Evidence of an association of plant cultivation and cultural forests on black Indian soil is found in the botanical identifications of the carbonized plants recovered from the soils. For example, in both

the urban Santarem site and the Santarem-phase site at Caverna da Pedra Pintada, the crop maize, cucurbits, and the important palms Pupunha, B. gasipaes and Acai, E. oleracea, were identified ( Roosevelt, 2000:472–473), as well as fruits from cultural forest species: forest nance, Proteasome inhibitor B. crispa, hog plum, Spondias mombin, cashew, Anacardium giganteum, Anacardium occidentale, Poupartia amazonica (Anacardiaceae), passionflower, Passiflora nitida, Norantea guianensis (Marcgraviaceae), Endopleura uchi (Humiriaceae), Silvia itauba (Lauraceae), Casimirella rupestris (Icacinaceae), Moutabea chodatiana (Polygalaceae), the palms

Acrocomia aculeata, E. oleracea, Mauritia excelsa (Fig. 14), Mauritiella armata, and Syagrus cocoides, etc. Even the small black soil site at Maicura in the Colombian interfluves had remains of maize, manioc, papaya, Acai and many other palm fruits ( Morcote-Rios, 2008). In their large, permanent settlements, late prehistoric humans created in Amazonia a regionally prominent type of bio-cultural deposit anthropic soil. For both past and current human economies, these black soils have been one of the most important http://www.selleckchem.com/products/DAPT-GSI-IX.html resources in the Amazon. The urban-scale populations of prehistoric cultural centers such as Santarem relied on the soils’ products for hundreds of years. The extensive dark soils near transportation hubs are still an agricultural resource and feed Amazonian cities with their products. They provide the substrate for subsistence farming, urban-supply truck gardening, and cash cropping for export. The small, isolated ones are sought-after resources for rural dispersed

settlements. Thus, certain ancient human activities created a resource for sustainable production. The venerable creations, however, are vulnerable Mirabegron to destruction and in many places have been removed or covered up. Often associated with Amazonian archeological dark soils and other types of prehistoric cultural deposits are the distinctive anthropic forests called cultural or oligarchic forests (Balee, 1989, Balee, 1994, Balee, 2013, Balee and Campbell, 1990, Balick, 1984, Clement, 1999, Goulding and Smith, 2007, Henderson, 1995, Peters et al., 1989, Politis, 2007, Roosevelt, 2010a and Smith et al., 2007) An alternative term, hyperdominant, see Steege et al., 2013, exaggerates the degree of dominance of individual species and was coined after the terms cultural and oligarchic, which thus take preference. The cultural forests occur at most current ethnographic settlements, fields, and their surroundings and at most known archeological sites. But the existence of archaeological sites (e.g., Evans and Meggers, 1968 and Smith, 1980) in oligarchic forest areas is not always acknowledged (e.g., Macia and Svenning, 2005).

Although the similarities between island systems are remarkable, with most islands showing at least some human www.selleckchem.com/products/pexidartinib-plx3397.html impact, another key lesson from island archeology is the variability in human occupation and environmental interactions through time. The cases of Tikopia and Mangaia currently provide the best examples of this (Kirch, 1997), where differences in island physical characteristics (island size, age, and productivity) coupled with human decision making and cultural changes (e.g., banishing pigs, instituting a highly managed system of aboriculture, and enforcing

population control measures on Tikopia) led to similar initial patterns of environmental degradation, but dramatically different end results for both island ecosystems and human sociocultural development. A key lesson from islands is that the record of extinction and declining biodiversity, invasive species dynamics, habitat degradation, and alteration that define many island (and continental) ecosystems today extend deep into the past and blur the divisions between natural

and anthropogenic changes. In most cases, archeological and paleoecological records on islands around the world contain evidence for significant anthropogenic change well before see more the beginning of the industrial era. In some cases (e.g., California’s Channel Islands and some Caribbean islands), they also document an acceleration through time in human influence on island ecology, with more Olopatadine recent historical changes, like the global fur and oil trade, often much sharper and more dramatic than those of prehistoric times. These deep historical records raise the question: from a global islands perspective, when did the Anthropocene begin? Debate continues on when (if at all) the Anthropocene era should begin, with estimates ranging from relatively

recent nuclear testing, pesticide use, etc. to as early as the Late Pleistocene megafaunal extinctions (Doughty et al., 2010 and Zalasiewicz et al., 2011b). In many ways, setting the onset of the Anthropocene is somewhat arbitrary, with most researchers offering compelling events (Industrial Revolution, megafaunal extinction, the development of agriculture, global erosion and sedimentation, etc.) that mark major human induced alterations on a global scale. In our view, all of these events are a continuum in the same process of human transformation of Earth’s ecosystems that began millennia ago, at least by the onset of the Holocene. During the Holocene, initial domestication of plants and animals, massive human migrations to virtually all parts of the planet, growing human populations, and widespread environmental impacts are discernible on a global scale (see Smith and Zeder, 2013).

