This shift in scale, intensity, and nature is significant for understanding new ecological baselines and the Anthropocene provides a framework for conceptualizing these changes. Yet it is precisely the rate and scale of change today that makes research into ecological histories and past human–environmental relationships

imperative. Only with an understanding of past human–environmental interactions, ecological histories, environmental resiliencies, and human adaptations to create historic baselines can we truly identify the scope of Anthropocene related developments today. Special thanks to Todd Braje, Douglas Kennett, Melinda Zeder, and two anonymous reviewers for their insightful comments and to Thomas Harper for creating the distribution map. PLX4032 research buy “
“Biologists should be wary when they discuss virgin Amazon ecosystems. Potsherds and black mTOR phosphorylation earth may lurk under control plots and pristine nature reserves. What appears to be untouched wilderness could have been a garden plot or bustling village, hundreds or thousands of years ago. The savannas of Roraima and the grasslands of Marajo are due partly to man-made fires. Open campina scrub on sandy soil was once cleared by Indians. More cultural surprises await beneath the forest mask ( Smith, 1980:566). Anthropocene theory and research on the

humid tropics in the 21st century have shifted away from 20th century environmental determinism. Anthropocene theory recognizes and analyzes variations in the human interaction with and impact on habitats (Mann, 2006). In contrast, mid-20th-century theoretical approaches focused on the impact of natural forces on humans and their landscapes, ignoring the possibilities of human agency. Human cultural development there was conceived as a unitary human adaptation to the tropical

forest habitat. The focus on tropical forests as marginal resources for human development became important in the late 19th and early 20th centuries during the height of western MycoClean Mycoplasma Removal Kit colonization of the tropics and exploitation of resources abroad (Roosevelt, 1991a and Roosevelt, 2005). This stance was a change from that of the initial explorers who depicted the tropics as a rich, blooming paradise for investment and settlement by Europeans (e.g., Ralegh, 1596). Mid-20th-century western scholars depicted tropical forest societies as culturally and biologically primitive compared to those of Eurasia (Steward, 1949). Because tropical peoples were supposedly unable to develop science and civilization, westerners justified their culture as a modernizing force to help indigenous peoples progress. Equilibrium theory, which privileged ecosystem stasis and control through natural forces, found favor in both social and natural science (Odum, 1975).

Once seen as the margins of our

planet (see Kirch, 1997), islands have emerged as centers of early human interaction, demographic expansion, and exploration (Erlandson and Fitzpatrick, 2006, Rainbird, 2007 and Fitzpatrick and Anderson, 2008). Islands are important both as microcosms of the patterns and processes operating on continents and as distinct locations with often greater isolation and unique biodiversity. Data from the Americas, Australia, Southeast Asia, the Pacific, North Atlantic, Mediterranean, and Caribbean demonstrate a deep history of maritime voyaging that suggests that for anatomically modern humans (Homo sapiens), the ocean was often a pathway of human interaction and discovery rather than a major obstacle or barrier

LBH589 price ( Anderson et al., 2010a, Erlandson, 2001, Erlandson, 2010a and Erlandson, 2010b). In other cases, ocean currents, winds, and other processes can influence travel across the waters surrounding islands ( Fitzpatrick and Anderson, 2008 and Fitzpatrick, 2013). Understanding when humans first occupied islands is important for understanding the geography and ramifications of ancient human environmental interactions. Here we outline

the antiquity of island colonization in major island groups around the world to contextualize our Veliparib concentration discussion of Polynesia, the Caribbean, and California. The earliest evidence for island colonization by hominins may be from Flores in Southeast Asia, which appears to have been colonized by Homo erectus 800,000 or more years ago ( Morwood et al., 1998 and Morwood Florfenicol et al., 2004). Evidence for maritime voyaging and island colonization is very limited, however, until after anatomically modern humans spread out of Africa about 70,000–60,000 years ago ( Erlandson, 2010a and Erlandson, 2010b). Australia and New Guinea were colonized roughly 45,000–50,000 years ago ( O’Connell et al., 2010 and O’Connor, 2010) in migrations requiring multiple sea voyages up to 80–90 km long. Several island groups in Southeast Asia were also settled between about 45,000 and 30,000 years ago, and some of these early maritime peoples appear to have had significant marine fishing capabilities ( O’Connor, 2010 and O’Connor et al., 2011). Additional long sea voyages were required for humans to colonize the Bismarck Archipelago in western Melanesia between 40,000 and 35,000 years ago ( Erlandson, 2010a).

