The number of lymphocytes, T-cells and PHA responsiveness are exa

The number of lymphocytes, T-cells and PHA responsiveness are examples of parameters useful for the evaluation of cell-mediated immunity and T-cell-related functions at bedside. However, abnormalities may not always be detected through such tests in all diseases, such as those involving STAT malfunctions, so caution

is necessary [38]. In addition, immunodeficiencies in which T-cell dysfunction is not important (eg. autoinflammatory diseases, polymorph abnormalities, complement abnormalities, slight T-cell immunodeficiency) were omitted from the list of indications for Palivizumab use, but as research progresses and risks for aggravated RSV infection are clarified, it will be necessary selleck chemical to review these current guidance again. In general, in the early recovery stages after transplantation and chemotherapy, when the level of immunosuppression and myelosuppression is still high, it may be thought that the risk of RSV

exposure is low during hospitalization. On the other hand, if RSV does happen to be transmitted to patients in such an advanced immunocompromised state, the risk of severe disease even to the point of death is considerable. In addition, most RSV infections in adults present with mild or even no symptoms, so the risk of infection from an adult during times when it is prevalent cannot be completely Stem Cell Compound Library mw prevented. That is why a section on preventing RSV infection during hospitalization was included in this guidance above. Therefore, it is important to be thorough in taking basic measures to prevent infection, considering the risk of infection, regional prevalence of RSV and the conditions and numbers or visitors, and to formulate a prevention plan. At the present time, while the prevention of RSV using Palivizumab in those with immunodeficiencies and Down’s syndrome has been SPTBN5 approved in Japan before anywhere else in the world, there is currently insufficient evidence of efficacy and safety of its use. Thus, the importance of collecting information

on Palivizumab use and reporting our experience with this antibody in our country to the international community cannot be overemphasized. I would like to express my deepest gratitude to the following doctors for their expert advice in preparing these guidelines. Dr. Katsuhiro Asonuma, Kumamoto University Hospital, Transplantation Department; Dr. Shinya Okamoto, Kyoto University Hospital, Pediatrics; Dr. Atsushi Kikuta, Fukushima Medical University Hospital, Clinical Tumor Center, Pediatrics Oncology Department; Dr. Katsuyoshi Yasu, Saitama Children’s Medical Center, Hematology and Oncology Department; Dr. Akihiko Saito, Niigata University Medical & Dental Hospital, General Research, Pediatrics; Dr. Shinichi Takatsuki, Toho University, Medical Center, Omori Hospital, Pediatrics; Dr. Mizue Tanaka, National Center for Global Health and Medicine Center Hospital, Pediatrics; Dr.

Bars, 500 nm Table 1 also lacked ± in correct locations and an a

Bars, 500 nm. Table 1 also lacked ± in correct locations and an additional * was inserted. The corrected table is presented here for reader convenience. Table 1. Comparison of number of ERb-EGFP cells Selleck Cisplatin in select brain regions. Brain region with map reference Female (N = 4; *p < 0.05) Male (N = 4) Lateral septum (Fig. 2B) 11.1 ± 0.4* 8.3 ± 1.0* Hypothalamic PVN (Fig. 2D) 17.0 ± 1.3 15.0 ± 2.6 Medial amygdala (between Fig. 2D and E) 10.3 ± 1.5

7.25 ± 1.1 Lateral amygdala (Fig. 2E) 7.8 ± 1.0* 4.0 ± 1.3* Endopyriform cortex (Fig. 2E) 12.5 ± 1.2* 5.8 ± 0.6* Somatosensory cortex, layer 5 (Fig. 2E) 9.5 ± 1.8 9.5 ± 0.7 Dorsal subiculum (Fig. 2 F) 17 ± 2.7 14.8 ± 1.4

