Missing data were replaced

by a negative answer for the latter analyses, A chi-square test was used when comparing groups while McNemar’s test was used to examine changes within groups from baseline to post-intervention for categorical variables. Independent t-tests were used to compare Anti-infection Compound Library groups while paired t-tests were used to examine changes within groups from baseline to post-intervention for continuous variables. The statistical significance for all analyses was set at p < 0.05 (two-sided). SPSS Version 20.0 (SPSS Inc. Chicago, IL, USA) was used for all analyses. Participants were recruited from 12 pharmacies. The response rate to the mailed invitation to enroll in the study among eligible participants identified by their pharmacists was 15%. A total of 144 participants who received the educational intervention

are included in this analysis. Table 1 shows demographic, general health status and prescription-related characteristics of the entire cohort at baseline. Participants were mostly female (73%), had an average age of 75, and the majority (83%) had no formal college or university education. Half of all participants Crenolanib in vitro had previously attempted benzodiazepine discontinuation, 25% of whom had successfully weaned off the drug at some point. Post-intervention, 45.1% (n = 65) of participants reported increased perceived risk from consumption of benzodiazepines. There were no statistical differences in baseline characteristics between individuals perceiving an increased risk (RISK) and those with no perceptions of increased

risk (NO RISK), except for a trend showing a shorter duration of benzodiazepine use among the RISK group (p = 0.08) ( Table 1). Knowledge about benzodiazepines was similar between groups at baseline. Changes in knowledge both within and between risk groups are described in Table 2. Eighty percent (52/65) of participants in the RISK group changed an answer from incorrect to correct on at least one knowledge question from pre- to post-intervention compared to only 41% (33/79) in the NO RISK group. The FER RISK group demonstrated a significantly higher proportion of correct answers post-intervention on the safety, side effects and alternatives questions compared to the NO RISK group (p < 0.001). Only participants in the RISK group who had the potential for knowledge acquisition showed a statistically significant increase on the overall knowledge score (mean change score 1.77 SD (1.3)). The change in overall score was significantly greater among these individuals in the RISK group post-intervention compared to the NO RISK group (mean change score 0.91 95% CI (0.5, 1.3)). Beliefs about benzodiazepines were similar between groups at baseline. Table 3a and Table 3b show changes in beliefs about the necessity, perceived negative consequences, and risk-benefit ratio of benzodiazepine use.

Although the current work only reflects the basic characterizations of the crystal structure following ball-milling, based on a previous paper we were able to infer that this method induces the starch to change the spatial arrangement disorder of its amylopectin and amylose thus leading to the destruction of its crystalline

areas and promoting the amorphous areas in each granule [8]. The surface morphology buy GSI-IX of the cold soluble and insoluble starch granules treated with ball-milling in either ceramic or stainless steel pots are presented in Fig. 3 and Fig. 4. The untreated maize starch granules were either oval or polyhedral and had uniform surfaces and smooth yet slightly porous surfaces. These results are similar to previous reports on native maize starch [18]. After 5 h of ball-milling, the starch granules were subjected to various forces (such as compression, impact, shear, and attrition) to cause a further physical breakdown of the granules and produce a range of fractions. Results revealed that the surface of the starch granules across the range of fractions lost their smoothness and became rough with some debris. Among them, highly hydrated

gel-forming and low molecular weight soluble fractions are known to be more likely attacked more rapidly by α-amylase as compared to intact granules. Consequently, ball-milling significantly not only increased the CWS but also damaged the physical properties of the starch (Fig. 1 and Fig. 3). Clear fissures and grooves were observed on the surface of a large number of starch Gefitinib nmr granules and a few fragments peeled off from the outer layer of the starch granules imparting excessive roughness on their surfaces. These phenomena are similar to that reported by Dhital et al. [19] who also proposed that fissures on the granule surface facilitate enzymatic diffusion and increase susceptibility oxyclozanide to amylolysis. In addition, they hypothesized that these fragments would have more surface area per unit mass and would thus be

expected to be more rapidly hydrolyzed than intact granules due to the enzymes having an easier access to the inside of the native granules via pores and channels. The current results also found that the ball-milling operation increased the enzymatic availability within the granule fractions. Moreover, the starch granules were broken into smaller particle sizes and clumped together either into lumps or adhering to the surface of the larger granules. All the above variations indicate that significant changes occur in the internal structure of the granule during the milling process. Finally, the results also reveal that the integrity and granule periphery remained intact even after 5 h of ball-milling time, indicating the stability of the starches process by this method.