One of the earliest DDRs is the activation selleck inhibitor of γH2AX as a result of a DSB. This response occurs

within minutes of the damage, thus making it a useful marker of DNA damage. The description of events involved in this activation in mammalian cells leading to γH2AX and beyond is a complex process that has been described in detail in previous reviews (Riches et al., 2008, Paull et al., 2000, Fernandez-Capetillo et al., 2004, Cann and Dellaire, 2011, Bekker-Jensen and Mailand, 2010, Srivastava et al., 2009 and Svetlova et al., 2010). Briefly, the earliest responding proteins are those of the phosphatidylinositol 3-kinase-like family of kinases (PIKK) including ataxia telangiectasia-mutated (ATM), ATM- and Rad3-related (ATR) and the catalytic subunit of DNA-dependent protein kinase (DNA-PKc). The proteins are activated by DNA damage and are rapidly recruited to the site of damaged chromatin. Once there, they phosphorylate the histone 2AX at serine residue 139 located selleck chemicals at the C-terminal tail resulting in the formation of γH2AX. However, to date it is still not fully

understood how DNA damage is detected by the cellular machinery. Cann et al. suggested two models. The first postulates that changes in the chromatin structure following a DSB release topological constraints on the DNA helix that ultimately activate ATM. The second model, however, postulates that the MRE11-RAD50-NBS1 (MRN) complex in its task of keeping both ends of the broken DNA together is the critical DSB sensor but also the initial repair force, recruiting ATM to the site where it becomes activated (Cann and Dellaire, 2011). Some investigations with cell

lines deficient in DNA-PK and ATM showed a limited increase in H2AX phosphorylation after DSB damage (Paull et al., 2000). The roles played by the PI3K enzymes are thought to be different depending on toxic stimulus or cell type (Yan et al., 2011 and Riches et al., 2008). Either way, after the initial γH2AX L-NAME HCl activation, a positive feedback loop is created between γH2AX and the PIKKs for further DDR. The signal amplification acts as a repair signal calling for the repair systems to move to the location of the damage (Nakamura et al., 2010). Within minutes of the damage occurring, γH2AX can be detected in high quantities in the areas surrounding the DSB (Rogakou et al., 1999). These areas are known as nuclear foci and could extend several megabases of chromatin around the site of damage (Riches et al., 2008). Multiple studies (Cann and Dellaire, 2011 and Xu and Price, 2011) suggest that γH2AX foci formation is mainly limited to euchromatin considered transcriptionally active and moderately compacted. Heterochromatin representing the transcriptionally inactive and highly compacted chromatin could be inaccessible to phosphorylation or more resistant to DNA damage. One could also hypothesise that DNA damage in the heterochromatin does not lead to genomic instability as there is no active transcription.

2). No such correlation was observed when using pHrodo Green-labeled particles, which were only fluorescent in acidic compartments (r = 0.13; p = 0.41). Consistent with the published data, the total number of particles ingested by M-CSF-derived macrophages was twice as high as those taken up into GM-CSF-derived macrophages, independent of the coating of the particles (MFI: 47.13 ± 17.05 vs. 24.53 ± 5.37; p < 0.0001).

Primary porcine microglia were generated by separating loosely adherent cells from confluent mixed cortical cultures. Labeling by phagocytosis and CD14 revealed a purity of approximately 80%. When incubated with the Aβ peptide-coated AF488-labeled Akt inhibitor E. coli, the findings with macrophages could be reproduced. Again, the preincubation of E. coli with Aβ1–42 and Aβ3p-42 increased its uptake by phagocytes, with Aβ3p–42 being more active than Aβ1–42 ( Fig. 5). The results obtained in human macrophages and microglia confirmed that the coating of particles with N-terminally truncated Aβ(x–42) facilitates phagocytosis more effectively than coating with the other tested Aβ-peptides. Although M-CSF-derived macrophages showed higher phagocytic activity, the impact of Aβ-peptides was independent of the polarization of the macrophages. The present study provides evidence for an immunological function of Aβ-peptides as soluble factors and as opsonins, both of which promote