Sollicité par Simon Flexner (1863–1946), MK-2206 clinical trial directeur de l’institut Rockefeller, il accepte un poste de chercheur dans cette institution et, en avril 1923, quitte La Haye pour New York. Landsteiner sera chercheur à l’institut Rockefeller jusqu’à sa retraite en 1939 et même, bénévolement, jusqu’à sa mort. Il peut s’adonner passionnément à la recherche et poursuit son exploration du système ABO : • avec son assistant Charles Philip Miller (1894–1985), il montre la présence des antigènes des groupes ABO sur les hématies des singes anthropoïdes ; En 1927, Landsteiner et Levine découvrent sur les

hématies humaines, deux « facteurs agglutinants », qu’ils désignent par les lettres M et N [9] and [10]. Indépendants des groupes ABO, ils sont

les premiers antigènes connus d’un ensemble complexe, le système MNS (ISBT no 2). Toujours en 1927, les mêmes découvrent l’antigène P du système P1 (ISBT no 3). Le 21 juin 1929, Landsteiner, sa femme et son fils deviennent citoyens des États-Unis d’Amérique. En 1930, Landsteiner est lauréat du prix Nobel de physiologie ou médecine see more pour sa « Découverte des groupes sanguins humains ». À Stockholm, où il se rend seul, il prononce la traditionnelle conférence des lauréats, en allemand, sur le thème des « Différences individuelles du sang humain » (Über individuelle Unterschiede des menschlichen Blutes). Il est traditionnel de voir dans la découverte du système Rhésus l’ultime contribution majeure de Landsteiner à la connaissance des groupes sanguins. La réalité est un peu différente : la mise en évidence du « facteur rhésus » revient indubitablement à Philip Levine en 1937 (qui avait

alors quitté Landsteiner et l’institut Rockefeller depuis 1932), avec la découverte de l’anticorps correspondant, dans le sérum d’une femme ayant récemment accouché d’un fœtus mort. Mais la publication du cas est repoussée jusqu’en 1939 [11]. C’est plus tard, en 1940–1941, que Landsteiner et Alexander Wiener (1907–1976) retrouvent ce facteur à l’aide d’un modèle expérimental d’hétéro-immunisation de lapin par des hématies de singe Macacus rhesus [12] and [13]. En juin 1939, Farnesyltransferase à 71 ans, Landsteiner quitte définitivement son poste à l’institut Rockefeller. Mais il garde à disposition un petit laboratoire où continuer ses recherches. C’est là que le 24 juin 1943, il est pris de violentes douleurs thoraciques, évocatrices d’un angor aigu. Il meurt le 26 juin 1943 à l’hôpital de l’institut. Son corps est incinéré, ses cendres enterrées au Prospect Hill Cemetery, dans l’ile de Nantucket, au large de la Nouvelle Angleterre. Hélène Landsteiner meurt peu après, le 25 décembre 1943.

, 1963). The low-frequency waves travel faster than high-frequency ones causing the frequency dispersion. Moreover, despite having a predominant forcing wind direction, waves also propagate at other directions around the predominant one, producing the directional dispersion. Due to these dispersion effects, the swell energy spectrum is narrower in both frequency and direction space, and swell waves are much lower than those initially generated in the storm (as illustrated in Fig. 3). Holthuijsen (2007) pointed out that ocean Ponatinib molecular weight waves barely lose energy outside

storms because the waves are not steep enough to break and therefore the reduction of HsHs is solely due to dispersion, without involving dissipation. However, swell dissipation has been observed across oceans, which might be attributed to air-sea friction or underwater processes (Ardhuin et al., 2009). Such dissipation increases with fetch (and selleckchem therefore it is very important in large oceans) and mostly affects steep

