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State College, PA, United States

Capelotti P.J.,Penn State Abington College
Polar Record | Year: 2010

In 1873, the British explorer Benjamin Leigh Smith concluded the private oceanographic and geographical explorations in the seas around Svalbard that he had begun in 1871 and continued in 1872. The logistics of the 1873 expedition, however, were far more complicated than those of the first two voyages. Rather than using a single ship as he had done with the sailing vessel Samson the previous summers, Leigh Smith chartered James Lamont's Arctic steamer Diana and employed Samson as a reserve supply tender. With the added supplies Samson afforded, Leigh Smith planned to round the northeast limit of Svalbard, which he had discovered in 1871, and survey Kong Karls Land. Among those invited to join to expedition was a twenty-three-year-old member of the Royal Engineers, Lieutenant Herbert C. Chermside, who would visit the Arctic for the first and last time in a long life of military service. It was to Chermside that Leigh Smith entrusted the keeping of the expedition's logbooks. These three unpublished journals, along with a log kept by Samson's captain, William Walker, provide details of an expedition that, while it failed in its primary objective to round Nordaustlandet, did succeed in relieving Adolf Erik Nordenskiöld's Swedish polar expedition beset near Mosselbukta. It also maintained an array of contacts with whalers and sealers, for example the Peterhead whaler David Gray and the Norwegian skipper Frederick Christian Mack, regarding local conditions around Svalbard. At Augustabukta, Chermside's observations of uplifted skeletons of remotely harvested whales give estimated death ranges of between 1569-1691 and 1764-1807. The expedition would end with a major island in Svalbard being named for Chermside. © Cambridge University Press 2010. Source


Between 1898 and 1905, three American expeditions attempted to reach the geographical North Pole from the archipelago of Zemlya Frantsa-Iosifa [Franz Josef Land] and each went to extraordinary and expensive lengths to stage their work. The third of these, the Ziegler polar expedition (1903-1905), led by Anthony Fiala and funded by the American baking soda tycoon William Ziegler, set up numerous camps and caches of supplies along its various expedition routes through the islands. The papers of Anton Vedoe and Ernest Leffingwell at the Rauner Special Collections Library at Dartmouth College reveal both the locations and contents of the caches Fiala ordered to be established in spring 1905, as he made his second and final attempt to reach the pole. These caches extend from the expedition base camp (Camp Abruzzi) at Bukhta Teplitsa [Teplitz Bay] on Ostrov Rudol'fa [Rudolf Island] to the main base of the preceding 1901-1902 Baldwin-Ziegler expedition (Camp Ziegler) on Ostrov Aldzher [Alger Island]. Little is known of the condition of these sites, especially the main cache site of Kane Lodge on Ostrov Grili [Greely Island]. As such, they hold the potential to provide new sources of archaeological data to study American polar ambitions at the turn of the 20th century. While these sites remain unexplored, increasing tourism in the islands necessitates informed planning and field research to establish the nature and stability of these remains so that they may be preserved and the potential effects of tourism mitigated. © Copyright 2010 Cambridge University Press. Source


Bloomer S.A.,Penn State Abington College | Bloomer S.A.,University of Iowa | Kregel K.C.,University of Iowa | Brown K.E.,Iowa City Veterans Administration Medical Center | Brown K.E.,University of Iowa
Archives of Gerontology and Geriatrics | Year: 2014

Elevations in hepatic iron content occur with aging and physiological stressors, which may promote oxidative injury to the liver. Since dysregulation of the iron regulatory hormone, hepcidin, can cause iron accumulation, our goal was to characterize the regulation of hepcidin in young (6 mo) and old (24 mo) Fischer 344 rats exposed to environmental heat stress. Liver and blood samples were taken in the control condition and after heating. Hepcidin expression did not differ between young and old rats in the control condition, despite higher levels of hepatic iron and IL-6 mRNA in the latter. Following heat stress, pSTAT3 increased in both groups, but C/EBPα and hepcidin mRNA increased only in old rats. Despite this, serum iron decreased in both age groups 2. h after heat stress, suggesting hepcidin-independent hypoferremia in the young rats. The differential regulation of hepcidin between young and old rats after hyperthermia may be due to the enhanced expression of C/EBPα protein in old rats. These data support the concept of "inflammaging" and suggest that repeated exposures to stressors may contribute to the development of anemia in older individuals. © 2013 Elsevier Ireland Ltd. Source


Bloomer S.A.,Penn State Abington College | Brown K.E.,Iowa City Veterans Administration Medical Center | Brown K.E.,University of Iowa
Cell Biochemistry and Function | Year: 2015

Although iron-catalysed oxidative damage is presumed to be a major mechanism of injury leading to cirrhosis and hepatocellular carcinoma in hemochromatosis, these events have been difficult to recapitulate in an animal model. In this study, we evaluated regulators of hepatocarcinogenesis in a rodent model of chronic iron overload. Sprague-Dawley rats were iron loaded with iron dextran over 6months. Livers were harvested and analysed for markers of oxidative stress, as well as the following proteins: p53, murine double minute 2, the Shc proteins p66, p52, p46; β-catenin, CHOP, C/EBPα and Yes-associated protein. In this model, iron loading is associated with hepatocyte proliferation, and indices of oxidative damage are mildly increased in tandem with augmented antioxidant defenses. Alterations potentially favouring carcinogenesis included a modest but significant decrease in p53 levels and increases in p52, p46 and β-catenin levels compared with control livers. Countering these factors, the iron-loaded livers demonstrated a significant decrease in CHOP, which has recently been implicated in the development of hepatocellular carcinoma, as well as a reciprocal increase in C/EBPα and decrease in Yes-associated protein. Our results suggest that chronic iron overload elicits both tumour suppressive as well as tumour-promoting mechanisms in rodent liver. © 2015 John Wiley & Sons, Ltd. Source


Bloomer S.A.,Penn State Abington College | Han O.,Pennsylvania State University | Kregel K.C.,University of Iowa | Brown K.E.,Iowa City Veterans Administration Medical Center | Brown K.E.,University of Iowa
Blood Cells, Molecules, and Diseases | Year: 2014

An increasing body of evidence suggests that dysregulation of iron metabolism contributes to age-related pathologies. We have previously observed increased hepatic iron with aging, and that environmental heat stress stimulates a further increase in iron and oxidative liver injury in old rats. The purpose of this study was to determine a mechanism for the increase in hepatic iron in old rats after heat stress. Young (6. mo) and old (24. mo) Fischer 344 rats were exposed to two heating bouts separated by 24. h. Livers were harvested after the second heat stress, and protein levels of the iron import protein, transferrin receptor-1 (TFR1), and the iron export protein, ferroportin (Fpn) were determined by immunoblot. In the nonheated condition, old rats had lower TFR1 expression, and higher Fpn expression. After heat stress, TFR1 declined in the old rats, and iron chelation studies demonstrated that this decline was dependent on a hyperthermia-induced increase in iron. TFR1 did not change in the young rats after heat stress. Since TFR1 is inversely regulated by iron, our results suggest that the increase in intracellular iron with aging and heat stress lower TFR1 expression. Fpn expression increased in both age groups after heat stress, but this response was delayed in old rats. This delay in the induction of an iron exporter suggests a mechanism for the increase in hepatic iron and oxidative injury after heat stress in aged organisms. © 2013 Elsevier Inc. Source

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