the Endocrinology antagonist phagocytosis of pathogens. The effect of the Aβ-peptides depends on N- and C-terminal modifications. A proinflammatory phenotype is particularly induced by Aβ-peptides that terminate at alanine 42. The phagocytosis of PSPs was facilitated by pre-incubation with all of the tested Aβ-peptide variants. Among them, Aβ(x–42) was more efficient

than Aβ(x–40). Similarly, an enhanced uptake of particles was previously observed in microglia after coating microspheres or yeast particles with Aβ(1–42) ( Kopec and Carroll, 1998 and Choucair-Jaafar et al., 2011). No such effect was reported after coating with Aβ1–40 ( Choucair-Jaafar et al., 2011). only These reports and our data indicate that the C-terminus strongly impacts the phagocytosis-inducing effect of Aβ-peptides. In primary monocytes and THP-1 macrophages, the phagocytosis of Aβ-coated particles was further increased by the N-terminal truncation of Aβ(x–42), i.e., Aβ(2–42) and Aβ(3p–42). As Aβ-peptides are highly hydrophobic, incubating particles with these peptides increases their hydrophobicity. Among the Aβ-peptides, those ending with alanine 42 are more hydrophobic than Aβ(x–40). N-truncation and pyroglutaminylation at amino acid residue 3 further enhance hydrophobicity due to the loss of charged groups ( Pike et al., 1995, Schilling et al., 2006, Schlenzig et al., 2009 and Meral and Urbanc, 2013). Hydrophobicity of the Aβ-peptides is also correlated with their aggregation propensity.

4A and B) and mRNA (Fig. 4C) levels were significantly increased (p < 0.01) in CUMS rats compared with Non-CUMS group, without change click here of ASC protein levels ( Fig. 4A and D). Furthermore, CUMS procedure induced significant activation of caspase-1 (cleaved caspase-1 P10, p < 0.001) in PFC of rats compared with Non-CUMS group ( Fig. 4A and E). These

data demonstrate PFC NLRP3 inflammasome activation in this animal model, being consistent with the induced maturation of IL-1β. In addition, CUMS procedure also caused PFC protein over-expression of other pro-inflammatory risk factors P2RX7 ( Fig. 4F and G) (p < 0.01), TLR2 ( Fig. 4F and H) (p < 0.01) but not TLR4 ( Fig. 4F and I) in rats compared with Non-CUMS group. Although a small but non-significant decrease of PFC NLRP3 mRNA in CUMS rats was detected after fluoxetine check details treatment, there were significant reduction of protein levels of PFC NLRP3 (p < 0.05) and cleaved caspase-1 P10 (p < 0.05), showing its suppression of PFC NLRP3 inflammasome activation in this animal model. Furthermore, fluoxetine treatment markedly down-regulated TLR2 protein

levels (p < 0.01), but showed no obvious effect on P2RX7 and TLR4 protein levels in PFC of CUMS animals. These results suggest that inhibition of PFC NLRP3 inflammasome activation and TLR2 up-regulation by fluoxetine may be involved in its antidepressant effect in CUMS rats. In above work, we demonstrated IL-1β over-expression and inflammatory signal activation in PFC of CUMS rats. Therefore, we determined

microglia and astrocyte changes in this animal model. Importantly, expression of microglia marker proteins CD11b (p < 0.001) and Iba1 (p < 0.05) ( Fig. 5A and B) were found to be increased in PFC of CUMS rats compared with Non-CUMS group. However, PFC astrocyte marker protein GFAP expression (p < 0.05) ( Fig. 5A and B) was decreased in this animal model. The similar results were observed by immunofluorescence analysis for the increased CD11b and Iba1 staining with relative increased number of amoeboid microglia, and the decreased GFAP staining with relative deceased number and short radiate of astrocyte in PFC of CUMS rats ( Fig. 5C). Fluoxetine treatment significantly inhibited microglial activation (decreased CD11b and Iba1, p < 0.05) and protected astrocyte (increased GFAP, p < 0.05) cAMP in PFC of CUMS rats ( Fig. 5). As shown in Fig. 6, there was no obvious co-location of NLRP3 and NeuN protein expression in PFC of CUMS rats. The increased co-location of NLRP3 and Iba1 protein expression further supported that microglia was primary contributor for the NLRP3 inflammasome activation and IL-1β-related inflammation in PFC of CUMS rats. Fluoxetine treatment significantly decreased microglial NLRP3 over-expression in PFC of CUMS rats. Then, we further examined PFC glutamine and glutamate levels as well as glutamine synthetase activity in CUMS rats. Although no change of PFC glutamate levels was detected (Fig.