Raphe magnus (Fig. 2 J) 10 ± 1.5 8.5 ± 0.9 Full-size table Selleckchem Y27632 Table options View in workspace Download as CSV “
“Opioid analgesics, such as morphine, are the most effective and frequently used substances for the relief of moderate to severe pain. The use of these analgesics has increased in the Neonatal Intensive Care Unit over the last few decades as a consequence of changes and advances in the understanding, identification, and treatment of pain in children (De Lima et al., 1996, El Sayed et al., 2007 and Suresh and Anand, 2001). In addition, improvements in short- and long-term clinical outcomes of critically ill neonates have necessitated the widespread use of opioid drugs for analgesia and sedation (Suresh and Anand, 2001). However, the consequences for the development of neurophysiological systems remain unknown. The efficacy of morphine in reducing pain in neonatal animals has already been demonstrated (Nandi and Fitzgerald, 2005 and Rozisky et al., 2008). Although descending inhibitory mechanisms are not completely formed until the Adenosine third week of life (Nandi and Fitzgerald, 2005), morphine and other opioid receptor agonists are effective

analgesics during the early neonatal period due to the presence of spinal opioid receptors from birth (Rahman and Dickenson, 1999). In a previous study by our group, using the tail-flick test (a measure of the pain threshold at the spinal level), we observed that animals in the second week of life showed an increased response to repeated morphine administration without developing tolerance. However, at P80 rats showed greater morphine analgesia and a classic tolerance effect. In addition, the animals that received morphine from P8 until P14 displayed a longer duration of morphine analgesia at the same age (P80) (Rozisky et al., 2008). These results indicate that early morphine exposure lead to the development of an altered opioid analgesic response that may be expressed into adulthood.

We have chosen not to get off that wave Thus, like surfers, we m

We have chosen not to get off that wave. Thus, like surfers, we must ride it. But we can choose, while going forward, to go straight ahead as the wave breaks, or ride the green water to either side. The latter option gives us the greatest possible measure of control. For instance we can, at a local or a regional level, make decisions as to what ecosystem services (benefits obtained by humans from the environment – Millenium Ecosystem Assessment, 1995) we want from estuarine or marine areas. Those services include, but are not restricted to: sources of food; provision of habitat for plants and animals; nutrient cycling; photosynthesis; and, sites for recreation and cultural activities

(e.g., spiritual, religious, aesthetic, and religious activities). Maintaining such ecosystem services will not require that all current species be maintained or that habitat not change, which will be impossible. Rather, it will require that we make GDC0199 proactive choices that will allow for the maintenance of such ecosystem services. For example, rather than letting chance decide which invasive species colonize new habitats, we can choose and encourage particular AZD1208 molecular weight species that will, though they change the species composition, maintain the ecosystem services we as humans want and need. We can ourselves change habitats before they are changed for us. Unfortunately, to be able to have some measure of control over

future ecosystem changes, we will have to not only change our mind-set, but also many of the laws L-gulonolactone oxidase that currently impede humans making any changes to ecosystems. For instance, in developed nations there are laws preventing intentional placement of invasive species in ecosystems or changes to habitat. It is arguable which will be more difficult: to change our view of ecosystems from maintenance of the status quo to manageable change; or, to change existing laws intended to maintain ecosystem

status quo. If we are successful in changing both our mind-set and the laws, we will probably have to depend more on best professional scientific judgment and common sense than on statistics or lawyers, arguably a positive effect of climate change. But changing ourselves in this manner will not be easy and may not be possible. After all, we have apparently chosen not to make changes that would limit global climate change. As the reality of climate change becomes more apparent can we make changes that will help us maintain what we need and want from ecosystems? I do not know, and I am not hopeful. All I know, and what we all need to recognize, is that we can now no longer go home again. Where we go and our future homes can be determined by default or by intent. The choice is wholly ours. “
“The authors regret that the decimal points were not displayed correctly in Table 1 of their article. The correct version of the table appears below. The authors would like to apologies for any inconvenience caused.

