, P.I. Daryani, A. Das, S.K. Das Gupta, R. Das Neves, J. Dasa, T.T. Dash, A.P. Davis, A.C. Davitoiu, D.V. Davletov, K. Dayama, A. De Courten, B. De Leo, D. Neve, J.W.D. De Steur, H. Degefa, M.G. Degenhardt, L. Degfie, T.T. Deiparine, S. Dellavalle, R.P. Demoz, G.T. Demtsu, B. Denova-Gutiérrez, E. Deribe, K. Dervenis, N. Dessie, G.A. Dey, S. Dharmaratne, S.D. Dhimal, M. Dicker, D. Dinberu, M.T. Ding, E.L. Djalalinia, S. Do, H.P. Dokova, K. Doku, D.T. Douwes-Schultz, D. Driscoll, T.R. Duan, L. Dubey, M. Dubljanin, E. Duken, E.E. Duncan, B.B. Duraes, A.R. Ebrahimpour, S. 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Homaie Rad, E. Hoogar, P. Horita, N. Hosgood, H.D. Hosseini, S.M. Hosseinzadeh, M. Hostiuc, M. Hostiuc, S. Hotez, P.J. Hoy, D.G. Hsairi, M. Hsiao, T. Hu, G. Huang, J.J. Hughes, C. Huynh, C.K. Igumbor, E.U. Ikeda, C.T. Ilesanmi, O.S. Iqbal, U. Irvani, S.S.N. Irvine, C.M.S. Islam, S.M.S. Islami, F. Ivers, R.Q. Izadi, N. Jacobsen, K.H. Jahangiry, L. Jahanmehr, N. Jain, S.K. Jakovljevic, M. Jalu, M.T. Jamal, A.A. James, S.L. Jassal, S.K. Javanbakht, M. Jayatilleke, A.U. Jeemon, P. Jha, R.P. Jha, V. Ji, J.S. Johnson, C.O. Johnson, S.C. Jonas, J.B. Jonnagaddala, J. Shushtari, Z.J. Joshi, A. Jozwiak, J.J. Jungari, S.B. Jürisson, M. Madhanraj, K. Kabir, Z. Kadel, R. Kahsay, A. Kahssay, M. Kalani, R. Kapil, U. Karami, M. Matin, B.K. Karanikolos, M. Karimi, N. Karimi, S.M. Karimi-Sari, H. Kasaeian, A. Kassa, D.H. Kassa, G.M. Kassa, T.D. Kassa, Z.Y. Kassebaum, N.J. Katikireddi, S.V. Kaul, A. Kawakami, N. Kazemi, Z. Karyani, A.K. Kazi, D.S. Prakash, K.C. Kebede, S. Keiyoro, P.N. Kemmer, L. Kemp, G.R. Kengne, A.P. Keren, A. Kesavachandran, C.N. Khader, Y.S. Khafaei, B. Khafaie, M.A. Khajavi, A. Khalid, N. Khalil, I.A. Khan, E.A. Khan, M.S. Khan, M.A. Khang, Y.-H. Khanna, T. Khater, M.M. Khatony, A. Khazaeipour, Z. Khazaie, H. Khoja, A.T. Khosravi, A. Khosravi, M.H. Khubchandani, J. Kiadaliri, A.A. Kiarie, H.W. Kibret, G.D. Kiirithio, D.N. Kim, D. Kim, J.Y. Kim, Y.-E. Kim, Y.J. Kimokoti, R.W. Kinfu, Y. Kinra, S. Kisa, A. Kissimova-Skarbek, K. Kissoon, N. Kivimäki, M. Kocarnik, J.M. Kochhar, S. Kokubo, Y. Kolola, T. Kopec, J.A. Kosek, M.N. Kosen, S. Koul, P.A. Koyanagi, A. Kravchenko, M.A. Krishan, K. Krohn, K.J. Defo, B.K. Kucuk Bicer, B. Kudom, A.A. Kulikoff, X.R. Kumar, G.A. Kumar, M. Kumar, P. Kutz, M.J. Kyu, H.H. Lachat, C. Lad, D.P. Lad, S.D. Lafranconi, A. Lagat, A.K. Lal, D.K. Lalloo, R. Lam, H. Lami, F.H. Lamichhane, P. Lan, Q. Lang, J.J. Lansingh, V.C. Lansky, S. Larson, H.J. Larsson, A.O. Laryea, D.O. Lassi, Z.S. Latifi, A. Lau, K.M.-M. Laxmaiah, A. 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Memiah, P.T.N. Memish, Z.A. Mendoza, W. Mengistu, D.T. Mengistu, G. Mensah, G.A. Mensink, G.B.M. Mereta, S.T. Meretoja, A. Meretoja, T.J. Mestrovic, T. Mezgebe, H.B. Miazgowski, B. Miazgowski, T. Millear, A.I. Miller, T.R. Miller-Petrie, M.K. Milne, G.J. Mini, G.K. Minnig, S.P. Mirabi, P. Mirarefin, M. Mirrakhimov, E.M. Misganaw, A.T. Mitchell, P.B. Moazen, B. Moghadamnia, A.A. Mohajer, B. Mohammad, K.A. Mohammadi, M. Mohammadifard, N. Mohammadnia-Afrouzi, M. Mohammed, M.A. Mohammed, S. Mohan, M.B.V. Mohan, V. Mohebi, F. Moitra, M. Mokdad, A.H. Molokhia, M. Monasta, L. Montañez, J.C. Moosazadeh, M. Moradi, G. Moradi, M. Moradi-Lakeh, M. Moradinazar, M. Moraga, P. Morawska, L. Morgado-da-Costa, J. Morisaki, N. Morrison, S.D. Mosapour, A. Moschos, M.M. Mountjoy-Venning, W.C. Mouodi, S. Mousavi, S.M. Muche, A.A. Muchie, K.F. Mueller, U.O. Muhammed, O.S.S. Mukhopadhyay, S. Mullany, E.C. Muller, K. Mumford, J.E. Murhekar, M. Murthy, G.V.S. Murthy, S. Musa, J. Musa, K.I. Mustafa, G. Muthupandian, S. Nabhan, A.F. Nachega, J.B. Nagarajan, A.J. Nagel, G. Naghavi, M. Naheed, A. Nahvijou, A. Naidoo, K. Naik, G. Naik, N. Najafi, F. Naldi, L. Nam, H.S. Nangia, V. Nansseu, J.R. Nascimento, B.R. Nawaz, H. Neamati, N. Negoi, I. Negoi, R.I. Neupane, S. Newton, C.R.J. Ngalesoni, F.N. Ngunjiri, J.W. Nguyen, A. Nguyen, G. Nguyen, H. Nguyen, H.L.T. Nguyen, H.T. Nguyen, M. Nichols, E. Nigatu, S.G. Ningrum, D.N.A. Nirayo, Y.L. Nisar, M.I. Nixon, M.R. Nolutshungu, N. Nomura, M. Norheim, O.F. Noroozi, M. Norrving, B. Noubiap, J.J. Nouri, H.R. Shiadeh, M.N. Nowroozi, M.R. Nyasulu, P.S. Obermeyer, C.M. Ofori-Asenso, R. Ogah, O.S. Ogbo, F.A. Oh, I.-H. Okoro, A. Oladimeji, K.E. Oladimeji, O. Olagunju, A.T. Olagunju, T.O. Olivares, P.R. Olsen, H.E. Olusanya, B.O. Olusanya, J.O. Ong, K.L. Ong, S.K. Oommen, A.M. Opio, J.N. Oren, E. Oros, A. Ortega-Altamirano, D.D.V. Ortiz, A. Ortiz, J.R. Ortiz-Panozo, E. Ota, E. Otstavnov, S.S. Owolabi, M.O. Mahesh, P.A. Pakhale, S. Pakhare, A.P. Pan, W.-H. Pana, A. Panda, B.K. Panda-Jonas, S. Pandian, J.D. Papantoniou, N. Park, E.-K. Parry, C.D.H. Parsian, H. Patel, S. Pati, S. Patle, A. Patton, G.C. Paturi, V.R. Paudel, D. Paulson, K.R. Pearce, N. Peprah, E.K. Pereira, D.M. Perico, N. Pervaiz, A. Pesudovs, K. Petri, W.A. Petzold, M. Phillips, M.R. Pigott, D.M. Pillay, J.D. Pirsaheb, M. Pletcher, M. Pond, C.D. Postma, M.J. Pourshams, A. Poustchi, H. Prabhakaran, D. Prakash, S. Prasad, N. Purcell, C.A. Pyakurel, M. Qorbani, M. Quansah, R. Radfar, A. Rafay, A. Rafiei, A. Rahim, F. Rahimi, K. Rahimi-Movaghar, A. Rahimi-Movaghar, V. Rahman, M. Rahman, M.S. Rahman, M.H.U. Rahman, M.A. Rahman, S.U. Rai, R.K. Rajati, F. Rajsic, S. Ram, U. Rana, S.M. Ranabhat, C.L. Ranjan, P. Rasella, D. Rawaf, D.L. Rawaf, S. Razo-García, C. Reddy, K.S. Reiner, R.C. Reis, C. Reitsma, M.B. Remuzzi, G. Renzaho, A.M.N. Resnikoff, S. Reynales-Shigematsu, L.M. Rezaei, S. Rezaeian, S. Rezai, M.S. Riahi, S.M. Ribeiro, A.L.P. Rios-Blancas, M.J. Roba, K.T. Roberts, N.L.S. Roever, L. Ronfani, L. Roshandel, G. Rostami, A. Roth, G.A. Roy, A. Rubagotti, E. Ruhago, G.M. Sabde, Y.D. Sachdev, P.S. Saddik, B. Sadeghi, E. Safari, H. Safari, Y. Safari-Faramani, R. Safdarian, M. Safi, S. Safiri, S. Sagar, R. Sahebkar, A. Sahraian, M.A. Sajadi, H.S. Salam, N. Salama, J.S. Salamati, P. De Freitas