Energy and nutrient intake and food patterns among Turkish university students

The goal of this study was to determine the nutritional value and nutrients provided by each meal and snack of consumed by university students. Subjects were randomly selected from volunteer students at five universities in Ankara. A sample of 400 students (167 female and 233 male) aged between 19 and 24 years participated in this study. A questionnaire designed to assess general characteristics, anthropometric measurements, and 24 hours dietary records was administered using face to face interviews. According to body mass index classifications, 69.5% of male students, and 77.7% of female students were found to be in the normal weight categories. Overweight categories were found to be 25.1% and 5.6% for males and females, respectively. Breakfast and lunch were the most frequently skipped meals, with a total of 47.7% of students skipping breakfast and 25.2% skipping lunch. The percentages of energy deficiency were found to be 78.4% in males, and 81.1% in females. Dinner was the main meal for consumption of energy and the other nutrients, except saturated fatty acids, for both genders. Also, dinner was the largest contributor of energy in both genders. Students ate more bread, cereals, and meat at dinner than during the other meals and snacks. Fruit was consumed more during snacks than at the other meals by all students. It was concluded that students need more nutritional information about healthy nutritional habits, adequate intake of nutrients, and ideal body weights.     

Reversible Cogan’s syndrome in a patient with human immunodeficiency virus (HIV) infection

Cogan’s syndrome is a rare, immune-mediated disorder characterized by chronic, bilateral vestibular-cochlear dysfunction and interstitial keratitis. We describe the first case of Cogan’s syndrome that resolved with antiretroviral therapy in a patient with human immunodeficiency virus infection. Plausible disease mechanisms are discussed.     

Sequential deregulation of NK cell subset distribution and function starting in acute HIV-1 infection

Natural killer (NK) cells are critical in the first-line defense against viral infections. Chronic HIV-1 infection leads to a perturbation in the NK cell compartment, yet the kinetics of this deregulation and the functional consequences are unclear. Here, we characterized changes in the NK cell compartment longitudinally by multiparameter flow cytometry, starting in acute HIV-1 infection. Acute HIV-1 infection was associated with elevated NK cell numbers, with an expansion of CD3(neg)CD56(dim)CD16(pos) NK cells and an early depletion of CD3(neg)CD56(bright)CD16(neg) NK cells. Ongoing viral replication resulted in a depletion of CD3(neg)CD56(dim)CD16(pos) NK cells with a paralleled increase in functionally anergic CD3(neg)CD56(neg)CD16(pos) NK cells, accompanied by reduced functional activity, as measured by CD107a expression and cytokine secretion. Taken together, these studies demonstrate a sequential impairment of NK cell function with persistent viral replication resulting from a progressive deregulation of NK cell subsets with distinct functional properties.     

Influence of oxygenated fuel additives and their metabolites on the binding of a convulsant ligand of the gamma-aminobutyric acid(A) (GABA(A)) receptor in rat brain membrane preparations

As a foundation for evaluating potential mechanisms of the neurological effects (e.g. headache, nausea, dizziness) of some octane boosters, we studied the gamma-aminobutyric acid(A) (GABA(A)) receptor in a series of binding assays in membranes from rat brain. The GABA(A) receptor was probed using the radioligand [3H]t-butylbicycloorthobenzoate ([3H]TBOB) which binds to the convulsant recognition site of the receptor. The results demonstrated that the short-chain t-ethers and their t-alcohol metabolites inhibit binding at the convulsant site of the GABA(A) receptor. The potency of the inhibition tended to correlate with carbon chain length. For agents having an equal number of carbon atoms, potency of inhibition of [3H]TBOB binding was greater in magnitude for the alcohols than for the ethers. The descending rank order of potency for the ethers and alcohols were as follows, t-amyl alcohol (TAA); t-amyl-methyl ether (TAME); ethyl-t-butyl ether (ETBE)>t-butyl alcohol (TBA)>methyl-t-butyl ether (MTBE)>ethanol. In additional saturation binding assays, MTBE reduced apparent density of convulsant binding (B(max)).     

HSPGs glypican-1 and glypican-4 are human neuronal proteins characteristic of different neural phenotypes

Generating neurons from human stem cells has potential for brain damage therapy and neurogenesis modeling, but current efficacy is limited by culture heterogeneity and the lack of markers. We have previously reported the heparan sulfate proteoglycans (HSPGs) glypican-1 (GPC1) and -4 (GPC4) as the markers of lineage-specific human neural stem cells (hNSCs) and mediators of hNSC lineage potential. Here, we further examined phenotypical characteristics and GPC1 and GPC4 during neural differentiation of hNSCs in the presence of two neurogenic growth factors reported to bind to heparan sulfate: brain-derived neurotrophic factor (BDNF) and platelet-derived growth factor-B (PDGF-B). In hNSC neural cultures, GPC1 and GPC4 were expressed along neurites and cell bodies in long-term (40–60 days) neural differentiation cultures demonstrating the areas of differential localization—suggesting potentially different functions. Neural differentiation cultures in the presence of BDNF or PDGF-B generated phenotypically different neural cells with BDNF treatment associated with higher GPC4 versus GPC1 expression, increased heterogeneity, and differential neuron subtype marker expression to PDGF-B cultures. PDGF-B cultures exhibited higher levels of spontaneous activity and reduced heterogeneity over long-term culture associated with decreased GPC4. Untreated neural cultures were highly variable, supporting the use of neuroregulatory growth factors for guided differentiation. Targeted siRNA downregulation of GPC1/4 reduced neural differentiation markers and altered response to exogenous BDNF and PDGF-B. This work confirms GPC1 and GPC4 as regulators of human neural differentiation and supports their use as novel markers of neural cell characterization.     