(short) waves (with higher frequencies). This explains why swell waves are usually long waves. Our study area does not have long fetches. Therefore, we do not explicitly account for dissipation; we only consider typical periods of swell waves, as shown later in this section. At any generation location m0m0, according to Rayleigh wave theory, wind-generated Hs(H0)Hs(H0) can be expressed as a function of the original wind-sea density spectrum E(t,f)E(t,f): equation(3) H0(t,m0)=4[∬E(t,f)D(θ)dfdθ]1/2=4[∫E(t,f)df]1/2,H0(t,m0)=4∬E(t,f)D(θ)dfdθ1/2=4∫E(t,f)df1/2,where not θθ is the angle deviation from the main direction, and D(θ)D(θ), the directional spreading function, whose integral over the whole range of directions is 1. D(θ)D(θ) can be expressed as (Denis and Pierson, 1953): equation(4) D(θ)=2πcos2(θ)where -90°⩽θ⩽90°-90°⩽θ⩽90°. As illustrated in Fig. 3, a swell wave train that is generated at location m0m0 and is associated with frequency bin (f1,f2)(f1,f2) and directional bin (θ1,θ2)(θ1,θ2)

will arrive at point mPmP after a certain time lag δδ. The swell wave height HswHsw is described by: equation(5) Hsw(t+δ,mP)=4∫f1f2∫θ1θ2E(t,f)D(θ)dfdθ1/2=4∫θ1θ2D(θ)dθ∫f1f2E(t,f)df1/2. Here, δ=d/Cgδ=d/Cg is the time needed by the wave train to travel from location m0m0 to location mPmP (over a distance d  ) at the associated average group velocity CgCg. Following Eqs. (3) and (5), Hsw(t+δ,mP)Hsw(t+δ,mP) can be rewritten as a portion of H0(t,m0)H0(t,m0) as follows: equation(6) Hsw(t+δ,mP)=[KfKθ]1/2H0(t,m0),where KfKf and KθKθ are the coefficient of reductions due to frequency and directional dispersion, respectively. They can be expressed as: equation(7) Kf=C∫f1f2E∼(x)dx, equation(8) Kθ=∫θ1θ2D(θ)dθwhere E∼(x) denotes the normalized density spectrum, and C   is chosen to satisfy: equation(9) C∫E∼(x)dx=1,with x=f/fpeakx=f/fpeak, and fpeakfpeak being the peak frequency.

Following his post-doc, Steve returned briefly to Ottawa and then accepted a faculty position in the Department of Psychology at Concordia University in Montreal. In 1998, we had the great fortune of recruiting

him to the Department of Psychiatry at the UMDNJ-New Jersey Medical School in Newark, where he established an exceptional basic science program in PNI. Steve buy Ivacaftor was also active in the school’s Interdisciplinary PhD program and in the Rutgers-UMDNJ Integrative Neuroscience Program, mentoring numerous pre-doctoral students and post-doctoral fellows. He became a key member of our largely clinical Department of Psychiatry, admired and sought after by clinical Residents as a teacher and research mentor, and appointed Director of Research in the department in 2009. Steve’s expertise, his respect for science and for colleagues, and his exceptional common sense made him a highly regarded member of NIH Study Sections and of the Editorial Board of BBI. His colleagues recall him as an outstanding champion of PNI research on study sections that often had only limited understanding of the field. Important funded research in PNI might never have happened if not for Steve’s erudite and articulate advocacy. And he stayed with the task,

even at the cost of having less time for his own work. Keith Kelley, who served on an NIH study section with Steve and then asked him to serve on the editorial board of BBI in Anacetrapib 2006, Screening Library screening noted his insightful, inquisitive mind and his knack for recognizing good science, as well as his warm, welcoming smile and infectious love for biomedical research. Recently, Steve co-edited “The Neuroimmunological Basis of Behavior and Mental Disorders” with Allan Siegel, a fitting expression of the scope of his interests. His trail-blazing collaboration with Siegel on cytokines and aggression has transformed that field, most recently elucidating TNF-alpha effects on aggressive

behavior. At the time of his death, Steve was especially excited about findings concerning effects of soluble IL-2 and IL-6 receptors on stereotypic behaviors and on the role of anti-streptococcus IgM and dopamine in mediating stereotypic movements. The first report, by Steve and his colleagues, on the specific role of IgM in precipitating unique behavioral disturbances is presented elsewhere in this issue of BBI (Zhang et al., 2012). Steve Zalcman devoted himself fully and unconditionally to the people he loved, the activities he valued, and the ideas he cherished. He inspired those around him, opening many minds to new ways of thinking and perceiving. He was individualistic and meticulous, with an unquenchable curiosity and an elegant mind. He challenged conventions with intellectual and personal integrity. Steve was taken from us as he was approaching the peak of his career.

