, 2006; Sisto et al., 2009; Fujimoto et al., 2011). Two primer sets have hitherto been reported as L. rhamnosus GG-specific primer sets (Brandt & Alatossava, 2003; Ahlroos & Tynkkynen, 2009). However, few studies have used the strain-specific primer sets, and the qualities

of the sets remain to be characterized. In this study, the two published L. rhamnosus GG-specific primer sets were evaluated by focusing on strain specificities of the sets for future use. All strains used in this study are shown in Table 1. L. rhamnosus GG (=ATCC 53103) was obtained from the American Type Culture Collection and used as positive control. L. rhamnosus DSM 20021T was from the German Collection of Microorganisms and Cell Cultures and Ipilimumab mouse used as negative control. A number of dairy isolates and human clinical isolates originating from different countries and identified as Seliciclib cell line L. rhamnosus were obtained from the Belgian Coordinated Collection of Microorganisms/LMG. The strains were cultured

in MRS broth at 37 °C for 20 h. Bacterial DNA was extracted from 1 mL of the cultured cells as previously described (Endo et al., 2007). Two different L. rhamnosus GG strain-specific PCR systems were used in this study, and all PCR primers used are shown in supporting information Table S1. The first PCR system targets a putative transposase gene in L. rhamnosus GG as described by Ahlroos & Tynkkynen (2009). Preparation of the reaction mixture and amplification of DNA

were conducted as described by Ahlroos & Tynkkynen (2009). The second PCR system targets a phage-related gene in L. rhamnosus GG as described by Brandt & Alatossava (2003). Preparation of the reaction mixture and amplification of DNA were according to a method previously described (Brandt & Alatossava, 2003). The amplification products were subjected to gel electrophoresis in 1.0% agarose, followed by ethidium bromide staining. Rep-PCR, RAPD, and ERIC PCR fingerprinting N-acetylglucosamine-1-phosphate transferase were carried out for strain differentiation in L. rhamnosus strains. (GTG)5 primer and a primer set REP1R-I and REP2-I were used for rep-PCR (Table S1). Preparation of the reaction mixture and amplification of DNA were according to the method described by Gevers et al. (2001). For RAPD fingerprinting, six different primers (C0540, 1251, OPA-03, D, E, and F) were used (Table S1). Preparation of the reaction mixture and amplification of DNA were performed as described elsewhere (Endo & Okada, 2006). PCR primers ERIC-1 and ERIC-2 were used for the ERIC PCR (Table S1). Preparation of the reaction mixture and amplification of DNA were by the method of Ventura et al. (2003). The amplification products were subjected to gel electrophoresis in 1.0% agarose, followed by ethidium bromide staining.

Here we built a neuro-computational model that allows us to simulate the effects of dopamine loss on synaptic plasticity in basal ganglia. Our simulations confirm that dysfunctional synaptic plasticity can indeed explain the emergence of both motor impairments and pathway imbalances in Parkinson’s disease, thus corroborating the novel concept. By predicting that dysfunctional plasticity results not only in reduced activation of desired responses, but also in their active inhibition, our simulations provide novel testable predictions. When Selleckchem IWR 1 simulating dopamine replacement

therapy (which is a standard treatment in clinical practice), we observe a new balance of pathway outputs, rather than a simple restoration of non-Parkinsonian states. In addition, high doses of replacement are shown to result in overshooting motor activity, in line with empirical evidence. Finally, our simulations provide an explanation for the intensely debated paradox that focused basal ganglia lesions alleviate Parkinsonian symptoms, but do not impair performance in healthy animals. Overall, our simulations suggest that the effects of dopamine loss on synaptic plasticity play an essential role in the development of Parkinsonian symptoms, selleck chemical thus arguing for a re-conceptualisation of Parkinsonian pathophysiology. “
“Innate differences in human temperament strongly influence how individuals cope with stress and also Y-27632 2HCl predispose towards specific types of

psychopathology. The present study examines the developing brain in an animal model of temperamental differences

