Late Little Ice Age palaeoenvironmental records from the Anzali and Amirkola Lagoons (south Caspian Sea): Vegetation and sea level changes

This is a postprint version of the article. The official published article can be found from the link below - Copyright @ 2011 Elsevier Ltd.Two internationally important Ramsar lagoons on the south coast of the Caspian Sea (CS) have been studied by palynology on short sediment cores for palaeoenvironmental and palaeoclimatic investigations. The sites lie within a small area of very high precipitation in a region that is otherwise dry. Vegetation surveys and geomorphological investigations have been used to provide a background to a multidisciplinary interpretation of the two sequences covering the last four centuries. In the small lagoon of Amirkola, the dense alder forested wetland has been briefly disturbed by fire, followed by the expansion of rice paddies from AD1720 to 1800. On the contrary, the terrestrial vegetation reflecting the diversity of the Hyrcanian vegetation around the lagoon of Anzali remained fairly complacent over time. The dinocyst and non-pollen palynomorph assemblages, revealing changes that have occurred in water salinity and water levels, indicate a high stand during the late Little Ice Age (LIA), from AD < 1620 to 1800–1830. In Amirkola, the lagoon spit remained intact over time, whereas in Anzali it broke into barrier islands during the late LIA, which merged into a spit during the subsequent sea level drop. A high population density and infrastructure prevented renewed breaking up of the spit when sea level reached its maximum (AD1995). Similar to other sites in the region around the southern CS, these two lagoonal investigations indicate that the LIA had a higher sea level as a result of more rainfall in the drainage basin of the CS.The coring and the sedimentological analyses were funded by the Iranian National Institute for Oceanography in the framework of a research project entitled “Investigation of the Holocene sediment along the Iranian coast of Caspian Sea: central Guilan”. The radiocarbon date of core HCGL02 was funded by V. Andrieu (Europôle Méditerranéen de l'Arbois, France) and that of core HCGA04 by Brunel University

The Sanandaj–Sirjan Zone in the Neo-Tethyan suture, western Iran: Zircon U–Pb evidence of late Palaeozoic rifting of northern Gondwana and mid-Jurassic orogenesis

The Zagros Orogen, marking the closure of the Neo-Tethyan Ocean, formed by continental collision beginning in the late Eocene to early Miocene. Collision was preceded by a complicated tectonic history involving Pan-African orogenesis, Late Palaeozoic rifting forming Neo-Tethys, followed by Mesozoic convergence on the ocean\u27s northern margin and ophiolite obduction on its southern margin. The Sanandaj-Sirjan Zone is a metamorphic belt in the Zagros Orogen of Gondwanan provenance. Zircon ages have established Pan-African basement igneous and metamorphic complexes in addition to uncommon late Palaeozoic plutons and abundant Jurassic plutonic rocks. We have determined zircon ages from units in the northwestern Sanandaj-Sirjan Zone (Golpaygan region). A sample of quartzite from the June Complex has detrital zircons with U-Pb ages mainly in 800-1050 Ma with a maximum depositional age of 547 ± 32 Ma (latest Neoproterozoic¿earliest Cambrian). A SHRIMP U-Pb zircon age of 336 ± 9 Ma from gabbro in the June Complex indicates a Carboniferous plutonic event that is also recorded in the far northwestern Sanandaj-Sirjan Zone. Together with the Permian Hasanrobat Granite near Golpaygan, they all are considered related to rifting marking formation of Neo-Tethys. Scarce detrital zircons from an extensive package of metasedimentary rocks (Hamadan Phyllite) have ages consistent with the Triassic to Early Jurassic age previously determined from fossils. These ages confirm that an orogenic episode affected the Sanandaj-Sirjan Zone in the Early to Middle Jurassic (Cimmerian Orogeny). Although the Cimmerian Orogeny in northern Iran reflects late Triassic to Jurassic collision of the Turan platform (southern Eurasia) and the Cimmerian microcontinent, we consider that in the Sanandaj-Sirjan Zone a tectonothermal event coeval with the Cimmerian Orogeny resulted from initiation of subduction and closure of rift basins along the northern margin of Neo-Tethys