elegans learning and memory ( Figure

1) Neuropeptides ca

elegans learning and memory ( Figure

1). Neuropeptides can function as direct or indirect modulators of synaptic output, as primary neuronal signaling molecules, or in a neuroendocrine fashion. Like small neurotransmitters, neuropeptides play key roles Ceritinib datasheet in a wide variety of processes, and their role in learning and memory is an emerging trend. It is predicted that the C. elegans genome has 119 neuropeptide precursor genes that are processed into over 250 peptides. These can be categorized into three groups: 1) the insulin-like peptides with 40 members; 2) the FMRFamide (Phe-Met-Arg-Phe-amide)-like peptide (flp) family with 31; and 3) the 48 general neuropeptide-like protein (nlp) genes whose only unifying characteristic is that they are Small Molecule Compound Library unlike the previous two families [7•]. In addition to the receptor tyrosine kinase insulin/IGF receptors encoded by daf-2, there are an estimated

128 neuropeptide G protein-coupled receptors, the majority of which remain functionally uncharacterized and orphaned. By reviewing recent findings for the role of neuropeptides in learning and memory we hope to highlight the advantages of behavioral genetics research in C. elegans ( Table 1). Zhang et al. [8] demonstrated that C. elegans can learn to avoid odorants released by strains of pathogenic bacteria, and to prefer odors released by non-pathogenic strains. Serotonin released from the chemosensory neuron ADF acts on various interneurons to associate infection with specific bacteria [8]. The target of the ADF serotonin signal Flucloronide is the serotonin-gated chloride channel MOD-1 [8]. Using known promoters to selectively express MOD-1 in specific neurons of MOD-1 defective mutants, Zhang

et al. [8] demonstrated that MOD-1 functions in several interneurons to modulate aversive learning. In a recent series of experiments, Chen et al. [9••] examined the potential role of insulin-like peptides (ILPs) in learned aversion to attractive pathogenic bacteria using strains with reduction of function alleles for the gene encoding the insulin/IGF-1 receptor, DAF-2. These mutants were defective in learning to avoid the smell of pathogenic bacteria [9••]. Learning was also disrupted by a semi-dominant mutation in ILP DAF-28 [9••]. DAF-28 has previously been shown to disrupt its own synthesis, as well as the synthesis of structurally related peptides expressed in the same cell [10]. After ruling out a role for DAF-28, further mutant analysis implicated the ILPs INS-6 and INS-7 as influential paracrine mediators of learned aversion to pathogens [9••]. Specifically, a learning deficit caused by loss of ins-6 could be suppressed by loss of ins-7 [9••]. Neuron specific rescue studies revealed that INS-6 is released from ASI sensory neurons to repress transcription of learning-inhibitory INS-7 [9••]. In ins-6 mutants, URX-generated INS-7 disrupts learning via the DAF-2 receptor on the RIA interneurons of the learning circuit [9••].

007), III-IV of TNM stage (HR, 1 727; 95% CI, 1 183-2 520; P = 0

007), III-IV of TNM stage (HR, 1.727; 95% CI, 1.183-2.520; P = .005) and AST > 40 U/l (HR, 1.888; 95% CI, 1.391-2.563; P < .001) were independent predictors

for DFS ( Table 3). High NLR (HR, 1.639; 95% CI, 1.212-2.218; P = .001), size of tumor > 5 cm (HR, 1.922; 95% CI, 1.168-3.162; P = .010), III-IV of TNM stage (HR, 1.806; 95% CI, 1.236-2.638; P = .002), and AST > 40 U/l (HR, 1.916; 95% CI, 1.415-2.595; P < .001) were independent predictors for OS ( Table 3). We established a preoperative prognostic score model by calculating the number of independent predictors (NLR, size of tumor, TNM stage, and AST) for each patient. Each factor was allotted a score of 1, and then patients were divided into five categories by Antidiabetic Compound Library manufacturer their risk scores (RSs) (0, 1, 2, 3, find protocol and 4). For example, “RS = 0” means patients without any of the above factors; this group occupied 8.59% (22 of 256). “RS = 4” means patients with all four factors; it occupied 26.56% (68 of 256) of patients carrying all four factors (Figure 3). Because no significant difference were observed in DFS and OS between patients whose RS equals 0 or 1 (Figure 3, A