to examine how altered neurodevelopment may engender differences in emotional reactivity that are stable throughout the animal’s life. We utilize selectively-bred High Responder (bHR) and Low Responder (bLR) rats that exhibit dramatic emotional behavior differences, with bHRs exhibiting exaggerated novelty-exploration, aggression, impulsivity and drug self-administration, and bLRs showing marked behavioral inhibition and exaggerated anxiety-like and depressive-like behavior. Using Affymetrix microarrays, we assessed bLR and bHR gene expression in the developing brain on postnatal days (P)7, 14 and 21, focusing on the hippocampus and nucleus accumbens, two regions related to emotionality and known to differ in adult bLR and bHR rats. We found dramatic gene expression differences between bLR and bHR in the P7 and P14 hippocampus, with minimal differences in the nucleus accumbens. Some of the most profound differences involved genes critical for neurodevelopment and synaptogenesis. Stereological studies evaluated hippocampal structure in developing bHR and bLR pups, revealing enhanced hippocampal volume and cell proliferation in bLR animals. Finally, behavioral studies showed that the characteristic bHR and bLR behavioral phenotypes emerge very early in life, with exploratory differences apparent at P16 and anxiety differences present by P25.

No data are available on the concentration of ZDV in the oral cavity. However, we expect that in the oral cavity the concentration of

the drug should be close to or lower than its Cmax (2 μg/mL). This assumption and previous data from studies investigating the effects of protease inhibitors on gingival tissues led us to use the concentrations indicated. The growth of the gingival epithelium was inhibited when the drug ZDV, an NRTI, was added at day 0 and was present throughout the growth period. In the present study, ZDV, even at lower concentrations (0.5 and 1 μg/mL), below the Cmax, affected the growth of the gingival epithelium, disrupting its proliferation and stratification status. These results support previous findings that indicated that the use of antiretroviral drugs resulted in the development of oral complications, especially with long-term use [2, 3, 5, 7, 9]. Our observations selleck products suggest that the oral epithelium in HIV-positive patients exposed to HAART, including ZDV, experiences drug-induced abnormalities

in the molecular and cellular biology of the tissue, which give rise to these oral complications. Epithelial tissues express different pairs of cytokeratin proteins depending on PS 341 the epithelial cell type and stage of differentiation [17, 18]. During the process of terminal differentiation, keratinocytes lose their ability to proliferate and migrate from the basal layer to the superficial layers while BCKDHA undergoing a coordinated series of morphological, biochemical and genetic changes. The terminal differentiated

cell is a flattened dead cell that consists of a network of cytokeratin filaments surrounded by an insoluble envelope of heavily cross-linked protein [37]. When cells make the commitment to terminally differentiate, one of the changes to occur is a switch in cytokeratin gene expression. Expression of cytokeratins 5 and 14 is shut off and that of cytokeratin 1 and 10 is turned on [38]. Cytokeratin 10 is indicative of terminal differentiation and is expressed in the suprabasal layer of keratinized epithelia. It has also been reported that cytokeratin 10 protects the epithelium from trauma and damage [31]. To examine the effect of ZDV on the proliferation and differentiation of oral keratinocytes, we treated raft cultures at day 0 and at day 8. Normally, gingival stratified epithelia express the cytokeratin pair of cytokeratins 5 and 14 only in the proliferative basal layer; however, the cytokeratin pair is maintained in all layers of tissue [28, 30]. In this study, cytokeratins 5 and 14 were detected in all layers of the tissue in untreated samples. Application of ZDV decreased the amount of cytokeratin 5 present in tissues (Fig. 3). The amount of cytokeratin 14 present in tissues was also reduced (data not shown).

No data are available on the concentration of ZDV in the oral cavity. However, we expect that in the oral cavity the concentration of

the drug should be close to or lower than its Cmax (2 μg/mL). This assumption and previous data from studies investigating the effects of protease inhibitors on gingival tissues led us to use the concentrations indicated. The growth of the gingival epithelium was inhibited when the drug ZDV, an NRTI, was added at day 0 and was present throughout the growth period. In the present study, ZDV, even at lower concentrations (0.5 and 1 μg/mL), below the Cmax, affected the growth of the gingival epithelium, disrupting its proliferation and stratification status. These results support previous findings that indicated that the use of antiretroviral drugs resulted in the development of oral complications, especially with long-term use [2, 3, 5, 7, 9]. Our observations check details suggest that the oral epithelium in HIV-positive patients exposed to HAART, including ZDV, experiences drug-induced abnormalities

in the molecular and cellular biology of the tissue, which give rise to these oral complications. Epithelial tissues express different pairs of cytokeratin proteins depending on Selleck Cobimetinib the epithelial cell type and stage of differentiation [17, 18]. During the process of terminal differentiation, keratinocytes lose their ability to proliferate and migrate from the basal layer to the superficial layers while crotamiton undergoing a coordinated series of morphological, biochemical and genetic changes. The terminal differentiated