This work was supported by the UK Medical Research Council (MC_A060_5PR10) and a study visit (L.G.B.) funded by the UK Experimental Psychology Society. We thank the editors of this special issue and two anonymous reviewers for feedback on an earlier draft of this work. “
“Our brains are constantly bombarded with signals from different sensory modalities. Although vision is usually considered the dominant modality, other senses, particularly audition, interact closely with vision to create a coherent representation of our surroundings (Shimojo and Shams, 2001). Some atypical forms of cross–modal interactions, such as synaesthesia, result in percepts

that do not represent events in the external world. Synaesthesia is an unusual phenomenon in which stimulation in one sensory modality elicits additional anomalous experiences. These additional

Y-27632 research buy experiences can occur in the same modality (e.g., seeing colours when viewing achromatic letters: grapheme–colour synaesthesia) or in a different modality (e.g., seeing colours when listening to music: sound–colour synaesthesia). The prevalence of synaesthesia is relatively low, with estimates ranging from .5% (Baron-Cohen et al., 1996; Rich et al., 2005) to 5% (Simner et al., 2006) of the population. Synaesthesia selleck chemicals has drawn much scientific attention in recent years due both to the interest inherent in anomalous brain phenomena, and to the insights these phenomena can give into normal mechanisms of perception and cognition. There are two major hypotheses regarding the neural mechanisms that give rise to synaesthesia. The first view, generally termed the cross-activation hypothesis, suggests that excessive neural connections between adjacent cortical areas

underlie synaesthetic experiences. Originally, this view postulated that grapheme–colour synaesthesia occurs as a result of excessive neural connections between colour-selective area V4 and the posterior temporal grapheme area (Hubbard and Ramachandran, 2005). More recently, these authors further proposed that the parietal lobe mediates the binding of synaesthetic colour and visual word form, presumably again through excessive connections with the temporal lobe (Hubbard, 2007; Hubbard et al., 2011). The idea that synaesthesia involves an anomalous form of Edoxaban feature binding, which implicates the parietal lobe, has also been raised by others, although not necessarily specifying excessive connections (Esterman et al., 2006; Mattingley et al., 2001; Robertson, 2003). The second view, generally called the disinhibited-feedback hypothesis, suggests that synaesthesia results from a ‘malfunctioning’ mechanism that fails to inhibit the crosstalk between brain areas normally inhibited in non-synaesthetic brain. According to different versions of this view, the disinhibition may occur in the feedback from multi-modal regions (e.g.

However, IL-1β is not consistently

elevated in the synovial fluid of OA patients [53] and [92] and the endogenous IL-1 receptor antagonist, which blocks IL-1 activity, is produced by synoviocytes at higher levels in OA than Selleckchem Osimertinib in RA [33]. Attempts to block IL-1 activity therapeutically in patients have been associated with only minimal symptom-reducing efficacy at best [18] and [20]. However, it is possible that IL-1 activity is important in specific clinical settings in OA. Production of active IL-1 requires activation of the NALP3 inflammasome; activation of the inflammasome by uric acid crystals has been implicated in flares of gouty arthritis [69]. Other crystals, including basic calcium phosphate [76] and hydroxyapatite [48] have recently been shown to activate inflammasome-mediated IL-1 production. Both hydroxyapatite and basic calcium phosphate crystal deposition occurs in patients with OA. Therefore, it is possible that IL-1 is important in patients with OA and evidence of crystalline deposition. TNF-α is readily detectable in SF in patients

with OA [92]. Like B-Raf inhibition IL-1, TNF can activate chondrocyte-mediated catabolic protease production [51]. The well-established clinical efficacy of TNF inhibition in the setting of RA, and the availability of blocking agents, led to trials of a TNF-inhibitor in an open-label pilot study to treat pain and inflammation in twelve patients with erosive hand OA [67]. Like the IL-1 trials, this trial did not demonstrate significant efficacy, but improvement in pain and physical function scores was reported for some individuals. It remains to be seen whether different patient subsets will respond to targeted therapies