and C; P = .132 and P = .145, respectively), these patients were merged as score ≤ 1 group. By combining four independent predictors, patients with different RSs showed distinguishable DFS (RS ≤ 1 vs RS = 2, P < .001; RS = 2 vs RS = 3, P = .037; and RS = 3 vs RS = 4, P < .001) ( Figure 3B) and OS (RS ≤ 1 vs RS = 2, P < .001; RS = 2 vs RS = 3,

P = .015; and RS = 3 vs RS = 4, P < .001) ( Figure 3D). Surprisingly, the proportion of patients with HCC with RS = 4 was very high, occupying 26.56% (68 of 256) of total patients ( Figure 3A). The DFS and OS in 68 patients with a score of 4 decreased sharply, and all these patients showed much shorter DFS and OS. Experimental and clinical data indicate that chronic inflammation significantly contributes to cancer development. The presence of systemic inflammation is associated with poor survival in certain tumors [15]. Inflammation can promote all stages of tumor development through multiple mechanisms, else which include predisposing tumor cell to proliferation and resistance to apoptosis, induction of DNA mutations, and promotion of angiogenesis, invasion, and metastasis [19]. The prognostic value of some systemic inflammatory markers such as C-reactive protein [15] and NLR have been investigated in tumor patients. Inflammatory environments can accelerate the progression of metastasis by neutrophi- mediated mechanisms [20]. NLR reflects an inflammatory status; a preoperatively high ratio is most likely to reflect more aggressive disease and hence represents poorer outcome. Patients with tumor and elevated NLR have a relative lymphocytopenia and neutrophilic leukocytosis, which denote that the balance is tipped in favor of protumor inflammatory response leading to poor oncologic outcome.

To successfully select those residues in the active site, a theor

To successfully select those residues in the active site, a theoretical model of RgPAL was constructed through homology modeling using RtPAL (PDB ID: 1T6J) as the template. As shown in Fig. 2, all of the residues that were

the superimposed with RtPAL showed an RMSD of 0.224 Å ( Fig. 2A), and the Ramachandran plot suggests that 94.9%, 3.2%, and 1.9% of the residues in derived model are in acceptable region, marginal HSP inhibition region and disallowed region, respectively ( Fig. 2B), These finding indicated that the model is reasonable and could be used in further molecular docking simulation. Using the AutoDock global–local evolutionary algorithm, we searched for those sites with the lowest free energy of binding between the ligand and the enzyme. As shown in Fig. 3, the active site cavity of RgPAL was bisected into

two regions ( Fig. 3A): one binds the amide group adjacent to the aromatic ring and the other binds the carboxyl group of the substrate. The phenyl ring of the substrate is roughly orthogonal to the plane of the MIO, and the methylidene of the MIO points to C2 of the aromatic ring ( Fig. 3A and B). In the carboxyl group binding pocket, the Arg361 residue is 3.2 Å from the carboxyl group of the substrate, and this residue might play a role in selleck screening library the binding of the carboxylate moiety of the substrate through a salt bridge. The Tyr358 residue is 2.7 Å from the β-H of substrate, which is close enough to act as the β-H abstracted base ( Fig. 3C). The Glu491 residue is the closet residue to the amino group of the substrate (2.8 Å, Fig. 3C) and might accept the amino group of substrate as the enzyme base, which is consistent with the results reported by Bartsch [1]. The Tyr358, Arg361 and Glu491 are highly conserved in PAL ( Fig. 1). In the aromatic ring binding pocket, the His136 residue points to the phenyl ring of the substrate. The imidzaole group

