International travel has become increasingly common, accessible, and affordable.1,2 In 2010, there were 711 million international outbound trips worldwide, a 7% increase from 2009.3 The number of international visitors to the United States rose to a record 60 million in 2010.4 This growth has provided more opportunities for pathogens to spread beyond geographic and political borders and has increased interest in preventing morbidity and mortality among international travelers. Previous studies of United States, Canadian, Scottish, and Australian civilians who died abroad have analyzed expatriate

death reports at consulates, embassies, and government agencies.5–17 Few studies have addressed passenger mortality during commercial travel on aircraft and cruise www.selleckchem.com/products/lgk-974.html ships.18–25 The U.S. Department of State (DOS) Web site lists data on some U.S. citizens who die in a foreign country because of non-natural causes (eg, injuries).26 However, this Web site does not include selleck screening library all deaths of U.S. military or government officials abroad, and DOS may not be notified about deaths of U.S. citizens who reside abroad. The Centers for Disease Control & Prevention’s (CDC) Division of Global Migration and Quarantine (DGMQ)

has statutory authority to make and enforce regulations to prevent the introduction or transmission of communicable diseases into the United States.27 The 20 CDC DGMQ quarantine stations have jurisdiction over all U.S. land border ports, seaports, and airports.28 The U.S. Code of Federal Regulations mandates that the pilot or captain of an international aircraft or ship reports illnesses

and deaths occurring aboard the vessel to the nearest CDC quarantine station.29 This reporting requirement does not apply to U.S. land borders, private physicians, hospitals, or clinics. U.S. Customs & Border Protection (CBP), domestic health departments, and others voluntarily report illnesses and deaths among international travelers to CDC quarantine stations.27 selleck products Our objective was to analyze data on public health investigations of death in international travelers arriving in the United States, and to describe the epidemiology of travelers’ deaths reported to CDC quarantine stations. We examined data from the CDC Quarantine Activity and Reporting System (QARS), a secure online database developed by CDC in 2005 to track illnesses and deaths among inbound international travelers of any citizenship entering the United States and that are reported to CDC quarantine stations. These QARS reports include individual traveler demographic data, clinical summaries, and travel itineraries. For reported deaths, quarantine station staff also collect information on the presumptive cause of death, chronic medical conditions, and when available, the official cause of death. This investigation was approved by CDC with a non-research determination.

, 2011; Marangolo et al., 2011, 2013) through additional

modulation of interhemispheric interactions via cathodic stimulation to the homologue contralesional area (Jung et al., 2011; Kang et al., 2011; You et al., 2011). Indeed, only after the real stimulation condition, articulatory errors significantly decreased and all patients were faster in repeating the stimuli compared to the sham condition. Most importantly, significant changes after therapy persisted at F/U and generalised to other tasks. Accordingly, most of the patients showed a significant improvement in different oral language tasks (picture description, noun and verb naming, word repetition and reading) administered before and after the treatment, an improvement which was still present 1 week after the therapy (see Table 2). This improvement revealed Inhibitor Library concentration CT99021 that the language treatment resulted in a positive effect on the production of stimuli not only treated but also belonging to other tasks. Indeed, after tDCS stimulation most patients were able to correctly produce the whole word and they showed

a reduction in phonological errors, the reduction being due to improvement in speech praxis. This is consistent with previous transcranial direct current stimulation–tDCS literature showing longer-term changes (at 1 month or more) in word retrieval and other language measures (Naeser et al., 2010, 2011; Marangolo et al., 2011, 2013). As far as