Does persistent organic pollutant PFOS (perfluorooctane sulfonate) negative impacts on the aquatic invertebrate organism,Astacus leptodactylus [Eschscholtz, 1823]

Highly persistent perfluorooctane sulfonate (PFOS) is an industrial fluorinated organic chemical with significant bioaccumulation and biomagnification properties. The purpose of this study was to determine the toxic effects of sublethal PFOS on the aquatic invertebrate organism, narrow-clawed crayfish [Astacus leptodactylus Eschscholtz, 1823]. The 96?h LC₅₀ value was determined as 48.81?mg/L (34.19–63.68?mg/L) with probit analysis. The sublethal experimental design was formed into four groups solvent control (DMSO, dimethyl sulphoxide), non-treated control group, and 1/10 (5?mg/L) and 1/100 (0.5?mg/L) of 96?h LC₅₀ of PFOS, and crayfish were exposed for 48?h, 7?d, and 21?d under laboratory conditions. Total haemocyte counts (THCs) decreased, while the haemolymph total antioxidant status (TAS) values increased (p?<?0.05) after exposure to 0.5 and 5?mg/L PFOS for 48?h, 7?d, and 21?d. Haemolymph total oxidative stress (TOS) levels significantly increased at 5?mg/L PFOS concentration (p?<?0.05). Catalase (CAT) activities increased at both concentrations after 48?h and 7?d and then returned to control levels after 21?d; whereas superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities did not change in muscle tissue (p?>?0.05). GPX and CAT activities decreased, but SOD activity increased in hepatopancreas tissue (p?<?0.05). SOD activity at both concentrations and CAT activity at 5?mg/L PFOS exposure decreased in gill tissue, while GPX activity increased at both concentrations of 48?h and 7?d and returned to control values on day 21 of exposure. Histopathological alterations were detected in hepatopancreas and gill tissues. Lamellar deformations, epithelial hyperplasia, and haemocytic infiltrations were observed in the gill tissues, whereas tubular degeneration, tubule loss, necrosis, and lesions in the hepatopancreas tissues were the major recorded alterations. As a result, the sublethal concentrations of PFOS have toxic effects on crayfish and histologically cause tissue damage. Our findings also support a better understanding of the early toxicological effects of PFOS in freshwater ecosystems. Also, it could be concluded that A. leptodactylus is a reliable model for examining histopathological alterations and differences in enzyme activities together with the haemolymph findings in toxicology studies amid aquatic species.

     

Testing the psychosis continuum: differential impact of genetic and nongenetic risk factors and comorbid psychopathology across the entire spectrum of psychosis

A growing number of studies demonstrate high rates of subthreshold psychotic experiences, but there is considerable heterogeneity in rates due to study cohort and design factors, obscuring how prevalent psychotic experiences may or may not relate to rare psychotic disorders. In a representative general population sample (n = 4011) in Izmir, Turkey, the full spectrum of expression of psychosis was categorized across 5 groups representing (1) absence of psychosis, (2) subclinical psychotic experiences, (3) low-impact psychotic symptoms, (4) high-impact psychotic symptoms, and (5) full-blown clinical psychotic disorder and analyzed for continuity and discontinuity in relation to (1) other symptom dimensions associated with psychotic disorder and (2) proxies of genetic and nongenetic etiology. Results were tested for linear and extralinear contrasts between clinical and nonclinical and between disorder and nondisorder expression of psychosis. Demographic variables, indexing premorbid social adjustment and socioeconomic status, impacted mostly linearly; proxy variables of genetic loading (more or more severely affected relatives) impacted in a positive extralinear fashion; environmental risk factors sometimes impacted linearly (urbanicity and childhood adversity) and sometimes extralinearly (cannabis), occasioning a disproportional shift in risk at the clinical disorder end of the spectrum. Affective symptoms were associated with a disproportionally higher risk below the disorder threshold, whereas a disproportionally higher risk above the threshold was associated with psychotic symptom load, negative symptoms, disorganization, and visible signs of mental illness. Liability associated with respectively affective and nonaffective symptom domains, in interaction with environmental risks, may operate by impacting differentially over a quasi-continuous extended psychosis phenotype in the population.