10 One of the major goals of the conference was to revisit the clinical diagnostic criteria published subsequent to the first International TSC Consensus Conference in 1998.11 Since 1998, one additional manuscript regarding the diagnostic criteria has been published that was designed to provide more guidance to practitioners by including pictures

of the major and minor findings.12 At the 2012 meeting, the most significant change recommended to the diagnostic criteria was the incorporation of genetic testing. Although the TSC1 and TSC2 genes were discovered before the 1998 conference, molecular testing was not widely available at that time. Molecular testing of the TSC1 and TSC2 genes yields a positive mutation result for 75-90% of TSC-affected individuals categorized as “definite” by the 1998 Consensus Conference Clinical Diagnostic Criteria. 2 The use of molecular testing in medicine has expanded click here greatly since the 1990s, becoming widely accepted as invaluable in the diagnosis of diseases with a genetic basis. Utilization of genetic testing for TSC was addressed along with refinement of clinical criteria. Comprehensive and reliable screens for TSC1 and TSC2

mutations are well-established, and many pathogenic mutations have been identified (www.lovd.nl/TSC1, www.lovd/TSC2). The recommendation of the Genetics Nivolumab cost Panel was to make identification of a pathogenic mutation in TSC1 or TSC2 an independent diagnostic criterion, sufficient

for the diagnosis or prediction of TSC regardless of the clinical findings ( Table part A). This will facilitate the diagnosis of TSC in some, particularly young individuals, allowing earlier implementation of surveillance and treatment with potential for better clinical outcomes. A “pathogenic” mutation was defined as a mutation that clearly prevents protein synthesis and/or inactivates the function of the TSC1 or TSC2 proteins (e.g., nonsense mutation or frameshift mutations, large genomic deletions) or is a missense mutation whose effect on protein function has been established by functional assessment. 13 and 14TSC1 and TSC2 genetic variants whose functional effect is less certain are not definitely pathogenic and would Bcl-w not be considered a major diagnostic criterion. A significant fraction (10-25%) of TSC patients have no mutation identified by conventional genetic testing. Therefore, a normal result does not exclude TSC. Nonetheless, if the mutation in an affected relative is known, testing for that mutation has very high predictive value for family members. Assembled experts at the Consensus Conference agreed with the recommendation that identification of a pathogenic mutation in TSC1 or TSC2 is an independent diagnostic criterion. In addition to diagnosis by genetic analysis, the clinical diagnostic criteria used to establish the diagnosis of TSC were also reviewed at the conference.

Patients were randomized to receive oral enobosarm at a dosage of 1 (n = 53) or 3 mg (n = 54) or placebo (n = 52) once daily for up to 113 days at centers in the United States or Argentina. The primary end point was defined as the change in total lean body mass from baseline as assessed by dual-energy X-ray absorptiometry (DEXA). After study termination, significant increases in total lean mass were noted in both enobosarm groups (enobosarm 1 mg: median 1.5 kg, range –2.1 to 12.6, P = .001 vs baseline, enobosarm 3 mg: 1.0 kg, –4.8 to 11.5, P = .046). The study drug was well

tolerated. POWER (Prevention and treatment Of muscle Wasting in patients with cancER) was a double-blind, randomized, placebo-controlled phase III trial of enobosarm 3 mg once daily that aimed to assess lean body mass and physical

function after treatment. Preliminary results were recently presented in abstract form. 75 A total HSP inhibitor of 641 patients Alpelisib purchase with stage 3 or 4 non–small cell lung cancer were randomized into 1 of 2 trials at initiation of first-line chemotherapy (platinum plus taxane or platinum plus nontaxane) plus add-on, consisting of either enobosarm or placebo for 5 months. The study’s coprimary end points, as assessed after 84 days of treatment, were physical function response assessed by stair-climb power and lean body mass as measured by DEXA. Compared with placebo, enobosarm treatment was associated with an increase in the stair-climb power and the lean body mass in the platinum plus taxane treatment arm, whereas in the platinum plus nontaxane arm, there was only a significant increase in the patients’ lean body mass (all P < .02). Using intramuscular testosterone replacement, Del Fabbro et al76 performed a randomized, double-blind, placebo-controlled trial in 29 patients with advanced cancer,