cell is a flattened dead cell that consists of a network of cytokeratin filaments surrounded by an insoluble envelope of heavily cross-linked protein [37]. When cells make the commitment to terminally differentiate, one of the changes to occur is a switch in cytokeratin gene expression. Expression of cytokeratins 5 and 14 is shut off and that of cytokeratin 1 and 10 is turned on [38]. Cytokeratin 10 is indicative of terminal differentiation and is expressed in the suprabasal layer of keratinized epithelia. It has also been reported that cytokeratin 10 protects the epithelium from trauma and damage [31]. To examine the effect of ZDV on the proliferation and differentiation of oral keratinocytes, we treated raft cultures at day 0 and at day 8. Normally, gingival stratified epithelia express the cytokeratin pair of cytokeratins 5 and 14 only in the proliferative basal layer; however, the cytokeratin pair is maintained in all layers of tissue [28, 30]. In this study, cytokeratins 5 and 14 were detected in all layers of the tissue in untreated samples. Application of ZDV decreased the amount of cytokeratin 5 present in tissues (Fig. 3). The amount of cytokeratin 14 present in tissues was also reduced (data not shown).

The clones from mucoid colonies were transferred to E. coli DH5α by triparental conjugation, and then reintroduced into strain Rm11105 to confirm the associated mucoid colony phenotype on YM agar. Five of these clones, designated Proteases inhibitor pCX92, pCX9M1, pCX9M3, pCX9M4, and pCX9M5, were found to exhibit unique BamH1 restriction patterns. PHB accumulation was confirmed in the transconjugants of all clones by PHB assay (Table 2) and by transmission electron

microscopy for the first clone isolated, pCX92 (Fig. 1). The differentiation of mucoid from dry colony phenotype on YM agar required close inspection, and the possibility of missing complemented colonies was a concern. We found that incorporation of 0.5 μg mL−1 Nile red into the YM agar (YM-NR) resulted in bright pink staining of PHB-producing colonies, with no staining of the colonies that did not produce PHB. Examination under long-wave UV light enhanced the fluorescence, but it was not necessary to differentiate NU7441 chemical structure between the PHB mutant and the wild-type colonies. The exoY∷Tn5 mutant Rm7055, in which the extracellular polysaccharide succinoglycan is not produced, formed colonies that were not mucoid on YM-NR. These dry colonies fluoresced brightly under UV illumination. Strain Rm11476, containing both exoY∷Tn5 and phaC∷Tn5-233 mutations, was constructed by transduction. On YM-NR, this

strain formed dry colonies that did not stain or fluoresce. This was found to be the best genetic background for the detection of PHB-accumulating clones, especially on densely populated plates, and was used to screen for complementing subclones of the originally isolated cosmid clones. BamH1 fragments were subcloned from the cosmid clones pCX92, pCXM4, 17-DMAG (Alvespimycin) HCl and pCXM5 individually into pBBR1MCS-5. Complementing subclones were identified after en masse conjugation

of transformants from E. coli DH5α into strain Rm11105 or Rm11476, screening transconjugants on YM-NR as described above. These subclones were subjected to in vitro mutagenesis with EZ∷TN 〈KAN-2〉 transposon to localize the complementing regions. Complete DNA sequences of the complementing BamH1 fragments were determined, facilitated by sequencing from the EZ∷TN 〈KAN-2〉 transposon insertions using transposon-specific primers, and from the ends of subcloned fragments using vector-specific primers. Thus, pMS1 carries a 16 456-bp fragment from pCX92, pMS2 carries a 5255-bp fragment from pCX9M4, and pMS3 carries a 5015-bp fragment from pCX9M5. In each case, analysis of the sequence confirmed the presence of phaC genes. The complete 33 810-bp sequence of pCX92 insert DNA was determined from a shotgun library prepared by cloning a partial Sau3A1 digest into vector pTZ19R. The identities of the nearest orthologs from a cultured organism and the predicted functions are presented in Table 3, with the relative gene orientations illustrated in Fig. 2.