M. Purcell and F. Bloch in 1952), the U.S. has played a leading

role in the development of NMR spectroscopy. Many of the critical developments in multidimensional NMR, in solid state NMR methods and their underlying theory, in see more DNP technology, and in the exploration of applications in chemistry, biochemistry, biology – ALL took place in the U.S. (MRI and functional MRI were also first proposed and demonstrated in the U.S.) However, there is a consensus in the NMR community that the U.S. leadership role has eroded over the past 10 years. This is certainly true in the area of high field NMR magnets. When 900 MHz (21.1 T) NMR magnets became available around 2002, approximately 15 were installed in the U.S., with approximately 10 being purchased with federal government funds (NIH or DOE, plus the wide-bore 900 MHz magnet constructed at NHMFL). selleck screening library Relatively few NMR magnets above 800 MHz (18.8 T)

were installed in the U.S. in subsequent years. Meanwhile, magnet technology has advanced to the point where a 1.0 GHz (23.5 T) NMR magnet was installed at the European Center for High Field NMR in Lyon, France in 2010. Plans exist to install at least one 1.2 GHz (28.2 T) NMR magnet in Europe, at a new NMR center in the Netherlands. Additional 1.2 GHz NMR Quisqualic acid magnets are under negotiation for other European sites. Two 950 MHz NMR magnets were installed recently in the U.S., one with federal funding (NIH), the other purchased entirely by private funds. Each increment in magnetic field strength produces an improvement in NMR data, through increased resolution and sensitivity, as explained above. Magnetic field strength is not the only significant parameter in an NMR-based research project. Innovations

in ancillary technology and RF pulse sequence methods, new approaches to data analysis, improvements in sample quality, and clever choices of scientific problems are also highly significant. For these reasons, NMR research groups in the U.S. that do not have access to the highest available fields can continue to make important scientific contributions. However, if the U.S. were to fall further behind in NMR magnet technology, the most interesting and important problems, involving systems with the greatest complexity, biological relevance, and technological impact, would be solved elsewhere. It would also become increasingly difficult for research groups in the U.S. to attract the brightest and most productive Ph.D. students and postdoctoral fellows, as it is natural for young scientists to prefer better-equipped research labs for their training. Investment in high-field NMR magnet technologies is highly leveraged.

The overall MES prevalence was 35.3% with a median MES number of

2.3/h. There was a strong correlation between MES activity and incidence of thromboembolism and times with events were predicted by MES activity with a moderate positive predictive value (0.37–0.7) and a high negative predictive value (0.82–1.0). Concerning therapy, patients on both medications, oral anticoagulants and antiplatelets, had less events (0.7% vs. 2.8%) and a lower MES prevalence (18.3% vs. 65.4%) than patients on anticoagulation alone. Therefore, MES detection seems very useful in patients with the Novacor device as it correlates with therapy and clinical events. In another study patients with the DeBakey were investigated [17]. 23 patients were monitored twice weekly with and without oxygen inhalation. Therapy and documentation of clinical events was identical to the first study. In these patients the embolic risk of 0.24%/per day was Selleckchem Linsitinib 80% less than for patients with the Novacor LVAD, although the prevalence of MES (35.1%) was the same as in Novacor patients and the number of MES was much higher (mean 81 ± 443/h) than in the Novacor device. The authors

found no correlation between MES activity and incidence Metformin of thromboembolism or hemostatic treatment for patients with the DeBakey device. The authors also found that the number of MES with the DeBakey device decreased significantly after oxygen inhalation suggesting Amrubicin a gaseous nature of most of the MES in patients with the DeBakey device. Gaseous MES have been shown to not correlate with stroke risk, something that has been observed with artificial heart valves in the past. Sliwka and Georgiadis retrospectively evaluated 369 patients with various types of artificial heart valves >3 months concerning the risk of stroke and the presence and number of MES [18]. They found significant differences in MES prevalence and counts depending on valve type. Although the prevalence of MES ranged from 9% (biological valves) to 92% (Björk Shiley) and the average MES numbers from 0 to 133 per hour there was no association

between MES counts and INR, age, cardiac rhythm, and implant duration. There was also no predictive value of MES for a history of neurological symptoms which were prevalent in 42 patients. In summary, MES detection seems useful in patients with Novacor LVAD to guide therapy and to predict clinical events. However this does not hold true for patients with the DeBakey LVAD and not for patients with artificial heart valves as most MES in these patients are from gaseous nature. MES are an infrequent finding in most cardiac sources of embolism and due to the low case numbers in most studies and the low absolute number of MES any conclusion is premature. Much larger studies would be needed with homogeneous study populations to address most questions covered in this review, especially to monitor therapeutic effects or to predict future strokes.