we know, this is the first study which has investigated the effects of bihemispheric stimulation on the recovery of language. As stated in the Introduction, several studies have already stressed the importance of associating specific language training with anodic unihemispheric tDCS stimulation over the perilesional language areas (Baker et al., 2010; Fiori et al., 2011; Fridriksson et al., 2011; Marangolo et al., 2013). This was based on the assumption that, in chronic patients, language recovery may be associated with the reactivation FAD of left-hemispheric perilesional structures (Warburton et al., 1999; Saur et al., 2006; Winhuisen et al., 2007). Although it is often assumed that the right homologue of Broca’s area takes over the function of the left if it is infarcted, the evidence for this is slender. Recent studies have stressed the importance of the left Broca’s area or adjacent tissue in the natural recovery from post-stroke aphasia (Saur et al., 2006, 2008). Coherently with this assumption, some studies have also shown that the suppression of the right homologue language areas through repetitive transcranial magnetic stimulation (Naeser et al., 2005, 2010, 2011) or unihemispheric cathodic tDCS (Jung et al., 2011; Kang et al., 2011; You et al., 2011), reducing the inhibition on the ipsilesional cortex exerted by the unaffected hemisphere via the transcallosal pathway, determines significant changes in language recovery.

Lopinavir/ritonavir treatments severely affected the growth of gingival epithelium when the drug was present throughout the growth period. To the best of our knowledge, the correlation between lopinavir/ritonavir levels in blood serum and in oral tissues has not been widely studied. However, earlier studies showed that drug levels were almost equal in blood serum and in saliva [23–25]. Therefore, we assumed that the blood levels of

lopinavir/ritonavir Idelalisib research buy would be the same as in the saliva. As the oral cavity is directly exposed to saliva, we expect that the intracellular concentration of the drug in the oral cavity tissues would be equal or close to its Cmax (9.8 μg/mL). In the present study, at even lower concentrations

of lopinavir/ritonavir (3 and 6 μg/mL), the growth of gingival epithelium was severely inhibited. To examine the Ivacaftor price effect of lopinavir/ritonavir on epithelium integrity using TEM, we treated raft cultures at day 8. TEM observations clearly illustrated that lopinavir/ritonavir treatments affected cell-to-cell packing by directly or indirectly reducing desmosome adhesiveness. As desmosomes are intercellular junctions that provide strong adhesion between cells and also give mechanical strength to tissues [19], the results of our study suggest that lopinavir/ritonavir treatments affected gingival epithelium integrity. The results of the present study are consistent with those of our previous study in which amprenavir treatments also affected epithelial growth and integrity [20]. However, the adverse impact of lopinavir/ritonavir on tissue growth and integrity was more severe compared with amprenavir treatments. Our results Anacetrapib support

previous findings that indicated that the use of antiretroviral drugs, including protease inhibitors, resulted in the development of oral complications [6,8–11]. These observations suggest the possibility that the oral epithelium in HIV-infected patients exposed to HAART develops drug-induced abnormalities in the cellular and molecular biology of the tissue which give rise to oral complications. However, our raft culture model is an in vitro model in which the study of growth kinetics is limited to a maximum of 20 days. In contrast, patients undergoing drug therapy have potentially been exposed to these drugs for a numbers of years. As a result, our raft culture system provides a snapshot of the drug effects during a limited growth period. However, the effects of the drugs are representative of the adverse oral effects reported in patients undergoing antiviral therapy. Different cytokeratins are differentially expressed during development and differentiation and vary in different types of epithelia [18,32]. Normally, cytokeratins 5 and 14 are expressed only in the proliferative basal layer of gingival stratified epithelia [28–30].

Lopinavir/ritonavir treatments severely affected the growth of gingival epithelium when the drug was present throughout the growth period. To the best of our knowledge, the correlation between lopinavir/ritonavir levels in blood serum and in oral tissues has not been widely studied. However, earlier studies showed that drug levels were almost equal in blood serum and in saliva [23–25]. Therefore, we assumed that the blood levels of

lopinavir/ritonavir Y-27632 purchase would be the same as in the saliva. As the oral cavity is directly exposed to saliva, we expect that the intracellular concentration of the drug in the oral cavity tissues would be equal or close to its Cmax (9.8 μg/mL). In the present study, at even lower concentrations