Saldanha, R. Saleem, Z. Salimi, Y. Salimzadeh, H. Salomon, J.A. Salvi, S.S. Salz, I. Sambala, E.Z. Samy, A.M. Sanabria, J. Sanchez-Niño, M.D. Santos, I.S. Milicevic, M.M.S. Jose, B.P.S. Sardana, M. Sarker, A.R. Sarrafzadegan, N. Sartorius, B. Sarvi, S. Sathian, B. Satpathy, M. Savic, M. Sawant, A.R. Sawhney, M. Saxena, S. Saylan, M. Sayyah, M. Schaeffner, E. Schmidt, M.I. Schneider, I.J.C. Schöttker, B. Schutte, A.E. Schwebel, D.C. Schwendicke, F. Seedat, S. Sekerija, M. Sepanlou, S.G. Serván-Mori, E. Seyedmousavi, S. Shabaninejad, H. Shackelford, K.A. Shafieesabet, A. Shaheen, A.A. Shaikh, M.A. Shams-Beyranvand, M. Shamsi, M.B. Shamsizadeh, M. Sharafi, H. Sharafi, K. Sharif, M. Sharif-Alhoseini, M. Sharma, J. Sharma, R. Sharma, S.K. She, J. Sheikh, A. Shey, M.S. Shi, P. Shibuya, K. Shields, C. Shifa, G.T. Shiferaw, M.S. Shigematsu, M. Shiri, R. Shirkoohi, R. Shirude, S. Shishani, K. Shiue, I. Shokraneh, F. Shoman, H. Shrime, M.G. Shukla, S.R. Si, S. Siabani, S. Sibai, A.M. Siddiqi, T.J. Sigfusdottir, I.D. Silpakit, N. Silva, D.A.S. Silva, J.P. Da Silva, N.T. Silveira, D.G.A. Singh, J.A. Singh, N.P. Singh, O.P. Singh, P.K. Singh, V. Sinha, D.N. Skiadaresi, E. Sliwa, K. Smith, A.E. Smith, M. Filho, A.M.S. Sobaih, B.H. Sobhani, S. Soljak, M. Soofi, M. Soosaraei, M. Sorensen, R.J.D. Soriano, J.B. Soshnikov, S. Soyiri, I.N. Spinelli, A. Sposato, L.A. Sreeramareddy, C.T. Srinivasan, R.G. Srinivasan, V. Stanaway, J.D. Starodubov, V.I. Stathopoulou, V. Steckling, N. Stein, D.J. Stewart, L.G. Stockfelt, L. Stokes, M.A. Straif, K. Sudaryanto, A. Sufiyan, M.B. Sunguya, B.F. Sur, P.J. Sutradhar, I. Sykes, B.L. Sylaja, P.N. Sylte, D.O. Szoeke, C.E.I. Tabarés-Seisdedos, R. Tabuchi, T. Tadakamadla, S.K. Tamirat, K.S. Tandon, N. Tanser, F.C. Tassew, A.A. Tassew, S.G. Tavakkoli, M. Taveira, N. Tawye, N.Y. Tehrani-Banihashemi, A. Tekalign, T.G. Tekle, M.G. Temesgen, H. Temsah, M.-H. Temsah, O. Terkawi, A.S. Teshale, M.Y. Teshome, D.F. Tessema, B. Teweldemedhin, M. Thakur, J.S. Thankappan, K.R. Theis, A. Thirunavukkarasu, S. Thomas, L.A. Thomas, N. Thomson, A.J. Thrift, A.G. Tilahun, B. To, Q.G. Tobe-Gai, R. Tonelli, M. Topor-Madry, R. Torre, A.E. Tortajada-Girbés, M. Tovani-Palone, M.R. Towbin, J.A. Tran, B.X. Tran, K.B. Tran, T.T. Tripathy, S.P. Troeger, C.E. Truelsen, T.C. Tsadik, A.G. Car, L.T. Tuzcu, E.M. Tymeson, H.D. Ukwaja, K.N. Ullah, I. Updike, R.L. Usman, M.S. Uthman, O.A. Vaduganathan, M. Vaezi, A. Vaidya, G. Valdez, P.R. Van Donkelaar, A. Varavikova, E. Vasankari, T.J. Venketasubramanian, N. Vidavalur, R. Villafaina, S. Violante, F.S. Vladimirov, S.K. Vlassov, V. Vollmer, S. Vollset, S.E. Vos, T. Vosoughi, K. Vujcic, I.S. Wagner, G.R. Wagnew, F.S. Waheed, Y. Walson, J.L. Wang, Y. Wang, Y.-P. Wassie, M.M. Weiderpass, E. Weintraub, R.G. Weiss, J. Weldegebreal, F. Weldegwergs, K.G. Werdecker, A. Werkneh, A.A. West, T.E. Westerman, R. Whisnant, J.L. Whiteford, H.A. Widecka, J. Widecka, K. Wijeratne, T. Wilner, L.B. Winkler, A.S. Wiyeh, A.B. Wiysonge, C.S. Wolde, H.F. Wolfe, C.D.A. Wu, S. Xavier, D. Xu, G. Xu, R. Yadollahpour, A. Jabbari, S.H.Y. Yakob, B. Yamada, T. Yan, L.L. Yano, Y. Yaseri, M. Yasin, Y.J. Ye, P. Yearwood, J.A. Yeshaneh, A. Yimer, E.M. Yip, P. Yirsaw, B.D. Yisma, E. Yonemoto, N. Yonga, G. Yoon, S.-J. Yotebieng, M. Younis, M.Z. Yousefifard, M. Yu, C. Zaman, S.B. Zamani, M. Zare, Z. Zavala-Arciniega, L. Zegeye, D.T. Zegeye, E.A. Zeleke, A.J. Zendehdel, K. Zerfu, T.A. Zhang, A.L. Zhang, X. Zhou, M. Zhu, J. Zimsen, S.R.M. Zodpey, S. Zoeckler, L. Zucker, I. Zuhlke, L.J.J. Lim, S.S. Murray, C.J.L. GBD 2017 SDG Collaborators