(3) A series of HTS assay positive lung

tumorigenesis inhalation studies have been conducted using whole-body exposure of A/J mice to an environmental tobacco smoke surrogate (ETSS) (Stinn et al., 2005 and Witschi, 2005). In these studies, mice were exposed for 5 months followed by a 4-month post-inhalation period (5 + 4-month schedule), which was needed for the smoke-induced tumors to develop beyond incidences found in sham-exposed controls. Using the same exposure schedule, studies on MS inhalation were also negative at the end of the 5-month inhalation period but positive at the end of the 4-month post-inhalation period (Curtin et al., 2004 and Stinn et al., 2010). In an 18-month study with A/J mice, the need for a post-inhalation period was confirmed for 5- and 10-month MS inhalation periods, but MS inhalation for 18 months was sufficient to elicit a concentration-dependent lung tumor response without the need for a further post-inhalation period (Stinn et al., 2012). The susceptibility of the A/J mouse to the development of spontaneous and chemically induced lung adenomas and adenocarcinomas seems to be related to a propensity of the

Kras proto-oncogene for mutation and increased transcription ( Chen et al., 1994 and To et al., 2006). Mutated Kras genes have frequently been found in human lung adenocarcinomas of smokers ( Porta et al., 2009). In view of the Selleckchem Target Selective Inhibitor Library above, this model warrants further

investigation of its reliability and biological relevance, two crucial requirements of toxicological method validation (e.g., Interagency Coordinating Committee on the Validation of Alternative Methods, 1997). With the aim of generating data towards validating the A/J mouse model, the objectives of the present study were • to generate data on intra-laboratory reproducibility of the lung tumor response in A/J mice exposed to MS inhalation for 18 months and to discuss inter-laboratory reproducibility based on published shorter-term smoke inhalation studies; Due to the objective of reproducing the data from the previous 18-month inhalation study (designated as Study 1, Stinn et al., 2012), Dolichyl-phosphate-mannose-protein mannosyltransferase the basic study design and methods were very similar for the current study (Study 2). In order to align as much as possible to regulatory guidance available for the carcinogenicity testing of chemicals (Organisation for Economic Co-operation and Development, 1981 and Organisation for Economic Co-operation and Development, 2009), Study 2 additionally included female mice as the second sex and the histopathological examination of extra-pulmonary organs and tissues. For a better characterization of the MS concentration–response curve, a third concentration was added, which was below the ones previously used, because the high concentration in Study 1 was considered the maximum tolerated MS concentration.

Once death was confirmed the pulmonary system was flushed with a heparin-solution (Wockhardt UK Ltd., Wrexham, UK) via catheter inserted into

the right ventricle or caudal vena cava. This was followed by Dublecco’s phosphate buffer solution (D-PBS, Sigma–Aldrich Olaparib in vivo Ltd., Gillingham, UK) to remove remaining blood from circulation. The lungs were inflated with around 3 ml of air and the trachea clamped; then the lungs, heart, and connective tissue were extracted en bloc. After extraction the lung’s trachea was cannulated and a syringe was used to breathe the lungs to ensure that they did not leak. Lungs were stored in glucose solution (5% glucose in water, Baxter Healthcare Ltd., Thetford, UK), chilled Navitoclax cell line to approximately 280 K until needed. Excised rat lungs were inserted into a custom-made, sealable, ventilation chamber that filled the entire coil region. The ventilation chamber and its operating procedures are described in detail in previous work [15]. Briefly, the trachea of the rat lung was cannulated with an adaptor that was attached to the top of the ventilation chamber. The ventilation chamber was filled to about 2/3 of its total volume with a 5% glucose solution (Baxter Healthcare Ltd., Thetford, UK). Hp gas was delivered to the storage volume VB after compression using one of the two Extraction