of lopinavir/ritonavir (3 and 6 μg/mL), the growth of gingival epithelium was severely inhibited. To examine the OSI-744 supplier effect of lopinavir/ritonavir on epithelium integrity using TEM, we treated raft cultures at day 8. TEM observations clearly illustrated that lopinavir/ritonavir treatments affected cell-to-cell packing by directly or indirectly reducing desmosome adhesiveness. As desmosomes are intercellular junctions that provide strong adhesion between cells and also give mechanical strength to tissues [19], the results of our study suggest that lopinavir/ritonavir treatments affected gingival epithelium integrity. The results of the present study are consistent with those of our previous study in which amprenavir treatments also affected epithelial growth and integrity [20]. However, the adverse impact of lopinavir/ritonavir on tissue growth and integrity was more severe compared with amprenavir treatments. Our results Astemizole support

previous findings that indicated that the use of antiretroviral drugs, including protease inhibitors, resulted in the development of oral complications [6,8–11]. These observations suggest the possibility that the oral epithelium in HIV-infected patients exposed to HAART develops drug-induced abnormalities in the cellular and molecular biology of the tissue which give rise to oral complications. However, our raft culture model is an in vitro model in which the study of growth kinetics is limited to a maximum of 20 days. In contrast, patients undergoing drug therapy have potentially been exposed to these drugs for a numbers of years. As a result, our raft culture system provides a snapshot of the drug effects during a limited growth period. However, the effects of the drugs are representative of the adverse oral effects reported in patients undergoing antiviral therapy. Different cytokeratins are differentially expressed during development and differentiation and vary in different types of epithelia [18,32]. Normally, cytokeratins 5 and 14 are expressed only in the proliferative basal layer of gingival stratified epithelia [28–30].

In recognition of the advanced status of

community pharmacists in the delivery of asthma disease-state management services in Australia,[45–49] the exemplary chronic disease of asthma was chosen as the chronic illness model around which to frame this research. A qualitative research approach was employed, utilising a theoretical framework and the collection of empirical data. Based on the literature and the Collaborative Working Relationships model,[15,50] a semi-structured interview guide was constructed (Table 1). The semi-structured interview guide was designed to elicit experiences and perceptions about professional relationships between GPs and pharmacists and collaboration around asthma management in the community. Note that the term ‘teamwork’ as well as ‘collaboration’ was used to gain Selleckchem LY2835219 feedback from the participants Osimertinib mw as the concept of teamwork was often found to be more intuitive for the participants. Following attainment of ethics approval from the University of Sydney Human Research

Ethics Committee, purposive sampling based on location (i.e. GPs and community pharmacists working in Western Sydney) was used to target recruitment of participants. Seventy-four pharmacists and 69 GPs were identified using business addresses from the telephone directory, and invited to participate by mail. Follow-up phone calls were made to pharmacies and GP surgeries to arrange a convenient appointment time at the usual place of business. Participants were given an information sheet and were

asked to sign a consent form before the interview occurred. Face-to-face interviews (conducted by RD) with pharmacists and GPs were recorded and transcribed. Following transcription of audio data, the following process of data analysis was undertaken: first-level coding was performed immediately after most interviews (RD and SBA), and concepts were identified from these interview transcripts by the researchers independently and later grouped into categories. Consensus of researchers was reached prior to finalisation of categories (RD and SBA). Selective coding then occurred as themes emerged from the conceptual categories. Recruitment continued until saturation of ideas and concepts was reached. Cytidine deaminase Interviews took between 30 and 45 min and were conducted at the workplace of participating GPs and pharmacists at a time of their convenience. HCPs were approached until saturation of data was achieved. In total 65 HCPs (25 pharmacists and 40 GPs) were approached to participate, with 25 interviews being were completed and analysed (saturation of data being reached with 18 community pharmacists and all seven willing GPs being interviewed). This corresponds to a response rate of 38% (25/65). Reasons for non-participation included lack of time or lack of interest. Some HCPs did not provide a reason, and others, mainly GPs, were unable to be contacted. Of the participants, eight were female.