of His136 is parallel to the phenyl ring and might generate a π–π interaction. Moreover, the imidazole of His136 and the adjacent amide group of Gln137 which points to the phenyl ring within a distance of 4.5 Å, form a hairpin motif to clamp the phenyl ring ( Fig. 3B and C). To verify the function of the hairpin, the His136, Gln137 were deleted (RgPAL-Δ136H, RgPAL-Δ137Q) and mutated to negative (RgPAL-H136E, Paclitaxel in vivo RgPAL-Q137E) and positive charges (RgPAL-H136K, RgPAL-Q137K) as well as uncharged amino acids (RgPAL-H136F, RgPAL-Q137L), respectively. The mutant and wild type RgPAL proteins appeared a single band of about 75 kDa on SDS-PAGE ( Fig. 4). The activities of RgPAL-Δ136H and RgPAL-Δ137Q were not detected (data not shown), suggesting that the residues at the two sites were essential for catalysis. The RgPAL-H136K, RgPAL-Q137K and RgPAL-H136E lost the enzymatic activity (data not shown), and the RgPAL-H136F, RgPAL-Q137L sharply decreased the activity ( Fig. 5). Compared with those mutants, the activity of RgPAL-Q137E decreased slightly ( Fig. 5).

Two studies were reanalyses of a prior publication; these were no

Two studies were reanalyses of a prior publication; these were not classified as new studies but were evaluated

and the findings are discussed. We fully reviewed and evaluated 112 studies. For these 112 studies, the level of evidence was determined based on criteria used in our prior reviews.1 and 2 Well-designed, prospective, RCTs were considered class I evidence; studies using selleck products a prospective design with quasi-randomized assignment to treatment conditions were designated as class Ia studies. Given the inherent difficulty in blinding rehabilitation interventions, we did not consider this as criterion for class I or Ia studies, learn more consistent with our prior reviews. Class II studies consisted of prospective, nonrandomized cohort studies; retrospective,

nonrandomized case-control studies; or multiple-baseline studies that permitted a direct comparison of treatment conditions. Clinical series without concurrent controls, or single-subject designs with adequate quantification and analysis were considered class III evidence. Studies that were designed as comparative effectiveness studies but did not include a direct statistical comparison of treatment conditions were considered class III; this occurred for 4 articles. Disagreements between the 2 primary reviewers (as occurred for 3 articles) were first addressed by discussion between reviewers to correct minor sources of disagreement,

and then by obtaining a third review. Of the 112 studies, 14 were rated as class I, 5 as class Ia, 11 as class II, and 82 as class III. The overall evidence within each predefined Bcr-Abl inhibitor area of intervention was synthesized and recommendations were derived from the relative strengths of the evidence. The level of evidence required to determine Practice Standards, Practice Guidelines, or Practice Options was based on the decision rules applied in our initial review ( table 1). All recommendations were reviewed for consensus by the entire task force through face-to-face discussion. We reviewed 2 class I studies9 and 10 and 6 class III studies11, 12, 13, 14, 15 and 16 addressing remediation of attention. A class I study9 investigated the effectiveness of cognitive remediation and cognitive-behavioral psychotherapy for participants with persisting complaints after mild or moderate TBI. The cognitive remediation consisted of direct attention training along with training in use of a memory notebook and problem-solving strategies. Cognitive-behavioral therapy was used to increase coping behaviors and reduce stress.

Resorbiertes MeHg bindet an SH-Gruppen von Proteinen in Blut und

Resorbiertes MeHg bindet an SH-Gruppen von Proteinen in Blut und Geweben, in geringerem Ausmaß dagegen an SH-Gruppen z. B. von Cystein und GSH. Durch die Zellmembran wird es hauptsächlich an Cystein gebunden transportiert, und zwar vom Large Neutral Amino Acid Transporter („Transporter für große neutrale Aminosäuren”) [58]. Darüber hinaus sind Selleck PFT�� noch weitere Mechanismen an der Aufnahme in Zellen beteiligt, darunter auch passive Diffusion [59]. Die Verteilung aus dem Blut in die Gewebe verläuft langsam und das Gleichgewicht stellt sich erst 4 Tage nach einer Exposition ein. Etwa 10% der Körperlast wird im Kopfbereich gefunden. Die Aufnahme ins Gehirn erfolgt langsamer als die in andere Organe. Das