low bioavailable testosterone, and a fatigue score higher than 3 of 10 on the ESAS. Unfortunately, 4 weeks of treatment did not change patients’ FACIT score values in the testosterone group (n = 13, administered every 2 weeks) as compared with the placebo group (n = 16). Improvements were noted in the testosterone group with regard to the Sexual Desire Inventory score (P = .05) and the patients’ performance status (P = .02). The authors therefore concluded Farnesyltransferase that “four weeks of intramuscular testosterone replacement in hypogonadal male patients with advanced cancer did not significantly improve quality of life.” 76 Another novel anabolic agent has recently been tested in a randomized, double-blind, controlled trial. MT-102, also known as espindolol, is a novel anabolic/catabolic transforming agent that appears to possess 3 potential pharmacological targets in cancer cachexia: (1) reduced catabolism through nonselective β-blockade, (2) reduced fatigue and thermogenesis through central 5-HT1a antagonism, and (3) increased anabolism through partial β-2 receptor agonism.

As alterações histológicas sugestivas de EEo são: a presença de 15 ou mais eosinófilos intraepiteliais por CGA,

microabcessos eosinofílicos, distribuição superficial dos eosinófilos, hiperplasia da zona basal. Com o novo consenso de 2011, passou-se a incluir um pequeno número de doentes com uma história clínica muito sugestiva de EEo, com menos de 15 eosinófilos por CGA, mas que apresentavam os outros achados histológicos de inflamação eosinofílica referidos anteriormente ou grânulos eosinofílicos extracelulares4. Vários estudos têm demonstrado que a EEo pode ser causada por múltiplos alergénios alimentares, através de um mecanismo imunológico de hipersensibilidade Ganetespib solubility dmso mista, mediado por IgE (hipersensibilidade tipo i) e por células (hipersensibilidade tipo iv ou tardia), sobretudo os linfócitos T13, 14, 21 and 22. Deste modo, após confirmação do diagnóstico de EEo, selleck screening library é importante a avaliação alergológica, de forma a detetar a sensibilização a possíveis alergénios (alimentares ou aeroalergénios)4. Os testes cutâneos por picada (TCP), com leitura imediata aos 15-20 min, avaliam a sensibilização a alergénios mediada por IgE e são os que têm maior sensibilidade. Os alimentos em que parece estar implicado

um mecanismo mediado por IgE são: o leite de vaca, ovo, soja, amendoim, trigo, arroz, marisco, peixe, tomate, leguminosas (ervilhas e feijão), carne de vaca e carne de frango/galinha23. Os testes epicutâneos, com leitura tardia às 48 e 96 horas, permitem detetar sensibilização mediada por células a alimentos, como o leite vaca, o ovo, o trigo, o milho, o arroz, a aveia, a soja, a batata, a carne de vaca e a carne de frango/galinha23. A associação dos TCP com os testes NADPH-cytochrome-c2 reductase epicutâneos parece aumentar a sensibilidade na deteção de sensibilização para

os alimentos mais frequentemente implicados na esofagite eosinofílica e tem um bom valor preditivo negativo (88-100%) para todos os alimentos exceto para o leite (41%)24. O doseamento sérico de IgE específica para alimentos não parece correlacionar-se com o resultado histológico da evicção do alergénio alimentar, não sendo recomendado na avaliação alergológica inicial com o objetivo de instituir as dietas alimentares. Por outro lado, a possibilidade de sensibilização a aeroalergénios deverá ser avaliada através dos TCP, dado que pode estar implicada na patogénese ou nos períodos de agravamento/exacerbação da EEo. Além disso, como os doentes com EEo têm uma elevada incidência de outras patologias alérgicas, a avaliação alergológica permite otimizar a abordagem terapêutica destas doenças, necessária em todos os doentes com EEo4.

The most serious, but rare, risk of ICG when administered intravenously in humans, according to the IC-GREEN (Akorn) product label, is anaphylactic death, which has been reported after IC-GREEN administration during cardiac catheterization.27, 28 and 29 A total of 147 patients were enrolled between July 2012 and July 2013 at 11 institutions in the United States, of whom 139 were eligible for final analysis. Ineligibility was secondary to planned anastomosis < 5 cm, no anastomosis, and/or

ileorectal anastomosis, as listed in Appendix 1 (online only). The average age of patients (±SD) was 58 ±14 years, and 53% of patients were male. Obesity (BMI >30 kg/m2) STA-9090 was prevalent in 30%, and the majority of patients were American Society see more of Anesthesiologists