The clones from mucoid colonies were transferred to E. coli DH5α by triparental conjugation, and then reintroduced into strain Rm11105 to confirm the associated mucoid colony phenotype on YM agar. Five of these clones, designated Dabrafenib cost pCX92, pCX9M1, pCX9M3, pCX9M4, and pCX9M5, were found to exhibit unique BamH1 restriction patterns. PHB accumulation was confirmed in the transconjugants of all clones by PHB assay (Table 2) and by transmission electron

microscopy for the first clone isolated, pCX92 (Fig. 1). The differentiation of mucoid from dry colony phenotype on YM agar required close inspection, and the possibility of missing complemented colonies was a concern. We found that incorporation of 0.5 μg mL−1 Nile red into the YM agar (YM-NR) resulted in bright pink staining of PHB-producing colonies, with no staining of the colonies that did not produce PHB. Examination under long-wave UV light enhanced the fluorescence, but it was not necessary to differentiate Afatinib concentration between the PHB mutant and the wild-type colonies. The exoY∷Tn5 mutant Rm7055, in which the extracellular polysaccharide succinoglycan is not produced, formed colonies that were not mucoid on YM-NR. These dry colonies fluoresced brightly under UV illumination. Strain Rm11476, containing both exoY∷Tn5 and phaC∷Tn5-233 mutations, was constructed by transduction. On YM-NR, this

strain formed dry colonies that did not stain or fluoresce. This was found to be the best genetic background for the detection of PHB-accumulating clones, especially on densely populated plates, and was used to screen for complementing subclones of the originally isolated cosmid clones. BamH1 fragments were subcloned from the cosmid clones pCX92, pCXM4, very and pCXM5 individually into pBBR1MCS-5. Complementing subclones were identified after en masse conjugation

of transformants from E. coli DH5α into strain Rm11105 or Rm11476, screening transconjugants on YM-NR as described above. These subclones were subjected to in vitro mutagenesis with EZ∷TN 〈KAN-2〉 transposon to localize the complementing regions. Complete DNA sequences of the complementing BamH1 fragments were determined, facilitated by sequencing from the EZ∷TN 〈KAN-2〉 transposon insertions using transposon-specific primers, and from the ends of subcloned fragments using vector-specific primers. Thus, pMS1 carries a 16 456-bp fragment from pCX92, pMS2 carries a 5255-bp fragment from pCX9M4, and pMS3 carries a 5015-bp fragment from pCX9M5. In each case, analysis of the sequence confirmed the presence of phaC genes. The complete 33 810-bp sequence of pCX92 insert DNA was determined from a shotgun library prepared by cloning a partial Sau3A1 digest into vector pTZ19R. The identities of the nearest orthologs from a cultured organism and the predicted functions are presented in Table 3, with the relative gene orientations illustrated in Fig. 2.

Second, strong support for this model was provided by a recent study by Pernia-Andrade et al. (2009) showing that CB1 receptors decrease GABA release from inhibitory interneurons in the dorsal horn, measured as inhibitory postsynaptic currents. The same study, using electron microscopic immunohistochemistry, selleck chemicals found CB1 receptors in axon terminals forming inhibitory synapses in the superficial dorsal horn. Third, the experiment shown

in Fig. 9 confirmed our prediction that the inhibition produced by AM251 was caused by an increase in GABA and opioid release. Thus, inhibition by AM251 was reversed by GABAB and μ-opioid receptor antagonists. Interestingly, the GABAB antagonist CGP55845 reversed the inhibition by AM251 when the dorsal root was stimulated TSA HDAC supplier at 1 Hz but not at 100 Hz. This

is consistent with our previous studies (Marvizon et al., 1999; Lao & Marvizon, 2005) showing that root stimulation at 1 Hz, but not at 100 Hz, induces the activation of GABAB receptors. The fact that CB1 receptors facilitate substance P release reveals an unexpected pronociceptive role of cannabinoids in the spinal cord. Because of the prominent role that substance P and NK1Rs play in the induction of central sensitization (Traub, 1996; Mantyh et al., 1997; De Felipe et al., 1998; Laird et al., 2000), an increase in substance P release would lead to sustained hyperalgesia. Furthermore, inasmuch as substance P release is an indicator of nociceptor activity (Hua & Yaksh, 2009), its facilitation could signal an increase in acute from nociception. Indeed, we show that CB1 receptors in the spinal cord increase acute thermal nociception (Fig. 8). Our findings are consistent with the study by Pernia-Andrade et al. (2009) showing pronociceptive effects of spinal CB1 receptors during hyperalgesia induced by cutaneous capsaicin injection. They found that spinal application of AM251 decreased neuronal firing evoked by stimuli delivered next to the capsaicin injection site. They also showed