Schemes described in this work. When a volume was pulled on the inhalation syringe pressure equalization forces the lungs to expand ( Fig. 8). This acts in a similar fashion to the thoracic diaphragm, as the expansion of the lungs causes it to inhale Chlormezanone gas from the volume VB. Rubidium filters were made from 60 mm

of Teflon tubing (outer-diameter = 9.4 mm, inner-diameter = 6.4 mm; Swagelok, Warrington, UK) with 100 g of glass wool (Corning glass works, Corning, NY, USA) loosely packed inside. Chemical indicator paper (Whatman plc, Maidstone, UK) was used to check the pH value of the 1.0 ml of distilled water used to wash the glass wool. The resulting pH of the rubidium wash was pH 5.0. After SEOP at 220 kPa, a transfer of 5 s in duration resulted in a pressure of approximately 11 kPa of hp gas in Vext. Valves A + B ( Fig. 3a) were closed and the connecting lines were evacuated. A selected pressure of O2 gas was then added to Vext and the connecting lines were evacuated again. After a 5 s time delay that allowed for mixing of the O2 with the hp gas, the mixture was delivered for the MR measurements performed using Extraction Scheme 2. All T  1 data were obtained at ambient temperature using a pulse sequence comprising of sixteen medium (θ=12°)(θ=12°) flip angle r.f. pulses evenly separated by time increment τ. T1 relaxation values were determined from the nonlinear least-square analysis of the time dependence of the NMR signal intensity f(t) in the presence of spin-destruction due to the r.f.

Radiocarbon dates were calibrated with OxCal software ( Bronk Ramsey 1995) using 3-MA order the Marine09 data set ( Reimer et

al. 2009), with the Baltic Sea regional ΔR value of –100 ± 100. Three sediment cores were taken and examined from Prorer Wiek (Figures 1, 2). The shallowest of these cores (core 246040, 15.7 m b.s.l.) consisted of three parts (Figure 3). The lowest part (E1) contained olive-grey clay silt with few plant remains. The sediments of this zone exhibited the highest contents in a core of biogenic silica (6%) and loss on ignition (6%), and the lowest content of terrigenous silica (69%). This zone was also characterized by lower ratios of Mg/Ca, Fe/Mn and Na/K than in other zones. The Na/K ratio was highest LDK378 clinical trial in this zone only at the base of zone E1. The second zone (E2) began at a depth of 265 cm and contained fine, olive-grey, silty sand with fine shell debris of the Ancylus, Pisidium and Spherium genera. The geochemical composition of this zone yielded a slightly higher contribution than in zone E1 of terrigenous silica and

higher ratio of Fe/Mn and Na/K, whereas the contribution of biogenic silica and loss of ignition decreased. The uppermost zone (F) of core 246040 began at a depth of 176 cm and consisted of fine, olive-grey sand with shells of the Macoma, Cerastoderma, Mytilus, and Hydrobia genera. The ratio of Mg/Ca, Fe/Mn and Na/K and the content of terrigenous silica (95%) were the highest observed in this core, while the content of biogenic silica and loss on ignition were the lowest.

Liothyronine Sodium Core 246050 was taken at a depth of 16.8 m b.s.l., to the south-east of core 246040 (Figures 1, 2). This core also consisted of three distinct zones (Figure 3). The lowest zone (E1; 283–610 cm) contained fine, olive-grey sand with humus particles and abundant plant remains. The geochemical composition of this zone exhibited a high content of terrigenous silica (95%) and Fe/Mn ratio, and a low content of biogenic silica (0–3%), loss of ignition (1.5–11%), and ratio of Mg/Ca and Na/K. This zone did not contain diatom flora. The central zone (E2; 136–283 cm) contained brownish-black peat gyttja and detritus gyttja (205–283 cm) with wood and reed remains, and fine, olive-grey sand (136–205 cm) with plant remains. The sediment in the gyttja portion of this zone was characterized by higher contents in the core of biogenic silica (9%) and loss on ignition (37%), a low content of terrigenous silica (44%) and low Mg/Ca, Na/K and Fe/Mn ratios. However, the sand portion of E2 contained the highest amount of terrigenous silica, and all the elemental ratios were the highest. Zone E2 contained benthic freshwater diatom species, such as Fragilaria martyi, F. brevistriata, F. pinnata and Amphora pediculus, and brackish-water species, such as F. guenter-grassi and F. geocollegarum.