The global burden of adolescent and young adult cancer in 2019: a systematic analysis for the Global Burden of Disease Study 2019

Background: In estimating the global burden of cancer, adolescents and young adults with cancer are often overlooked, despite being a distinct subgroup with unique epidemiology, clinical care needs, and societal impact. Comprehensive estimates of the global cancer burden in adolescents and young adults (aged 15–39 years) are lacking. To address this gap, we analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, with a focus on the outcome of disability-adjusted life-years (DALYs), to inform global cancer control measures in adolescents and young adults. Methods: Using the GBD 2019 methodology, international mortality data were collected from vital registration systems, verbal autopsies, and population-based cancer registry inputs modelled with mortality-to-incidence ratios (MIRs). Incidence was computed with mortality estimates and corresponding MIRs. Prevalence estimates were calculated using modelled survival and multiplied by disability weights to obtain years lived with disability (YLDs). Years of life lost (YLLs) were calculated as age-specific cancer deaths multiplied by the standard life expectancy at the age of death. The main outcome was DALYs (the sum of YLLs and YLDs). Estimates were presented globally and by Socio-demographic Index (SDI) quintiles (countries ranked and divided into five equal SDI groups), and all estimates were presented with corresponding 95% uncertainty intervals (UIs). For this analysis, we used the age range of 15–39 years to define adolescents and young adults. Findings: There were 1·19 million (95% UI 1·11–1·28) incident cancer cases and 396 000 (370 000–425 000) deaths due to cancer among people aged 15–39 years worldwide in 2019. The highest age-standardised incidence rates occurred in high SDI (59·6 [54·5–65·7] per 100 000 person-years) and high-middle SDI countries (53·2 [48·8–57·9] per 100 000 person-years), while the highest age-standardised mortality rates were in low-middle SDI (14·2 [12·9–15·6] per 100 000 person-years) and middle SDI (13·6 [12·6–14·8] per 100 000 person-years) countries. In 2019, adolescent and young adult cancers contributed 23·5 million (21·9–25·2) DALYs to the global burden of disease, of which 2·7% (1·9–3·6) came from YLDs and 97·3% (96·4–98·1) from YLLs. Cancer was the fourth leading cause of death and tenth leading cause of DALYs in adolescents and young adults globally. Interpretation: Adolescent and young adult cancers contributed substantially to the overall adolescent and young adult disease burden globally in 2019. These results provide new insights into the distribution and magnitude of the adolescent and young adult cancer burden around the world. With notable differences observed across SDI settings, these estimates can inform global and country-level cancer control efforts. Funding: Bill &amp; Melinda Gates Foundation, American Lebanese Syrian Associated Charities, St Baldrick's Foundation, and the National Cancer Institute

The global burden of adolescent and young adult cancer in 2019 : a systematic analysis for the Global Burden of Disease Study 2019