The mechanism involved in this facilitation appears to be the inhibition of the release of GABA and opioids from dorsal horn neurons, leading to

disinhibition of the effect of GABAB receptors and μ-opioid receptors on substance P release. Our results indicate that CB1 receptors facilitate substance P release from primary afferent terminals. This facilitation was observed primarily Selleckchem NVP-LDE225 as an inhibition of evoked NK1R internalization produced by the CB1 receptor antagonists AM251, AM281 and rimonabant (Kano et al., 2009). AM251 and AM281 inhibited substance P release and not the NK1R internalization mechanism itself, as they did not decrease NK1R internalization induced by exogenous substance P. The fact that AM251 inhibited substance P release evoked by stimulating the dorsal root with selleckchem capsaicin indicates that CB1 receptors facilitate substance P release from nociceptors. Although a few A-fibers contain substance P (Lawson et al., 1993), they do not have TRPV1 receptors, so this experiment shows that AM251 is able to inhibit substance P release from C-fibers. Importantly, intrathecal AM251 inhibited NK1R internalization evoked by a noxious stimulus in vivo, showing that facilitation of substance P release by CB1 receptors takes place in physiological conditions.

The effect of AM251 and AM281 was dose-dependent, with IC50 values (13 nm and 6 nm, respectively) consistent with the affinity of these compounds for CB1 receptors (Gatley et al., 1997, 1998; Lan et al., 1999a,b). The inhibition that they produced was partial, leveling off at ∼ 50% of the NK1R internalization L-NAME HCl found in control slices. This partial

inhibition was found independently of the stimulus used to evoke substance P release: electrical stimulation at low (1 Hz) and high (100 Hz) frequency (Marvizon et al., 1997; Lao & Marvizon, 2005; Adelson et al., 2009) or capsaicin applied to the root (Lao et al., 2003). One possible explanation for this partial inhibition is that CB1 receptors facilitate substance P release from a subset of the substance P-containing terminals. Alternatively, the effect of CB1 receptors may consist of disinhibition of mechanisms that only partially decrease substance P release (see below). The facilitatory effect of CB1 receptors was also detected as an increase in the evoked NK1R internalization by the selective CB1 receptor agonist ACEA (Hillard et al., 1999; Pertwee, 1999). The decrease in NK1R internalization produced by the antagonist AM251 and the increase produced by the agonist ACEA cancelled each other, supporting the idea that these effects were mediated by opposing actions at CB1 receptors. However, the increase produced by ACEA was small compared with the inhibition produced by the antagonists. This was probably because the effect of ACEA was masked by the release of endocannabinoids.

The Km for the substrate 1-H2NA remained unaltered

in the presence of NADPH or NADH (Table 5). The enzyme showed similar Km for NADPH and NADH (Table 5). The saturation plot for FAD was hyperbolic and Km was determined to be 4.7 μM (Table 5). Alcaligenes sp. strain PPH degrades phenanthrene, hydroxybenzoates (o-, m- and p-) and o-phthalate (Deveryshetty et al., 2007). Based on metabolic analysis, the proposed pathway for phenanthrene degradation is: phenanthrene 1-H2NA 1,2-DHN salicylaldehyde salicylic acid catechol. The steps involved in the metabolism of 1-H2NA to salicylic acid are similar to that involved in naphthalene degradation and hence referred to as the ‘naphthalene selleck products route’. The generated catechol enters the central carbon cycle via the meta ring-cleavage pathway. Organisms capable of degrading phenanthrene via the ‘naphthalene route’ have the ability to degrade naphthalene (Davies & Evans, 1964; Evans et al., 1965; Menn et al., 1993; Sanseverino et al., 1993; Kiyohara et al., 1994; Takizawa et al., 1994; Yang et al., 1994). Interestingly, strain PPH failed to metabolize naphthalene as the carbon source; this could be due to lack of naphthalene dioxygenase or the presence of highly specific phenanthrene dioxygenase in this strain. Compared to salicylate,