Gehirn weist jedoch eine höhere Affinität für MeHg auf, und es wurde gezeigt, dass die Konzentration im Gehirn 3- bis 6-mal höher ist als im Blut. Etwa 20% des MeHg im Gehirn ist wasserlöslich und liegt hauptsächlich als MeHg-GSH-Komplex vor. Im übrigen Körper

ist MeHg mehr oder weniger gleichmäßig verteilt, obwohl in der Leber und der Niere einige konzentrationsabhängige Effekte auftreten. MeHg wird durch die Plazenta transportiert und im Fetus abgelagert. Im Gleichgewicht kann das Gehirn des Fetus MeHg in derselben Konzentration enthalten wie das Gehirn der Mutter. Jedoch ist beim Menschen die Konzentration im fetalen u. U. höher als im mütterlichen Blut. Möglicherweise liegt dies an Unterschieden check details beim Hämoglobin, da dies das wichtigste Bindungsprotein für MeHg in Erythrozyten ist und sich der Hämoglobingehalt zwischen Mutter und Fetus unterscheidet. Es wurde gezeigt, dass bei langfristiger Verabreichung von MeHg an Affen die Hg2+-Menge nur langsam ansteigt [60]. Das anorganische Quecksilber reichert sich Urocanase vor allem in Astrozyten und der Mikroglia an. Die Bedeutung dieses Prozesses im Rahmen der Neurotoxizität von MeHg wird später diskutiert. Die Exkretion von MeHg erfolgt

hauptsächlich über die Galle und die Nieren. Die tägliche Netto-Exkretionsrate von 1% der Körperlast resultiert in einer Halbwertszeit von etwa 70 Tagen. Diese Schätzung passt sehr gut zu den Daten in der umfangreichen Datenbank, die während der Vergiftungsepidemie im Irak [61] erstellt wurde. Die enterohepatische Rezirkulation von MeHg ist ein wichtiger Faktor im Zusammenhang mit der Exkretion von MeHg über die Faeces. Clarkson et al. entwickelten ein SH-Harz zur oralen Einnahme, um den enterohepatischen Kreislauf zu unterbrechen und so die Exkretionsrate von MeHg zu erhöhen [62]. Demethylierung im Darm kann signifikant zu einer erhöhten fäkalen Exkretion beitragen, da Hg2+ über den enterohepatischen Kreislauf nicht im demselben Ausmaß reabsorbiert wird wie MeHg. MeHg hat eine hohe Affinität zu SH-Gruppen; der logK liegt im Bereich von 15 bis 23 [63]. Trotz der hohen Affinität findet ein äußerst rascher Austausch des MeHg zwischen SH-Gruppen statt, der zu einer schnellen Umverteilung des MeHg führt, wenn neue SH-Gruppen verfügbar werden [64].

However, there are two factors that could potentially resolve the

However, there are two factors that could potentially resolve the apparent discrepancy. First, although these areas typically deactivate when participants perform demanding tasks, this may not be true of semantic tasks specifically. Second, even if they were more active during rest, strong activation of these regions in task-free situations might indicate daydreaming and undirected thoughts that contain rich semantic content ( Binder et al., 1999). If this

were the case, then we would expect other elements of the semantic network, including the ATL, to also Epacadostat purchase show greater activity at rest. We therefore assessed the relationship between areas showing semantic effects and areas showing positive or negative activity with respect to a resting baseline. Twenty healthy participants took part (11 male, mean age = 25, range = 20–39). Data from one participant was discarded due to image artefacts. All participants were native English speakers with no history of neurological or psychiatric disorders and normal or corrected-to-normal vision. The study was approved by the local ethics board. Participants completed a synonym judgement task similar to that used in previous neuropsychological (Jefferies, Patterson, Jones, & Lambon Ralph, 2009), transcranial KU-60019 magnetic stimulation (Hoffman et al., 2010; TMS; Pobric et al., 2007) and fMRI (Binney et al., 2010) studies. On each trial, participants