that capsaicin-induced mechanical hyperalgesia in mice was decreased by intrathecal AM251 and knockout of the CB1 receptor gene, both global and restricted to the spinal cord. Importantly, CB1 receptor deletion restricted to primary afferents did not decrease capsaicin-induced hyperalgesia, showing that the pronociceptive effect is caused by CB1 receptors in dorsal horn neurons. Our results show that this pronociceptive effect of CB1 receptors is not limited to hyperalgesia but can also be detected during acute nociception. In conclusion, CB1 receptors in dorsal horn interneurons produce pronociceptive effects by decreasing the release of GABA and opioids next to primary afferent terminals. The resulting decrease in the activity of the GABAB and μ-opioid receptors in these terminals facilitates substance P release by producing disinhibition.

All vaccines were administered by nurses in the immunization clinic and all medications were dispensed from the campus pharmacy. Institutional review board (IRB) approval was obtained prior to initiating the study. Basic characteristics of the travelers and the frequencies (or the average numbers) of the pretravel recommendations between the PTC and the PCP groups were compared by using chi-square test (or Fisher’s exact test) for categorical variables, and two-sample t-test or Wilcoxon–Mann–Whitney test (non-parametric version of independent-samples t-test) for continuous variables, if the normality assumptions

underlying the t-test were violated. The primary outcomes for vaccines and medications were (1) indicated and ordered, (2) indicated

and not ordered (excluding refused/declined), (3) not indicated and ordered, (4) and ordered and received (excluding refused/declined). The univariate and multivariate logistic selleck products regressions (results not shown in tables) were performed to help to rate the findings according to their importance as risk/protective factors. All variables that showed an association with pretravel recommendations in the univariate models having p values below 0.10 were entered into the more comprehensive multiple logistic regression models, which included visit type (PTC or PCP), trip duration, purposes of travel (study abroad and volunteer work), and destination (Southeast Asia). All statistical significance was assessed using an alpha level of 0.05. Statistical analysis was performed find more using SAS 9.2. In 2007, 513 travelers were identified, 172 were seen by a PCP and 341 were seen in the PTC. Travelers who were seen in the PTC were more often prescribed antibiotics for self-treatment of travelers’ diarrhea when indicated (96% vs 50%, p < 0.0001), while

travelers seen by Guanylate cyclase 2C a PCP were more likely to be prescribed antibiotics not consistent with guidelines (not ordered when indicated 49% vs 6%, p < 0.0001 and ordered when not indicated 21% vs 3%, p < 0.0001) (Table 1). Furthermore, patients who were seen in the PTC were more likely to pick up their antibiotic from the pharmacy than those who were prescribed antibiotics by a PCP (75% vs 63%, p = 0.04). Travelers seen in the PTC were also more often prescribed antimalarials when indicated (98% vs 81%, p < 0.0001), while those seen by a PCP were more frequently prescribed antimalarials not consistent with guidelines (not ordered when indicated 15% vs 1%, p < 0.0001 and ordered when not indicated 19% vs 2%, p < 0.0001). There was no statistically significant difference in antimalarial pickup rates from the pharmacy between the two groups (Table 1). Results regarding the ordering and receipt of vaccines were similar to those of antibiotics and antimalarials. To account for multiple vaccines ordered at the same time, the primary outcomes for vaccines were calculated per patient and were used for comparison purposes.

After cooling, the extracts were centrifuged at 8000 × g for 20 min. The collected supernatants were filtered with qualitative filter papers (Whatman) and transferred to glass flasks at 40 °C until solvent was completely evaporated (approximately 72 h). The dry glucosinolate-containing precipitate was reconstituted with 1 mL of 0.2 mol L−1 HEPES–KOH buy GDC-0449 (pH 7.0) in the same container. An extract aliquot (10 μL), which was previously reconstituted in 0.2 mol L−1 HEPES–KOH (pH 7.0), was incubated with 5 μL of a thioglucosidase solution