Abstract

Background: Efforts to establish the 2015 baseline and monitor early implementation of the UN Sustainable Development Goals (SDGs) highlight both great potential for and threats to improving health by 2030. To fully deliver on the SDG aim of “leaving no one behind”, it is increasingly important to examine the health-related SDGs beyond national-level estimates. As part of the Global Burden of Diseases, Injuries, and Risk Factors Study 2017 (GBD 2017), we measured progress on 41 of 52 health-related SDG indicators and estimated the health-related SDG index for 195 countries and territories for the period 1990–2017, projected indicators to 2030, and analysed global attainment. Methods: We measured progress on 41 health-related SDG indicators from 1990 to 2017, an increase of four indicators since GBD 2016 (new indicators were health worker density, sexual violence by non-intimate partners, population census status, and prevalence of physical and sexual violence [reported separately]). We also improved the measurement of several previously reported indicators. We constructed national-level estimates and, for a subset of health-related SDGs, examined indicator-level differences by sex and Socio-demographic Index (SDI) quintile. We also did subnational assessments of performance for selected countries. To construct the health-related SDG index, we transformed the value for each indicator on a scale of 0–100, with 0 as the 2·5th percentile and 100 as the 97·5th percentile of 1000 draws calculated from 1990 to 2030, and took the geometric mean of the scaled indicators by target. To generate projections through 2030, we used a forecasting framework that drew estimates from the broader GBD study and used weighted averages of indicator-specific and country-specific annualised rates of change from 1990 to 2017 to inform future estimates. We assessed attainment of indicators with defined targets in two ways: first, using mean values projected for 2030, and then using the probability of attainment in 2030 calculated from 1000 draws. We also did a global attainment analysis of the feasibility of attaining SDG targets on the basis of past trends. Using 2015 global averages of indicators with defined SDG targets, we calculated the global annualised rates of change required from 2015 to 2030 to meet these targets, and then identified in what percentiles the required global annualised rates of change fell in the distribution of country-level rates of change from 1990 to 2015. We took the mean of these global percentile values across indicators and applied the past rate of change at this mean global percentile to all health-related SDG indicators, irrespective of target definition, to estimate the equivalent 2030 global average value and percentage change from 2015 to 2030 for each indicator. Findings: The global median health-related SDG index in 2017 was 59·4 (IQR 35·4–67·3), ranging from a low of 11·6 (95% uncertainty interval 9·6–14·0) to a high of 84·9 (83·1–86·7). SDG index values in countries assessed at the subnational level varied substantially, particularly in China and India, although scores in Japan and the UK were more homogeneous. Indicators also varied by SDI quintile and sex, with males having worse outcomes than females for non-communicable disease (NCD) mortality, alcohol use, and smoking, among others. Most countries were projected to have a higher health-related SDG index in 2030 than in 2017, while country-level probabilities of attainment by 2030 varied widely by indicator. Under-5 mortality, neonatal mortality, maternal mortality ratio, and malaria indicators had the most countries with at least 95% probability of target attainment. Other indicators, including NCD mortality and suicide mortality, had no countries projected to meet corresponding SDG targets on the basis of projected mean values for 2030 but showed some probability of attainment by 2030. For some indicators, including child malnutrition, several infectious diseases, and most violence measures, the annualised rates of change required to meet SDG targets far exceeded the pace of progress achieved by any country in the recent past. We found that applying the mean global annualised rate of change to indicators without defined targets would equate to about 19% and 22% reductions in global smoking and alcohol consumption, respectively; a 47% decline in adolescent birth rates; and a more than 85% increase in health worker density per 1000 population by 2030. Interpretation: The GBD study offers a unique, robust platform for monitoring the health-related SDGs across demographic and geographic dimensions. Our findings underscore the importance of increased collection and analysis of disaggregated data and highlight where more deliberate design or targeting of interventions could accelerate progress in attaining the SDGs. Current projections show that many health-related SDG indicators, NCDs, NCD-related risks, and violence-related indicators will require a concerted shift away from what might have driven past gains—curative interventions in the case of NCDs—towards multisectoral, prevention-oriented policy action and investments to achieve SDG aims. Notably, several targets, if they are to be met by 2030, demand a pace of progress that no country has achieved in the recent past. The future is fundamentally uncertain, and no model can fully predict what breakthroughs or events might alter the course of the SDGs. What is clear is that our actions—or inaction—today will ultimately dictate how close the world, collectively, can get to leaving no one behind by 2030. Funding: Bill & Melinda Gates Foundation. © 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license

Published
2018

43. Phytochemical investigation on Myristica fragrans stem bark

Author

Sajin K. Francis, James, Beena, Varughese, Sunil, and Mangalam S. Nair

Abstract

Myristica fragrans Houtt., the source of very important spice ‘nutmeg’ used world over is native to India, Indonesia, Sri Lanka, South Africa and Southeast Asia. Phytochemical investigation of M. fragrans stem bark led to the isolation of bis-aryl dimethyl tetrahydrofuran lignans, such as grandisin [(7S,8S,7′S,8′S)-3,3′,4,4′,5,5′-hexamethoxy-7,7′,8,8′-lignan] and (7S,8S,7′R,8′R)-3,3′,4,4′,5,5′-hexamethoxy-7,7′,8,8′-lignan along with important lignans and neolignans, licarinA, licarin B, odoratisol A, (2S, 3R)-7-methoxy-3-methyl-5-((E)-prop-1-enyl)-2-(5-methoxy,3,4-methylenedioxyphenyl)-2,3-dihydrobenzofuran, elemicin, fragransin B1, raphidecursinol B, erythro-(7S,8R)-Δ8′-4,7-dihydroxy-3,5,3′-trimethoxy-8-O-4′-neolignan, erythro-(7S,8R)-Δ8′-7-hydroxy-3,4,3′,5′-tetramethoxy-8-O-4′-neolignan, surinamensin.and β-sitosterol. Structures of the 12 compounds isolated were unambiguously identified by various spectroscopic methods. The former two compounds were isolated from M. fragrans for the first time. Furthermore, the X-ray crystal structure of odoratisol A is reported in this paper for the first time.

