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Apricot (Prunus armeniacaL.), which belongs to the genus Prunus, is one of the most commonly commercialized fruits produced in Turkey. Apricot pomace, the most common byproduct of apricot nectar processing, is the press residue of the fruit flesh. Ultrasound assisted extraction (UAE) is known as one of the most efficient techniques for separation of valuable ingredients from raw materials with enhanced extraction yield. In this study, UAE parameters (temperature and time) were optimized by using Response Surface Methodology with a central composite design for maximization of the total phenolic and flavonoid contents as well as the antiradical (DPPH scavenging) activity and extraction yield. Phenolic composition and CUPRAC, ABTS and FRAP values of the extract at the highest extraction yield point was also determined. In the results, the highest phenolic and flavonoid contents, antiradical activity and extraction efficiency were determined as 1.206 mg GAE/g DM, 1.015 mg CE/g DM, 79.85% and 7.86% in apricot pomace samples at 50 °C and 90 min trial points, respectively. HPLC–DAD showed that p-coumaric acid, ferulic acid and rutin were the most abundant phenolics found in the extract. CUPRAC, ABTS and FRAP values of the extract were 30.00, 32.30 and 18.80 mg TE/100 g, respectively. In conclusion, this study provided valuable findings to food industry and other related fields for extraction of valuable bioactive compounds from apricot pomace using UAE as an eco-friendly extraction technique.

Data on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) guide therapy in severe traumatic brain injury (TBI), but current linear analytic methods are insufficiently sensitive and specific for prognosis in dynamic situations over time.

Calculation of integer heart rate variability (HRVi) permits monitoring over extended periods. We asked whether continuous monitoring of HRVior integer pulse pressure (PP) variability (PPVi) could predict intracranial hypertension, defined as ICP >20 mm Hg, cerebral hypoperfusion, defined as CPP<60 mm Hg, mortality or functional outcome after severe traumatic brain injury. Dense integer data collected during continuous intensive care unit monitoring for periods of 1 to 11 days on 25 patients admitted to our Level I trauma center with Glasgow Coma Scale <9 provided 1,715,000 data points over a mean 106±62 hours. PP, HRVi, and PPViincreased in response to increasing ICP when CPP >60 mm Hg (P<0.001), but HRViand PPVidecreased when CPP <60 mm Hg and P<50 mm Hg, even with ICP <20 mm Hg (P<0.001). ICP up to 40 mm Hg still evoked an increase in HRViand PPVi(P<0.001), but both were suppressed with CPP <50 mm Hg and ICP >40 mm Hg (actual or impending brain death). Mean HRViand PPVipredicted in-hospital mortality (sensitivity, 67; specificity, 91 to 100). Combining HRViand PPVias an “autonomic index” (AI) best predicted long-term functional outcome Area Under the Curve 0.84±0.08 for AI <0.5. Our data show that HRViand PPVican be monitored and calculated automatically and can provide useful prognostic information in patients with severe traumatic brain injury, particularly when combined into a single index.

Earlier, more accurate assessment of secondary brain injury is essential in management of patients with traumatic brain injury (TBI). We assessed the accuracy and utility of high-resolution automated intracranial pressure (ICP) and cerebral perfusion pressure (CPP) recording and their analysis in patients with severe TBI.

Certain anesthetics exhibit neurotoxicity in the brains of immature but not mature animals. Gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the adult brain, is excitatory on immature neurons via its action at the GABAAreceptor, due to a reversed transmembrane chloride gradient. GABAAreceptor activation in immature neurons is sufficient to open L-type voltage-gated calcium channels. As propofol is a GABAAagonist, we hypothesized that it and more specific GABAAmodulators would increase intracellular free calcium (Ca2i), resulting in the death of neonatal rat hippocampal neurons. Neuronal Ca2iwas monitored using Fura2-AM fluorescence imaging. Cell death was assessed by double staining with propidium iodide and Hoechst 33258 at 1 hour (acute) and 48 hours (delayed) after 5 hours exposure of neurons to propofol or the GABAAreceptor agonist, muscimol, in the presence and absence of the GABA receptor antagonist, bicuculline, or the L-type Ca2channel blocker, nifedipine. Fluorescent measurements of caspase-3,-7 activities were performed at 1 hour after exposure. Both muscimol and propofol induced a rapid increase in Ca2iin days in vitro (DIV) 4, but not in DIV 8 neurons, that was inhibited by nifedipine and bicuculline. Caspase-3,-7 activities and cell death increased significantly in DIV 4 but not DIV 8 hippocampal neuronal cultures 1 hour after 5 hours exposure to propofol, but not muscimol, and were inhibited by the presence of bicuculline or nifedipine. We conclude that an increase in Ca2i, due to activation of GABAAreceptors and opening of L-type calcium channels, is necessary for propofol-induced death of immature rat hippocampal neurons but that additional mechanisms not elicited by GABAAactivation alone also contribute to cell death.

Dead fungal biomass prepared from Phanerochaete chrysosporium and Funalia trogii was tested for their efficiency in removal of textile dyes. The effects of contact time, initial dye concentration, amount of dead biomass and agitation rate on dye removal have been determined. Removal of all dyes required a very short time (60 min). Experimental results show that, P. chrysosporium was more effective than F. trogii . An increase in the amount of dead biomass positively affected of the dye removal. The removal efficiency of different amount of biomass was in order 1 g > 0.5 g > 0.2 g > 0.1 g. The highest removal was obtained at 150–200 rpm. Slightly lower removing activities were found at lower agitation rates. This study showed that it was possible to remove textile dyes by dead biomass of P. chrysosporium . (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

Numerous studies have recently been conducted to investigate genetic mechanisms in cancer causes and pathogenesis. Some of these studies have shown that there were certain specific chromosomal defects in normal cells of cancer patients and in their first-degree relatives. It was suggested that these individuals were susceptible to cancer development when compared with people without these defects. Chromosomal anomalies, such as gaps, breaks, and acentric fragments, and fragile site expression rates were determined in peripheral blood lymphocyte cultures in 14 head and neck cancer patients, 17 first-degree relatives of these patients, and 20 healthy individuals as a control group in this study. RPMI 1640 medium, composed of aphidicolin, 5-bromodeoxyuridine, and caffeine were used for the induction of fragile sites. In cytogenetic and statistical evaluation, it was observed that both chromosomal aberration rates and fragile site expression frequencies in head and neck cancer patients and in their first-degree relatives were significantly greater than the control group (p &lt; .05). It was found that fragile site expression was site specific in head and neck cancer patients and in their first-degree relatives. These specific sites were determined to be 1p21-22, 1q21, 1q25, 2q21, 2q31-33, 3p14, 16q22-23, 18q21, and 22q12 sites. These findings support studies showing that the fragile sites might be unstable factors in human genomes and their expression could be affected by some genetic factors, such as tumor suppressor genes and mismatch repair genes, and by some environmental factors, such as benzo (a) pyrene, dimethylnitrosamine, and dimethylsulfate. In conclusion, fragile sites may be playing an important role in the genetic tendency to head and neck cancer. Overexpression of these sites in normal lymphocytes may be used as a reliable marker to determine the genetic susceptibility in head and neck cancer patients and in their first-degree relatives. © 2000 John Wiley & Sons, Inc. Head Neck 22: 591–598, 2000.