(0.12 U). The thioglucosidase solution contained myrosinase purified from Sinapis alba L. (Sigma–Aldrich), which was buffered in 0.2 mol L−1 HEPES–KOH (pH 7.0) at 37 °C for 24 h; this procedure was in accordance with the methodology of Li and Kushad (2005) which was performed in 3 mL test tubes. In agreement with the degradation reaction of glucosinolates by thioglucosidase, the measurement is accomplished on glucose produced upon glucosinolate hydrolysis. Glucosinolate content was quantified according to the stoichiometry proposed by Palmieri, Iori, and Leoni (1987), which states that 1 mol of released glucose is

equivalent to 1 mol of see more total glucosinolate. The enzymatic catalysis was stopped with the addition of 5 μL of 18 mmol L−1 perchloric acid solution (HClO4). To detect the background levels of glucose in the samples, a control was prepared. The control contained buffered extract (10 μL) with 18 mmol L−1 HClO4 (5 μL), and 5 μL of the thioglucosidase solution was rapidly added. The liberated total glucose was assayed enzymatically by using a glucose oxidase/peroxidase kit (CELM, Brazil). Sinigrin, an allyl-glucosinolate (Sigma), was used

as a calibrant and as a positive control. The sample extraction procedure was identical to the one described for total glucosinolates (n = 3, each in triplicate). The extracts were filtered on Millex™ polyvinylidene fluoride (PVDF) membranes (0.45 μm, Millipore) prior to HPLC injection. The methodology used for the determination of benzylglucosinolate was described by Kiddle et al. (2001) and modified by Rossetto et al. (2008). The calibration curve for benzylglucosinolate and the internal standardization for the sample recovery test were carried out according to Rossetto et al. (2008). A single chromatographic Racecadotril run with an internal standard (50 μL of 12 nmol L−1sinigrinin 1 mL of 70:30 MeOH (mL):water (mL) that also contained 1.49 g L−1 TFA) was also completed to determine the sinigrin (allyl-glucosinolate) retention time. Benzylglucosinolate was isolated by HPLC, which was coupled to an automatic injector and a quaternary pump (HP 1100). The substance was detected by a diode array (PDA) detector at a spectral range of 200–400 nm. A reverse phase column (Luna C18, 250 × 4.6 mm, 5 μm) developed by Phenomenex was used, and the column was coupled to a Security Guard pre-column (Phenomenex). The column temperature was maintained at 25 °C.

The salinity was measured with an inductive salinometer (model MI-150). The water temperature was measured with a mercury thermometer graduated to 0.1 °C. The seaweed samples were analysed in triplicate for their proximate lipid content using the Bligh and Dyer (1959) method. Samples were homogenised with a 1:2 mixture of chloroform and methanol and incubated in the dark overnight. The residues were extracted 2–3 times

with buy Seliciclib a small amount of chloroform and methanol. The chloroform layer was removed with a separating funnel and then vaporised in an evaporator. The lipid content was calculated by weighing the residues and was expressed as a percentage of dry weight. The fatty acids were converted to methyl esters using the method of Christie (1998). The samples were esterified in 1% sulphuric acid in absolute methanol and extracted with hexane to separate the layers. The hexane layer was washed with water containing potassium bicarbonate and dried over anhydrous sodium sulphate. The solvent was evaporated using a rotary evaporator. The fatty acid methyl esters (FAMEs) were analysed on a Shimadzu gas-liquid chromatographer equipped with a flame ionisation detector with a packing column with Hp-5 material. The carrier gas was nitrogen, and the short speed was 5 mm/min. For the identification and quantification

of FAMEs, their retention times were compared with standards. The values are Dabrafenib molecular weight expressed as a percentage of the total fatty acids mixture. The variation in fatty acid composition between the species during different seasons was evaluated using principal component analysis (PCA) (SPSS IBM version 20) with the mean of three individual samples as the variables. Three principal component analyses

(PCAs) were performed oxyclozanide separately on the total, saturated and unsaturated fatty acids. The outcome was plotted in two dimensions (PCA1, PCA2). The score loading was analysed and identified in the bi-plot of PCA1 versus PCA2. The seawater parameters, such as pH, salinity and temperature, showed limited variations during the different seasons (Table 1). The pH value varied between a maximum of 8.11 during spring and a minimum of 7.60 during summer, whereas the pH value during autumn was in between (7.78). The average values of water salinity decreased in the order of autumn (32.15 g/L), spring (36.21 g/L) and summer (38.32 g/L). The seasonal temperature variations followed the climate conditions. There was significant variation between the seasons, with the highest values during the summer (29.30 °C). Furthermore, the lowest values fluctuated between 21.50 °C and 20.90 °C in the autumn and spring, respectively. The seasonal variations in the total lipid content based on the dry weight of J. rubens are shown in Table 2. The highest lipid content was 2.51% in the spring, followed by 2.42% in the summer, and the lowest value was 1.56% in autumn.