Background In estimating the global burden of cancer, adolescents and young adults with cancer are often overlooked, despite being a distinct subgroup with unique epidemiology, clinical care needs, and societal impact. Comprehensive estimates of the global cancer burden in adolescents and young adults (aged 15-39 years) are lacking. To address this gap, we analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, with a focus on the outcome of disability-adjusted life-years (DALYs), to inform global cancer control measures in adolescents and young adults. Methods Using the GBD 2019 methodology, international mortality data were collected from vital registration systems, verbal autopsies, and population-based cancer registry inputs modelled with mortality-to-incidence ratios (MIRs). Incidence was computed with mortality estimates and corresponding MIRs. Prevalence estimates were calculated using modelled survival and multiplied by disability weights to obtain years lived with disability (YLDs). Years of life lost (YLLs) were calculated as age-specific cancer deaths multiplied by the standard life expectancy at the age of death. The main outcome was DALYs (the sum of YLLs and YLDs). Estimates were presented globally and by Socio-demographic Index (SDI) quintiles (countries ranked and divided into five equal SDI groups), and all estimates were presented with corresponding 95% uncertainty intervals (UIs). For this analysis, we used the age range of 15-39 years to define adolescents and young adults. Findings There were 1.19 million (95% UI 1.11-1.28) incident cancer cases and 396 000 (370 000-425 000) deaths due to cancer among people aged 15-39 years worldwide in 2019. The highest age-standardised incidence rates occurred in high SDI (59.6 [54.5-65.7] per 100 000 person-years) and high-middle SDI countries (53.2 [48.8-57.9] per 100 000 person-years), while the highest age-standardised mortality rates were in low-middle SDI (14.2 [12.9-15.6] per 100 000 person-years) and middle SDI (13.6 [12.6-14.8] per 100 000 person-years) countries. In 2019, adolescent and young adult cancers contributed 23.5 million (21.9-25.2) DALYs to the global burden of disease, of which 2.7% (1.9-3.6) came from YLDs and 97.3% (96.4-98.1) from YLLs. Cancer was the fourth leading cause of death and tenth leading cause of DALYs in adolescents and young adults globally. Interpretation Adolescent and young adult cancers contributed substantially to the overall adolescent and young adult disease burden globally in 2019. These results provide new insights into the distribution and magnitude of the adolescent and young adult cancer burden around the world. With notable differences observed across SDI settings, these estimates can inform global and country-level cancer control efforts. Copyright (C) 2021 The Author(s). Published by Elsevier Ltd.Peer reviewe

The Effect of Atorvastatin on Depression by Forced Swimming Stress model in Gonadectomized Male Mice

Introduction: Depression is one of the most common mental disorders, which its effective treatment maintains an acceptable level of performance in patients. Concerning the different effects of sexual glands on various physiological phenomena such as depression, the purpose of this study was investigation of the effect of Atorvastatin on depression by forced swimming stress model in gonadectomized male mice. Methods: 24 male rats with an average weight of 30-35 g were used in the study. Rats were randomly divided into 3 groups (n=8). Those groups included a group which was not gonadectomized, the gonadectomized group received DMSO and gonadectomized group received Atorvastatin. At first, mice were gonadectomized. One week after the operation, treatments were administered intraperitoneally half an hour before the test. Depression was assessed by the forced swimming test. In this test, mice were placed into a cylindrical glass (25 cm height, 12 cm in diameter) containing a column of 8 cm of water at 25&plusmn;1&deg;C. In 10 minutes, the number of immobile, swimming and climbing wall were recorded. The data were analyzed by one way variance analysis and Tukey&rsquo;s test using SPSS. Results: Intraperitoneal injection of Atorvastatin (40 mg/kg) significantly increased the immobility time in the gonadectomized mice taking the drug or solvent DMSO in forced swimming test. The gonadectomy had an increase in depression compared to healthy mice (p<0.05). Conclusion: The findings of the present study indicated that taking Atorvastatin having a two-folded increase in depression of gonadectomized mice

Yield, Yield Components, Correlation Coefficients and Path Analysis of Cotton Cultivars under Drought Stress

Determining environment &ndash; associated alterations in grain yield is important in yield assessment under drought stress. Therefore this study was carried out to determine the correlation coefficients and direct and indirect effects of effective components on yield in four drought - tolerant and susceptible cotton cultivars. Cotton cultivars were considered as sub plots and 3 levels of irrigation regime [33% (I33%), 66% (I66%) and 100% (I100% of water requirement)], designated as main plots in a split plot based on complete block design with three replications at Agricultural Research Station of Kashmar, Razavi Khorasan of Iran in 2011. The results showed that all yield components, except boll weight, were negatively and significantly affected by drought stress. The results also showed that retention of greater boll numbers per plant was the main component of cultivars difference in terms of cotton seed yield. High and significant correlations were observed between yield and boll number per plant, biological yield and harvest index under drought stress. While there was only significant correlations between seed yield with plant height and biological yield under non-stress condition. Path analysis showed that the most important component of cotton seed yield is biological yield under both drought stress and non-stress conditions and other components such as: boll number and weight, earliness percent and harvest index caused an increase in cotton seed yield by indirect effect on this component