Published
2018
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44. Population and fertility by age and sex for 195 countries and territories, 1950–2017: a systematic analysis for the Global Burden of Disease Study 2017

Author

Murray, C.J.L. Callender, C.S.K.H. Kulikoff, X.R. Srinivasan, V. Abate, D. Abate, K.H. Abay, S.M. Abbasi, N. Abbastabar, H. Abdela, J. Abdelalim, A. Abdel-Rahman, O. Abdi, A. Abdoli, N. Abdollahpour, I. Abdulkader, R.S. Abebe, H.T. Abebe, M. Abebe, Z. Abebo, T.A. Abejie, A.N. Aboyans, V. Abraha, H.N. Abreu, D.M.X. Abrham, A.R. Abu-Raddad, L.J. Abu-Rmeileh, N.M.E. Accrombessi, M.M.K. Acharya, P. Adamu, A.A. Adebayo, O.M. Adedeji, I.A. Adekanmbi, V. Adetokunboh, O.O. Adhena, B.M. Adhikari, T.B. Adib, M.G. Adou, A.K. Adsuar, J.C. Afarideh, M. Afshin, A. Agarwal, G. Agesa, K.M. Aghayan, S.A. Agrawal, S. Ahmadi, A. Ahmadi, M. Ahmed, M.B. Ahmed, S. Aichour, A.N. Aichour, I. Aichour, M.T.E. Akanda, A.S. Akbari, M.E. Akibu, M. Akinyemi, R.O. Akinyemiju, T. Akseer, N. Alahdab, F. Al-Aly, Z. Alam, K. Alebel, A. Aleman, A.V. Alene, K.A. Al-Eyadhy, A. Ali, R. Alijanzadeh, M. Alizadeh-Navaei, R. Aljunid, S.M. Alkerwi, A. Alla, F. Allebeck, P. Almasi, A. Alonso, J. Al-Raddadi, R.M. Alsharif, U. Altirkawi, K. Alvis-Guzman, N. Amare, A.T. Ammar, W. Anber, N.H. Andrei, C.L. Androudi, S. Animut, M.D. Ansari, H. Ansha, M.G. Antonio, C.A.T. Appiah, S.C.Y. Aremu, O. Areri, H.A. Arian, N. Ärnlöv, J. Artaman, A. Aryal, K.K. Asayesh, H. Asfaw, E.T. Asgedom, S.W. Assadi, R. Atey, T.M.M. Atique, S. Atteraya, M.S. Ausloos, M. Avokpaho, E.F.G.A. Awasthi, A. Ayala Quintanilla, B.P. Ayele, Y. Ayer, R. Ayuk, T.B. Azzopardi, P.S. Babalola, T.K. Babazadeh, A. Badali, H. Badawi, A. Bali, A.G. Banach, M. Barker-Collo, S.L. Bärnighausen, T.W. Barrero, L.H. Basaleem, H. Bassat, Q. Basu, A. Baune, B.T. Baynes, H.W. Beghi, E. Behzadifar, M. Behzadifar, M. Bekele, B.B. Belachew, A.B. Belay, A.G. Belay, E. Belay, S.A. Belay, Y.A. Bell, M.L. Bello, A.K. Bennett, D.A. Bensenor, I.M. Bergeron, G. Berhane, A. Berman, A.E. Bernabe, E. Bernstein, R.S. Bertolacci, G.J. Beuran, M. Bhattarai, S. Bhaumik, S. Bhutta, Z.A. Biadgo, B. Bijani, A. Bikbov, B. Bililign, N. Bin Sayeed, M.S. Birlik, S.M. Birungi, C. Biswas, T. Bizuneh, H. Bleyer, A. Basara, B.B. Bosetti, C. Boufous, S. Brady, O.J. Bragazzi, N.L. Brainin, M. Brazinova, A. Breitborde, N.J.K. Brenner, H. Brewer, J.D. Briant, P.S. Britton, G. Burstein, R. Busse, R. Butt, Z.A. Cahuana-Hurtado, L. Campos-Nonato, I.R. Campuzano Rincon, J.C. Cano, J. Car, M. Cárdenas, R. Carrero, J.J. Carvalho, F. Castañeda-Orjuela, C.A. Rivas, J.C. Castro, F. Catalá-López, F. Çavlin, A. Cerin, E. Chalek, J. Chang, H.-Y. Chang, J.-C. Chattopadhyay, A. Chaturvedi, P. Chiang, P.P.-C. Chin, K.L. Chisumpa, V.H. Chitheer, A. Choi, J.-Y.J. Chowdhury, R. Christopher, D.J. Cicuttini, F.M. Ciobanu, L.G. Cirillo, M. Claro, R.M. Collado-Mateo, D. Constantin, M.-M. Conti, S. Cooper, C. Cooper, L.T. Cornaby, L. Cortesi, P.A. Cortinovis, M. Costa, M. Cromwell, E.A. Crowe, C.S. Cukelj, P. Cunningham, M. Daba, A.K. Dachew, B.A. Dandona, L. Dandona, R. Dargan, P.I. Daryani, A. Gupta, R.D. Neves, J.D. Dasa, T.T. Dash, A.P. Davis Weaver, N. Davitoiu, D.V. Davletov, K. 