blocking the actions of TNF. The perivascular inflammatory cell infiltrates observed in the OA synovium are largely composed of lymphocyte populations [7]. Based on this observation, our group investigated the expression and activity of cytokines involved in lymphocyte biology in OA synovium. We focused our efforts on the common-γ chain family of cytokines (including IL-2, IL-15, and IL-21) which are involved in recruitment, survival and activity of lymphocytes [89]. IL-15 was consistently Anacetrapib detectable and elevated in patients with early stage OA, compared with end-stage OA patients undergoing total knee arthroplasty. In rheumatoid synovial fibroblasts, TLR-2 and -4 stimulation were shown to induce IL-15 production in vitro [49]. Both synoviocytes [89] and chondrocytes (Scanzello, unpublished results) from OA patients express the specific IL-15 receptor, suggesting there may be multiple cellular targets of IL-15. Serum IL-15 detected using a proteomic approach was associated with the presence and progression of radiographic OA [62]. Studies by Long et al. showed that IL-7, another common-γ chain cytokine which activates lymphocytes, is produced by chondrocytes [66].

The lysate was centrifuged at 12 000 × g for 10 min at 4 °C, after which the supernatant was withdrawn and stored at − 20 °C until use. The methanol extract was evaporated to dryness, and the dried extract dissolved in Trametinib concentration an aliquot of filtered sea water. Bloom extracts, culture extracts and the medium of batch cultures (extracellular exudates) were diluted with sterilized sea water to give a dilution series of 1, 2, 3, 5, 10, 20, 50 and 100%. Sterilized sea water was used as the control. 500 μl of each

dilution was added to a 5 ml culture tube containing 25 nauplii of 48 h-hatched cysts of A. salina. The tubes were incubated at 20 °C under a continuous light flux of 90 μmol photons m− 2 s− 1. After 48 h, the percentage mortality of nauplii was calculated compared to controls. The LC50 value was determined by probit analysis ( Finney 1963). Haemolytic activity was

tested by erythrocyte lysis assay (ELA) according to Eschbach et al. (2001) and its modification by Ling & Trick (2010). ELA was carried out on bloom samples, on algal cells and on extracellular exudates of exponentially growing cultures (6 days after inoculation) of H. akashiwo. An aliquot with a known number Cell Cycle inhibitor of Heterosigma cells was centrifuged (6000 × g for 10 min at 4 °C), and the supernatant containing extracellular exudates following filtration through a 0.45 μm pore size GF/C filter was collected. Algal samples were prepared following the protocols of Eschbach et al. (2001), modified Montelukast Sodium by Ling & Trick (2010). The cells of bloom samples (10 ml) and pellets of centrifuged cultures were ruptured in ELA buffer, prepared as

described by Eschbach et al. (2001) (150 mM NaCl, 3.2 mM KCl, 1.25 mM MgSO4, 3.75 mM CaCl2 and 12.2 mM TRIS base; pH adjusted to 7.4 with HCl) by sonication for 60 s at 20 °C in a bath-type sonicator. Complete cell rupture was confirmed by microscopic observation. Ultrasonicated algal samples and supernatants were kept in the freezer until use. The dry methanol extract of H. akashiwo cells prepared for the Artemia salina assay was re-dissolved in ELA buffer before use in ELA. Blood freshly collected from a rabbit was immediately mixed with 0.1 ml 10% sodium citrate to prevent it from coagulating. For the ELA, erythrocytes were harvested from the blood by centrifugation in a 1.5 ml microcentrifuge tube at 1500 × g for 5 min at 4 °C. The pelleted erythrocytes were washed twice with ELA buffer by vortexing and centrifugation at 1500 × g for 5 min at 4 °C. Erythrocyte suspensions were adjusted to the appropriate cell density (5 × 106) in ELA buffer with a haemocytometer. The ELA method was basically that of Eschbach et al. (2001) with modifications by Ling & Trick (2010). Briefly, 0.5 ml of erythrocyte suspension and 0.5 ml of cell extract or extracellular exudates of H. akashiwo were added to 1.

, 2008, Oliveira-Brett et al., 2002 and Rauf et al., 2005).