Kupffer Cells Mediate Leptin-Induced Liver Fibrosis

BACKGROUND & AIMS: Leptin has profibrogenic effects in liver, although the mechanisms of this process are unclear. We sought to elucidate the direct and indirect effects of leptin on hepatic stellate cells (HSCs). METHODS: HSCs from Sprague-Dawley rats were exposed to leptin and expression of collagen-I, tissue inhibitor of matrix metalloproteinases-1 (TIMP1), transforming growth factor beta 1 (TGF-beta 1), and connective tissue growth factor (CTGF/CCN2) was assessed. The effects of medium from Kupffer cells (KCs) and sinusoidal endothelial cells (SECs) following leptin were evaluated in HSCs; alpha-smooth muscle actin (alpha SMA) production and KC signaling were analyzed. RESULTS: HSCs were not activated by incubation with leptin. However, HSCs cultured with medium taken from KCs that were incubated with leptin had increased expression of collagen 1, TIMP1, TGF-beta 1, and CTGF/CCN2, as well as aSMA protein levels and proliferation. These effects were leptin receptor dependent because conditioned medium from KCs isolated from leptin receptor-deficient Zucker (fa/fa) rats did not activate HSCs. In KCs incubated with leptin, messenger RNA and protein expression of TGF-beta 1 and CTGF/CCN2 increased. Leptin potentiated signal transducer and activator of transcription 3, AKT, and extracellular signal-related kinase 1/2 phosphorylation in KCs and increased AP-1 and nuclear factor-kappa B DNA binding. Finally, addition of anti-TGF-beta to KC-conditioned medium inhibited HSC expression of collagen I, TIMP1, and CTGF/CCN2, whereas signal transducer and activator of transcription 3 inhibitor attenuated TGF-beta 1 production by KC. CONCLUSIONS: Leptin mediates HSC activation and liver fibrosis through indirect effects on KC; these effects are partly mediated by TGF-beta 1

Adiponectin attenuates liver fibrosis by inducing nitric oxide production of hepatic stellate cells

Adiponectin protects against liver fibrosis, but the mechanisms have not been fully elucidated. Here, we showed that adiponectin upregulated inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) and protein expression in hepatic non-parenchymal cells, particularly in hepatic stellate cells (HSCs), and increased nitric oxide (NO2-/NO3-) concentration in HSC-conditioned medium. Adiponectin attenuated HSC proliferation and migration but promoted apoptosis in a NO-dependent manner. More advanced liver fibrosis with decreased iNOS/NO levels was observed in adiponectin knockout mice comparing to wide-type mice when administered with CCI4 while NO donor supplementation rescued the phenotype. Further experiments demonstrated that adiponectin-induced iNOS/NO system activation is mediated through adipoR2-AMPK-JNK/Erk1/2-NF-κB signaling. These data suggest that adiponectin inhibits HSC function, further limiting the development of liver fibrosis at least in part through adiponectin-induced NO release. Therefore, adiponectin-mediated NO signaling may be a novel target for the treatment of liver fibrosis. KEY MESSAGES: • Adiponectin activates HSC iNOS/NO and SEC eNOS/NO systems. • Adiponectin inhibits HSC proliferation and migration but promotes its apoptosis. • Adiponectin inhibits CCL4-induced liver fibrosis by modulation of liver iNOS/NO. • Adiponectin stimulates HSC iNOS/NO via adipoR2-AMPK-JNK/ErK1/2-NF-κB pathway