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Mansournia, M.A. Mantovani, L.G. Mapoma, C.C. Marami, D. Maravilla, J.C. Marcenes, W. Marina, S. Martins-Melo, F.R. März, W. Marzan, M.B. Mashamba-Thompson, T.P. Masiye, F. Mason-Jones, A.J. Massenburg, B.B. Mathur, M.R. Maulik, P.K. Mazidi, M. McGrath, J.J. Mehata, S. Mehendale, S.M. Mehndiratta, M.M. Mehrotra, R. Mehrzadi, S. Mehta, K.M. Mehta, V. Mekonnen, T.C. Meles, H.G. Meles, K.G. Melese, A. Melku, M. Memiah, P.T.N. Memish, Z.A. Mendoza, W. Mengesha, M.M. Mengistu, D.T. Mengistu, G. Mensah, G.A. Mereta, S.T. Meretoja, A. Meretoja, T.J. Mestrovic, T. Mezgebe, H.B. Miangotar, Y. Miazgowski, B. Miazgowski, T. Miller, T.R. Miller-Petrie, M.K. Mini, G.K. Mirabi, P. Mirica, A. Mirrakhimov, E.M. Misganaw, A.T. Moazen, B. Mohammad, K.A. Mohammadi, M. Mohammadifard, N. Mohammadi-Khanaposhtani, M. Mohammed, M.A. Mohammed, S. Mokdad, A.H. Mola, G.D. Molokhia, M. Monasta, L. Montañez, J.C. Moradi, G. Moradi, M. Moradi-Lakeh, M. Moradinazar, M. Moraga, P. Morgado-Da-Costa, J. Mori, R. Morrison, S.D. Mosapour, A. Moschos, M.M. Mousavi, S.M. Muche, A.A. Muchie, K.F. Mueller, U.O. Mukhopadhyay, S. Murphy, T.B. Muller, K. Murthy, G.V.S. Musa, J. Musa, K.I. Mustafa, G. Muthupandian, S. Nachega, J.B. Nagel, G. Naghavi, M. Naheed, A. Nahvijou, A. Naik, G. Naik, P. Najafi, F. Naldi, L. Nangia, V. Nansseu, J.R. Nascimento, B.R. Nawaz, H. Ncama, B.P. Neamati, N. Negoi, I. Negoi, R.I. Neupane, S. Newton, C.R.J. Ngalesoni, F.N. Ngunjiri, J.W. Nguyen, G. Nguyen, L.H. Nguyen, T.H. Ningrum, D.N.A. Nirayo, Y.L. Nisar, M.I. Nixon, M.R. Nomura, S. Noroozi, M. Noubiap, J.J. Nouri, H.R. Nourollahpour Shiadeh, M. Nowroozi, M.R. Nyandwi, A. Nyasulu, P.S. Odell, C.M. Ofori-Asenso, R. Ogah, O.S. Ogbo, F.A. Oh, I.-H. Okoro, A. Oladimeji, O. Olagunju, A.T. Olagunju, T.O. Olivares, P.R. Olusanya, B.O. Olusanya, J.O. Ong, S.K. Ortiz, A. Osgood-Zimmerman, A. Ota, E. Otieno, B.A. Otstavnov, S.S. Owolabi, M.O. Oyekale, A.S. Mahesh, P.A. Pakhale, S. Pakhare, A.P. Pana, A. Panda, B.K. 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Tsilimparis, N. Car, L.T. Ukwaja, K.N. Ullah, I. Usman, M.S. Uthman, O.A. Uzun, S.B. Vaduganathan, M. Vaezi, A. Vaidya, G. Valdez, P.R. Varavikova, E. Varughese, S. Vasankari, T.J. Vasconcelos, A.M.N. Venketasubramanian, N. Villafaina, S. Violante, F.S. Vladimirov, S.K. Vlassov, V. Vollset, S.E. Vos, T. Vosoughi, K. Vujcic, I.S. Wagnew, F.S. Waheed, Y. Walson, J.L. Wang, Y. Wang, Y.-P. Weiderpass, E. Weintraub, R.G. Weldegwergs, K.G. Werdecker, A. Westerman, R. Whiteford, H. Widecka, J. Widecka, K. Wijeratne, T. Winkler, A.S. Wiysonge, C.S. Wolfe, C.D.A. Wu, S. Wyper, G.M.A. Xu, G. Yamada, T. Yano, Y. Yaseri, M. Yasin, Y.J. Ye, P. Yentür, G.K. Yeshaneh, A. Yimer, E.M. Yip, P. Yisma, E. Yonemoto, N. Yoon, S.-J. Yotebieng, M. Younis, M.Z. Yousefifard, M. Yu, C. Zadnik, V. Zaidi, Z. Zaman, S.B. Zamani, M. Zare, Z. Zeleke, M.M. Zenebe, Z.M. Zerfu, T.A. Zhang, X. Zhao, X.-J. Zhou, M. Zhu, J. Zimsen, S.R.M. Zodpey, S. Zoeckler, L. Lopez, A.D. Lim, S.S. GBD 2017 Population Fertility Collaborators