2,2-Dimethyl-(3H)-3-(N-3′-nitrophenylamino)naphtho[1,2-b]furan-4,5-dione (QPhNO2, C20H16O5N2, molecular mass ABT-263 cost 364.35 g/mol) was prepared as described previously ( da Silva Júnior et al., 2007). Stock solutions for pharmacological assays were prepared by dissolving QPhNO2 and nor-beta in 0.1% DMSO immediately prior to use. Doxorubicin hydrochloride (adriamycin, CAS No. 25316-40-9) (Dox) was purchased from Sigma Aldrich Co. (St. Louis, MO, USA). RPMI 1640 growth medium supplemented with 2% glutamine, fetal bovine serum, streptomycin and penicillin was purchased from Gibco® (Invitrogen, Carlsbad, CA, USA). Calf thymus dsDNA (sodium salt, type I) was purchased from Sigma (St. Louis, MO, USA). Aqueous acetate buffer solutions (0.1 M, pH 4.5), which were used in the electrochemical

experiments involving DNA, were prepared from analytical grade reagents and purified water (conductivity < 0.1 μS/cm) Z-VAD-FMK obtained from a Millipore (Milford, MA, USA) Milli-Q system. Dimethylformamide (DMF) and tetrabutylammonium tetrafluoroborate (TBABF4) were used in the electrochemical experiments (aprotic medium) and prepared from analytical grade reagents supplied by Sigma Aldrich. HL-60 cells (human promyelocytic leukemia line) were grown in RPMI-1640 medium supplemented with 10% fetal bovine serum, 100 μg/mL streptomycin and 100 U/mL penicillin 17-DMAG (Alvespimycin) HCl at 37 °C in a 5% CO2 atmosphere. The cytotoxicity

of compounds (0.009–5 μg/mL) was evaluated using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) reduction assay ( Mosmann, 1983) after 24 h of incubation. Doxorubicin was used as a positive control. In a second set of experiments, N-acetyl-l-cysteine (NAC, 5 mM) was pre-incubated with the cells for 1 h before drug addition, and after 24 h, cytotoxicity was measured, as previously described. Additional experiments were performed to elucidate the mechanisms involved in the cytotoxic action of nor-beta and QPhNO2 using HL-60 cells (3 × 105 cells mL−1) after drug exposure for 24 h. Compounds were dissolved in DMSO to make a 1 mg mL−1 stock solution and added to the cell culture to obtain a final concentration of 0.5, 1.0 or 2.0 μM QPhNO2, based on its IC50 value, or 1.0 or 2.0 μM nor-beta. Doxorubicin (0.5 μM) was used as a positive control. After the quinone treatment, cells were loaded with 2′,7′-dichlorodihydrofluorescein diacetate (H2-DCF-DA) (20 μM) and incubated at 37 °C for 30 min in the dark, as proposed by Lebel et al. (1992). Doxorubicin and beta-lapachone were used as positive controls. The experiments were repeated in the presence of NAC (5 mM) pre-incubated with the cells for 1 h before drug addition. The cells were then harvested, washed, resuspended in PBS and analyzed immediately by flow cytometry at excitation and emission wavelengths of 490 and 530 nm, respectively.

, 1997). The mechanism by which acridine and thiazolidine derivatives act has been continuously researched. Thiazolidine derivatives activate peroxisome proliferator-activated receptors (Barros et al., 2010). Meanwhile, acridine derivatives used in cancer chemotherapy have biological targets, such as DNA topoisomerases I and/or II, telomerase/telomeres and kinases (Castillo-González et al., APO866 in vivo 2009, Guo et al., 2009 and Oppegard et al., 2009). Our understanding of ATZD’s cytotoxic mechanisms have been limited to results from double stranded-DNA biosensors and single stranded-DNA solutions, which show a positive interaction

with these ATZD that couple acridine and thiazolidine (Barros et al., 2012). Here, we demonstrate that ATZD inhibit DNA topoisomerase I activity. The cytotoxicity of DNA topoisomerase I inhibitors is caused by blocking DNA topoisomerase I cleavage complexes or by inhibiting DNA topoisomerase I catalytic activity. Then, DNA topoisomerase I inhibitors work by stabilising the DNA topoisomerase I cleavage complexes, which cause DNA damage (Hsiang et al., 1989, Pommier et al., 1998 and Stewart et al., 1998). Because malignant cells often contain greater amounts of DNA topoisomerase I than normal cells, tumour cells should be more sensitive to the

toxic effects of these inhibitors. The malignant cells that often contain great amounts of DNA topoisomerase I include colon adenocarcinoma, several types of non-Hodgkin’s Cytidine deaminase lymphoma, leukaemias, melanoma and carcinomas of the stomach, breast EPZ015666 purchase and lung (Potmesil, 1994). This partially explains the selective cytotoxic effects of ATZD. However, the exact mechanism of this selective antitumor activity remains to be determined. Previous studies have reported that some acridine and thiazolidine derivatives are somatic- and germ-cell mutagenic agents capable of inducing both numerical and structural chromosome aberrations in vitro and in vivo (Attia, 2008, Attia, in press, Kao-Shan et al.,