(ASA) II (53%). Diverticulitis (44%), rectal cancer (25%), and colon cancer (21%) were the most prevalent preoperative diagnoses. Of the patients with rectal cancer (n = 35), 43% underwent preoperative pelvic radiation (Table 1). Cardiovascular disease (44%), and urogenital disease (40%) were the most prevalent comorbidities (Table 2). Laparoscopic resection was used in 86% and robotic surgery in 14% of the patients imaged. There was an overall conversion rate of 7.8% (n = 12); 5 of these patients were imaged, and 7 patients were not included due to a decision not to image. The splenic flexure was mobilized in 81% of patients, and a high ligation of the IMA was performed in 61.9% of cases. Successful imaging was obtained in 98.6% of cases in which perfusion imaging was attempted. 4��8C Imaging was unsuccessful in 2 patients secondary to equipment malfunction. Fluorescence angiography imaging

changed the surgical plan in 11 (7.9%) patients. This included revision of the point of proximal colon transection (Video 1), as indicated by perfusion assessment in 9 patients (6.5%); takedown and revision of the completed anastomosis after transanal perfusion assessment in 1 patient; and confirmation of viability of anastomosis with concerns of malperfusion based on traditional methods of assessing viability of the anastomosis under white light in 1 patient. The use of transanal fluorescence angiography with findings of adequate perfusion altered the intraoperative plan for diversion to no diversion in this patient. There were no anastomotic leaks in the 11 patients in whom a change in the surgical plan occurred based on fluorescence angiography findings (Table 3). The rate of splenic flexure mobilization was similar in patients with change in surgical plan (82%) and those who did not require revision (81%). There were no reported cases in which change in surgical plan was based on standard assessment of bowel before the use of fluorescence angiography. Postoperative complications were observed in 17% of patients; 12% of these were secondary to the surgical procedure and 2 (1.4%) were severe in nature (Table 4). The 2 abscesses reported were not associated with an anastomotic leak.

Taking into consideration the importance of Lake Timsah with regard to fisheries, tourism and recreational activities, it is important to identify the present status of the lake. Since up-to-date information about zooplankton community dynamics in the lake is desirable, the aim of the present investigation was to study the composition, abundance and species diversity of the zooplankton community in Lake Timsah and to establish its space-time variations in relation to the environmental conditions. Lake Timsah lies adjacent to Ismailia City near the middle of the Suez Canal at a point 80 km south of Port Said. It

covers about 16 km2 and is between 3 and 16 m in depth. The lake is considered one of the most productive along the Suez Canal AZD9291 (Fouda 1993, Ahmed 2005, Madkour et al. 2006). On the western side, the lake is connected to a small, shallow lagoon via a narrow passage. The human population of Ismailia is around 1 million. As estimated by ETPS (1995), the western lagoon receives about 833 000 m3 day−1 of domestic and

agricultural wastewaters from many drains (the Elmahsama, Abu-Gamouss, Abu-Attwa and Elbahtini drains). On the northern side, the lake receives occasional inputs from the Ismailia freshwater Everolimus molecular weight canal (ETPS 1995, Madkour et al. 2006). During the last decade, the efficiency of water treatment plants has improved and the Elbahtini drain has been closed. Despite the diminishing amounts of wastewaters, the lake is still under threat from pollutants (El-Moselhy et al. 2005, Kaiser et al. 2009) as a result of extensive human settlement where domestic agricultural

and industrial effluents are continuously discharged. To some extent, this affects the ecological and biological conditions of the lake. Such changes will be manifested in the flourishing or avoidance of some organisms including zooplankton. The study area covered Lake Timsah and the western lagoon. Ten sites were sampled seasonally from autumn Sitaxentan 2005 to summer 2006. They were chosen to cover different localities representing variable impacts on the lake (Figure 1). Sites 1–3 were located in the northern, middle and southern parts of the Canal’s shipping lane respectively. Sites 4–9 were distributed inside the lake, and site 10 lay in the western lagoon. Zooplankton samples were collected at sites 1–9 by vertical hauls (from bottom to the surface) using a plankton net of 150 μm mesh and 40 cm diameter. At site 10, 50 litres of water were collected with a bucket and sieved with the same net. The samples were preserved in 5% neutral formalin solution and their volumes concentrated to 100 ml. Three replicates of 5 ml were transferred to a Bogrove counting tray, and each zooplankter was identified and counted under a binocular research microscope. The zooplankton organisms were identified according to Giesbrecht (1892), Rose (1933), Tregouboff & Rose (1957) and Edmondson et al. (1959).