Abstract

Background: Population estimates underpin demographic and epidemiological research and are used to track progress on numerous international indicators of health and development. To date, internationally available estimates of population and fertility, although useful, have not been produced with transparent and replicable methods and do not use standardised estimates of mortality. We present single-calendar year and single-year of age estimates of fertility and population by sex with standardised and replicable methods. Methods: We estimated population in 195 locations by single year of age and single calendar year from 1950 to 2017 with standardised and replicable methods. We based the estimates on the demographic balancing equation, with inputs of fertility, mortality, population, and migration data. Fertility data came from 7817 location-years of vital registration data, 429 surveys reporting complete birth histories, and 977 surveys and censuses reporting summary birth histories. We estimated age-specific fertility rates (ASFRs; the annual number of livebirths to women of a specified age group per 1000 women in that age group) by use of spatiotemporal Gaussian process regression and used the ASFRs to estimate total fertility rates (TFRs; the average number of children a woman would bear if she survived through the end of the reproductive age span [age 10–54 years] and experienced at each age a particular set of ASFRs observed in the year of interest). Because of sparse data, fertility at ages 10–14 years and 50–54 years was estimated from data on fertility in women aged 15–19 years and 45–49 years, through use of linear regression. Age-specific mortality data came from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 estimates. Data on population came from 1257 censuses and 761 population registry location-years and were adjusted for underenumeration and age misreporting with standard demographic methods. Migration was estimated with the GBD Bayesian demographic balancing model, after incorporating information about refugee migration into the model prior. Final population estimates used the cohort-component method of population projection, with inputs of fertility, mortality, and migration data. Population uncertainty was estimated by use of out-of-sample predictive validity testing. With these data, we estimated the trends in population by age and sex and in fertility by age between 1950 and 2017 in 195 countries and territories. Findings: From 1950 to 2017, TFRs decreased by 49·4% (95% uncertainty interval [UI] 46·4–52·0). The TFR decreased from 4·7 livebirths (4·5–4·9) to 2·4 livebirths (2·2–2·5), and the ASFR of mothers aged 10–19 years decreased from 37 livebirths (34–40) to 22 livebirths (19–24) per 1000 women. Despite reductions in the TFR, the global population has been increasing by an average of 83·8 million people per year since 1985. The global population increased by 197·2% (193·3–200·8) since 1950, from 2·6 billion (2·5–2·6) to 7·6 billion (7·4–7·9) people in 2017; much of this increase was in the proportion of the global population in south Asia and sub-Saharan Africa. The global annual rate of population growth increased between 1950 and 1964, when it peaked at 2·0%; this rate then remained nearly constant until 1970 and then decreased to 1·1% in 2017. Population growth rates in the southeast Asia, east Asia, and Oceania GBD super-region decreased from 2·5% in 1963 to 0·7% in 2017, whereas in sub-Saharan Africa, population growth rates were almost at the highest reported levels ever in 2017, when they were at 2·7%. The global average age increased from 26·6 years in 1950 to 32·1 years in 2017, and the proportion of the population that is of working age (age 15–64 years) increased from 59·9% to 65·3%. At the national level, the TFR decreased in all countries and territories between 1950 and 2017; in 2017, TFRs ranged from a low of 1·0 livebirths (95% UI 0·9–1·2) in Cyprus to a high of 7·1 livebirths (6·8–7·4) in Niger. The TFR under age 25 years (TFU25; number of livebirths expected by age 25 years for a hypothetical woman who survived the age group and was exposed to current ASFRs) in 2017 ranged from 0·08 livebirths (0·07–0·09) in South Korea to 2·4 livebirths (2·2–2·6) in Niger, and the TFR over age 30 years (TFO30; number of livebirths expected for a hypothetical woman ageing from 30 to 54 years who survived the age group and was exposed to current ASFRs) ranged from a low of 0·3 livebirths (0·3–0·4) in Puerto Rico to a high of 3·1 livebirths (3·0–3·2) in Niger. TFO30 was higher than TFU25 in 145 countries and territories in 2017. 33 countries had a negative population growth rate from 2010 to 2017, most of which were located in central, eastern, and western Europe, whereas population growth rates of more than 2·0% were seen in 33 of 46 countries in sub-Saharan Africa. In 2017, less than 65% of the national population was of working age in 12 of 34 high-income countries, and less than 50% of the national population was of working age in Mali, Chad, and Niger. Interpretation: Population trends create demographic dividends and headwinds (ie, economic benefits and detriments) that affect national economies and determine national planning needs. Although TFRs are decreasing, the global population continues to grow as mortality declines, with diverse patterns at the national level and across age groups. To our knowledge, this is the first study to provide transparent and replicable estimates of population and fertility, which can be used to inform decision making and to monitor progress. Funding: Bill & Melinda Gates Foundation. © 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license

Published
2018

45. Nimbolide from Azadirachta indica and its derivatives plus first-generation cephalosporin antibiotics: a novel drug combination for wound-infecting pathogens

Author

S. R. Dhanya, Vandana Sankar, S. Nishanth Kumar, B. S. Dileep Kumar, Mangalam S. Nair, and Kozhiparambil Gopalan Raghu

Subjects
biology, Chemistry, medicine.drug_class, General Chemical Engineering, Antibiotics, General Chemistry, Pharmacology, Azadirachta, Antimicrobial, medicine.disease_cause, biology.organism_classification, In vivo, Staphylococcus aureus, Toxicity, medicine, Bacteria, Cephalosporin Antibiotic
Abstract