1984 and Nishi et al., 1989). These compounds are highly cytotoxic/genotoxic to normal lymphocyte cells. Therefore, to improve our understanding of the ATZD’s cytotoxic actions, we assessed their genotoxic effects in human peripheral lymphocytes. Previously, the cytotoxicity of these compounds was assessed against normal lymphocyte cells (Barros et al., 2012); however, the genotoxicity had not been investigated. The genotoxic effects of ATZD were determined using an alkaline comet assay and a chromosome aberration assay; the anti-telomerase activity was determined using a pan telomeric probe. In our studies, none of these ATZD agents showed genotoxicity and/or anti-telomerase activity in cultured human lymphocytes at the experimentally tested concentrations.

115360), resources of which are composed of financial contribution from the European Union’s

Seventh Framework Programme (FP7/2007-2013) and EFPIA buy Cobimetinib companies’ in kind contribution. “
“Lynne S. Steinbach Karen G. Ordovas David Saloner, Jing Liu, and Henrik Haraldsson The quality of the medical imaging is a key component for accurate disease diagnosis. Optimizing image quality while maintaining scan time efficiency and patient comfort is important for routine clinical MRIs. In this article, we review both practical and advanced techniques for achieving high image quality, especially focusing on optimizing the trade-offs between the image quality (such as signal-to-noise and spatial resolution) and acquisition time. We provide practical examples for optimizing the image quality and scan time. Maria Clara N. Lorca, Henrik Haraldsson, and Karen G. Ordovas Magnetic resonance assessment of regional myocardial function is a novel potentially important tool for early identification of cardiac pathology. Many cardiac magnetic resonance techniques have been developed for detection and quantification of regional strain abnormalities including steady-state free-precession CINE, tagging, displacement encoding with stimulated echoes, strain encoding imaging, learn more and

feature tracking. Potential clinical applications of magnetic resonance strain imaging include early detection of systolic dysfunction in heart failure patients with both ischemic and nonischemic etiologies. Nicholas S. Burris and Michael D. Hope Aortic disease is routinely monitored with anatomic imaging, but until the recent advent of 3-directional phase contrast

MRI (4D) flow, blood flow abnormalities have gone undetected. 4D flow measures aortic hemodynamic markers quickly. Qualitative flow visualization has spurred the investigation of new quantitative markers. Flow displacement and wall shear stress can quantify the effects of valve-related aortic Atazanavir flow abnormalities. Markers of turbulent and viscous energy loss approximate the increased energetic burden on the ventricle in disease states. This article discusses magnetic resonance flow imaging and highlights new flow-related markers in the context of aortic valve disease, valve-related aortic disease, and aortic wall disease. Juliano Lara Fernandes and Carlos Eduardo Rochitte T1 mapping, one form of tissue characterization performed with a parametric approach, has been gaining rapid popularity, as different sequences have been developed to integrate image acquisition into a clinical routine. This technique allows fast progression from the basics of sequence development to its application in normal individuals and distinct diseases, sometimes overriding the more gradual steps taken with other cardiovascular magnetic resonance advances.

Results depicted in Fig. 4 indicate that complex I inhibition by Ebs, (PhSe)2 and (PhTe)2 was not modified by the addition of SOD (Fig. 4A), CAT (Fig. 4B) or SOD + CAT (Fig. selleck compound 4C). In order to test the hypothesis that organochalcogens-induced complex I inhibition is mediated by oxidation of thiol groups, we investigated the efficacy of GSH

to reverse the organochalcogens-induced inhibition of complex I. Fig. 5 shows that GSH (500 μM) completely reversed the organochalcogens-induced complex I inhibition in hepatic (Fig. 5A) and in renal (Fig. 5B) membranes. In order to check the inhibitory effect of different organochalcogens in mitochondria complex II activity, we carried out experiments at two different conditions. In brief, in condition 1 the membranes were incubated with the organocompounds (at different concentrations) in the presence of succinate