were presented with a written probe word with three choices below it (a semantically related target and two unrelated foils). They were asked to select the word that was most similar in meaning to the probe (see Table 1 for

examples). Prior to each enough synonym judgement, participants were presented with a written cue consisting of two short sentences. On half of the trials, the cue ended with the probe word and placed it in a particular meaningful context (contextual cue condition). On the remaining trials, the cue did not contain the probe and was not related in meaning to the subsequent judgement (irrelevant cue condition). Participants were unaware when reading the cue whether it would be helpful for their next decision, meaning that neural differences between the two conditions only occurred in the decision phase. We assumed that reading the cue would activate semantic information related to its content and that this information would be strongly active when the subsequent synonym judgement was presented. On contextual cue trials, the pre-activated semantic information was highly relevant to the judgement, which was likely to have two effects. First, processing of the probe word would benefit from the prior activation of the word’s meaning and its context, leading to the retrieval of a richer semantic representation. Retrieval of a greater quantity of semantic knowledge leads to stronger activation in areas associated with semantic representation (Whitney, Jefferies, et al., 2011).

The authors also would like to thank professor Sandra Regina Paul

The authors also would like to thank professor Sandra Regina Paulon Avancini for her assistance in obtaining the necessary resources, masters Márcio Zílio and Aureanna Negrão for their help to perform the analysis and the Santa Catarina State University for giving space and equipment to perform the research. “
“The definition Apitolisib solubility dmso of quality is very complex within the food industry. In the literature

it is very common to find a mixture of quality, the concept, with quality, the measurement or attribute (Bremner, 2002, chap. 10). Botta (1995) defined some main quality attributes with respect to seafood: safety, nutritional characteristics, availability, convenience, integrity and freshness. The most important methods to evaluate freshness of seafood are the sensory methods (Bonilla, Sveinsdóttir, & Martinsdóttir, 2007). Freshness loss of seafood is the result of postmortem biochemical, physicochemical and microbiological processes characteristic of each species and influenced by handling on board and on land and by technological processing (Huidobro, Pastor, & Tejada, 2000). These changes are perceived and can be evaluated in sensory

terms by sight, touch, smell and taste (Huidobro et al., 2000). The Quality Index Method (QIM), originally FK866 developed by the Tasmanian Food Research Unit (TFRU), is a descriptive, fast and simple method to evaluate the freshness of seafood (Huidobro et al., 2000). This seafood freshness grading system (Sveinsdóttir, Martinsdóttir,

Jorgensen & Kristbergsson, 2002) is based on significant sensory parameters NADPH-cytochrome-c2 reductase for raw fish and a score system from 0 to 3 demerit points (Barbosa and Vaz-Pires, 2004, Branch and Vail, 1985, Bremner, 1985 and Larsen et al., 1992). It evaluates sensory parameters and attributes that change most significantly, in each species, during degradation processes (Huidobro et al., 2000). Therefore higher scores are given as storage time progresses. Each fish species has its own characteristic spoilage patterns and indicators, and consequently QIM schemes must be species-specific (Hyldig and Green-Petersen, 2004, Nielsen and Green, 2007 and Sveinsdóttir et al., 2002). Barbosa and Vaz-Pires (2004) compiled a list of the QIM schemes available. At the time, 21 different fish species or products had specifically designed QIM schemes, while between 2002 and 2009 additional QIM schemes were built for 16 new seafood items. Table 1 summarises the schemes that were created and made available in the scientific literature within that period. In the second period (2002–2009), some of the schemes proposed for the first 21 species were repeated and/or corrected; these recent advances and new schemes can be found on the site of the international project QIM-EUROFISH (www.qim-eurofish.com).