The shortage of effective drugs against wound-infecting pathogens poses a serious public health threat. Combination treatment may represent a good choice for treating infections caused by these pathogens. The aim of the present study is to evaluate the in vitro efficacy of nimbolide, desacetylnimbin isolated from Azadirachta indica, and the amide derivatives of nimbolide in combination with first-generation cephalosporin antibiotics against major wound-associated bacterial pathogens. The antibacterial activities of the compounds and antibiotics were studied by calculating minimum inhibitory concentrations and minimum bactericidal concentrations. The checkerboard and time–kill assay were used to evaluate the interactions between the compounds and antibiotics. Nimbolide recorded the highest antimicrobial activity against all tested strains followed by desacetylnimbin, but the amide derivatives of nimbolide were found to be less active. The MICs of the tested compounds ranged from 64 to 2000 μg mL−1. In the checkerboard test, nimbolide and its derivatives markedly reduced the MIC values of the antibiotics. A significant synergistic effect was recorded with nimbolide as well as desacetylnimbin in combination with antibiotics, and this combination recorded significant reduction in the number of colony forming units (CFUs) in the time kill assay, and the maximum reduction was recorded between 4 and 12 h. The above combination was also found to be effective against methicillin-resistant Staphylococcus aureus (MRSA), an important drug-resistant bacterium. The cytotoxicities of the compounds were tested against H9c2 and they recorded no toxicity up to 200 μM. In summary, the combination of nimbolide/desacetylnimbin and antibiotics demonstrated synergistic activity against the major wound-associated bacteria tested in this study. Furthermore, these compounds may potentially widen the therapeutic window of antibiotics, suggesting that these combinations could be used clinically to control infections caused by wound pathogens after in vivo experiments.

Published
2015
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46. Epoxyazadiradione Purified from the Azadirachta indica Seed Induced Mitochondrial Apoptosis and Inhibition of NFκB Nuclear Translocation in Human Cervical Cancer Cells

Author

G, Shilpa, J, Renjitha, R, Saranga, Francis K, Sajin, Mangalam S, Nair, Beena, Joy, B S, Sasidhar, and S, Priya

Subjects
Limonins, Azadirachta, Seeds, NF-kappa B, Humans, Uterine Cervical Neoplasms, Apoptosis, Female, HeLa Cells, Mitochondria
Abstract

Epoxyazadiradione (EAD) is an important limonoid present in Neem (Azadirachta indica) plant. In the present study, we have purified EAD from Neem seed and studied its anticancer potential in human cervical cancer (HeLa) cells. Cell proliferation inhibition studies indicated that the GI

Published
2017

47. A new approach to high-speed flow measurements using constant voltage anemometry

Author

Mangalam, S. M, Sarma, G. R, Kuppa, S, and Kubendran, L. R

Subjects
Instrumentation And Photography
Abstract

The paper addresses the basic features of conventional instrumentation, such as the constant temperature (CTA) and the constant current (CCA) anemometers, their limitations, and describes a totally new approach to high-speed dynamic measurements using a constant voltage anemometer (CVA). The paper describes the design features of a newly developed CVA and compares preliminary results obtained with CVA and conventional anemometry in low- and high-speed flows.

Published
1992

48. In-flight detection of flow separation, stagnation, and transition

Author

Mangalam, S. M and Kuppa, S

Subjects
Aircraft Instrumentation
Abstract

Flight tests were conducted to demonstrate the feasibility of simultaneous determination of: (1) boundary-layer instability and transition characteristics; (2) flow separation region; and (3) the location of the leading-edge stagnation point. Surface mounted, multi-element, micro-thin, hot-film sensors were used in conjunction with a bank of constant-temperature anemometers and a PC-based 8-channel simultaneous data acquisition system. Conventional techniques were used to determine the boundary-layer instability and transition characteristics while the flow separation and the stagnation points were determined through the presence of phase reversal signatures.

Published
1992

49. In vitro and in vivo antitumor activity of deoxyelephantopin from a potential medicinal plant Elephantopus scaber against Ehrlich ascites carcinoma

Author

Remani Prathapan, Farha Arakkaveettil Kabeer, Dhanya Sethumadhavan Rajalekshmi, and Mangalam S. Nair

Subjects
0106 biological sciences, Antitumor activity, Deoxyelephantopin, Bioengineering, Pharmacology, Biology, biology.organism_classification, medicine.disease, 01 natural sciences, Applied Microbiology and Biotechnology, In vitro, Elephantopus scaber, Ehrlich ascites carcinoma, In vivo, 010608 biotechnology, Ascites, medicine, Neoplasm, medicine.symptom, Agronomy and Crop Science, 010606 plant biology & botany, Food Science, Biotechnology
Abstract

Elephantopus scaber Linn. is a perennial medicinal herb widely used in Asian traditional medicine for the treatment of different kinds of neoplasm. The aim of the present study was to appraise the in vitro and in vivo antitumor activity of deoxyelephantopin (DOE) - the active principle isolated from E. scaber against murine Ehrlich ascites carcinoma (EAC). Intraperitoneal administration of DOE (25 mg/kg) reduced the ascites tumor volume to a better extend than the treatments with same concentrations of 5-Flourouracil (5-FU) in EAC ascites tumor model and increased the life span of treated mice with respect to control mice (p ˂ 0.001). Moreover, treatment with 25 mg/kg DOE reduced the tumor volume and tumor burden in EAC solid tumor model and showed the best overall survival responses (Log-Rank p value

Published
2019
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