5 mM for 10 min. The reaction was stopped 3 min after MTT by addition of ethanol. In condition 2, the mitochondrial membranes Pembrolizumab purchase were incubated with various concentrations of organocompounds in the absence of succinate for 10 min. Succinate (5 mM) and MTT were then added and the reaction stopped after 3 min by the addition of ethanol. Statistical analysis indicates that Ebs and (PhTe)2 significantly inhibited both hepatic and renal complex II activity in both conditions (Fig. 6). In contrast, (PhSe)2 did not change the mitochondrial complex II activity from liver (Fig. 6A and B), but inhibited renal complex II activity under condition ADAM7 1 (Fig. 6C), without inhibiting it under experimental condition 2 (Fig. 6D). The IC50 (μM) values for inhibition by organochalcogens of mitochondrial complex II activity, in both conditions, are showed in Table 1. Malonate (8 mM) caused a significant inhibition of the mitochondrial complex II activity that varied from 40% to 70% inhibition (see Fig. 6A–D). GSH (500 μM) completely reversed the organochalcogens-induced complex II inhibition both in hepatic (Fig.

7A) and renal (Fig. 7B) membranes. Ebs and (PhTe)2 inhibited the mitochondrial complexes II–III activity from liver (Fig. 8A) and kidney (Fig. 8B). (PhSe)2 did not inhibit hepatic complexes II–III activity (Fig. 8A), but significantly inhibited renal complexes II–III activity (Fig. 8B). The IC50 (μM) values for inhibition by organochalcogens of mitochondrial complexes II–III activity are showed in Table 1. Statistical analysis revealed that Ebs did not modify the hepatic (Fig. 9A) or renal (Fig. 9B) complex IV activity. (PhSe)2 slightly inhibited complex IV activity from liver and kidney (Fig. 9A and B), whereas (PhTe)2 did not change the renal complex IV activity (Fig. 9B); but it inhibited hepatic complex IV activity at 50 μM (Fig. 9A). The IC50 (μM) value for inhibition by (PhSe)2 of mitochondrial complex IV activity is showed in Table 1.

The saltern lies about 500 m from the Mediterranean Sea in the north. It consists of a series of shallow ponds with depths of 0.5–1.5 m and surface areas varying from 70 to a few hundred ha (Figure 1). Seawater is pumped from the Suez Canal through an intake to a large pond (P1) where solar energy and wind combine and evaporation begins. The water volume is reduced and salinity levels gradually build up through consecutive evaporation ponds (P2–P3) and the production pond (P4). As the salinity increases, low-soluble salts precipitate

Roxadustat clinical trial as carbonates and sulphates. The saturated brine then passes through smaller ponds (P5, crystallizer ponds) where evaporation continues (Figure 2). Once the volume has been reduced to about 10% of the original, any furtherk concentration results in the deposition of sodium chloride. Five ponds with different salinities were sampled in summer (June 2010).

Water samples were collected 20 cm below the surface using a 2-L Van Dorn bottle. Water temperature, transparency and pH were measured immediately in situ after sampling using a mercury CP 868596 glass thermometer graduated in 0.1 °C, a Secchi disc and a portable pH meter (Model HI 9124) respectively. Salinity was estimated as total dissolved salts (TDS) according to APHA (1995). A well-mixed sample was passed through a glass fibre filter, after which the filtrate was evaporated to dryness in a weighed

dish, then dried to constant weight at 180 °C. The increase in dish weight represents the salt content [g l− 1]. The total weight of major ions generally Proteasome inhibitor constitutes over 99% of the total salinity (Wetzel & Likens 2000). Nitrates and phosphates were determined in filtered seawater using GF/C filters according to the methods described by Parsons et al. (1984). For phytoplankton examination, water samples were preserved immediately using Lugol’s iodine and concentrated by decanting. The algal count was conducted under an inverted microscope using Utermöhl’s method (Utermöhl 1958) and identified to genus or species level by consulting the works of Prescott (1951), Hendey (1964), Dodge (1982) and Komárek & Anagnostidis (2005). Pearson’s correlation coefficient was performed using the SPSS 17 software program to examine the potential relationships among physicochemical variables and phytoplankton diversity and density. Relations highly significant to the 0.05 level were noted. The waters of the Port Fouad saltworks were always clear, with the Secchi depth corresponding to the maximum depth of water due to the shallowness of the ponds (Table 1). The water of the shallower, more saline pond (P5, crystallizer pond) was warmer (29.3 °C) than that of the deeper, less saline pond (P1, 25.6 °C). The water salinity increased progressively throughout the series of interconnected ponds, giving a value of 340.