phenanthrene-grown cells showed higher specific activity of 1-hydroxy-2-naphthoic acid hydroxylase (Table 2). As observed for several aromatic degradative pathways (Grund et al., 1990; Gescher et al., 2002; Phale et al., 2007; Swetha et al., Smad inhibitor 2007; Deveryshetty & Phale, 2009), enzymes of phenanthrene

degradation in strain PPH were also found to be inducible in nature. The upper-pathway enzymes of naphthalene degradation (naphthalene to salicylic acid) have been proposed to be involved in the conversion of phenanthrene to 1-H2NA and anthracene to 2-hydroxy-1-naphthoic acid (Menn et al., 1993). Further, 1-H2NA was metabolized to 1,2-DHN by salicylate-1-hydroxylase and reported to have broad substrate specificity (Balashova et al., 2001). In Alcaligenes sp. strain PPH, enzyme induction pattern and heat stability studies suggested the existence of two different enzymes, 1-hydroxy-2-naphthoic acid hydroxylase Baricitinib and salicylate-1-hydroxylase, responsible for the conversion of 1-H2NA to 1,2-DHN and salicylic acid to catechol, respectively. The enzyme responsible for the hydroxylation of 1-H2NA has not been reported so far. This is the first study reporting the existence of 1-hydroxy-2-naphthoic acid hydroxylase. The property of heat stability helped to resolve 1-hydroxy-2-naphthoic acid hydroxylase from salicylate hydroxylase and was exploited to partially purify the protein (Table 3). The enzyme was yellow in color and showed characteristic flavoprotein absorption spectrum (Fig. 2), as observed for several other hydroxylases (Yamamoto et al., 1965; Hesp & Calvin, 1969; White-Stevens & Kamin, 1972).

The Km for the substrate 1-H2NA remained unaltered

in the presence of NADPH or NADH (Table 5). The enzyme showed similar Km for NADPH and NADH (Table 5). The saturation plot for FAD was hyperbolic and Km was determined to be 4.7 μM (Table 5). Alcaligenes sp. strain PPH degrades phenanthrene, hydroxybenzoates (o-, m- and p-) and o-phthalate (Deveryshetty et al., 2007). Based on metabolic analysis, the proposed pathway for phenanthrene degradation is: phenanthrene 1-H2NA 1,2-DHN salicylaldehyde salicylic acid catechol. The steps involved in the metabolism of 1-H2NA to salicylic acid are similar to that involved in naphthalene degradation and hence referred to as the ‘naphthalene Roxadustat price route’. The generated catechol enters the central carbon cycle via the meta ring-cleavage pathway. Organisms capable of degrading phenanthrene via the ‘naphthalene route’ have the ability to degrade naphthalene (Davies & Evans, 1964; Evans et al., 1965; Menn et al., 1993; Sanseverino et al., 1993; Kiyohara et al., 1994; Takizawa et al., 1994; Yang et al., 1994). Interestingly, strain PPH failed to metabolize naphthalene as the carbon source; this could be due to lack of naphthalene dioxygenase or the presence of highly specific phenanthrene dioxygenase in this strain. Compared to salicylate,

phenanthrene-grown cells showed higher specific activity of 1-hydroxy-2-naphthoic acid hydroxylase (Table 2). As observed for several aromatic degradative pathways (Grund et al., 1990; Gescher et al., 2002; Phale et al., 2007; Swetha et al., Alectinib order 2007; Deveryshetty & Phale, 2009), enzymes of phenanthrene

degradation in strain PPH were also found to be inducible in nature. The upper-pathway enzymes of naphthalene degradation (naphthalene to salicylic acid) have been proposed to be involved in the conversion of phenanthrene to 1-H2NA and anthracene to 2-hydroxy-1-naphthoic acid (Menn et al., 1993). Further, 1-H2NA was metabolized to 1,2-DHN by salicylate-1-hydroxylase and reported to have broad substrate specificity (Balashova et al., 2001). In Alcaligenes sp. strain PPH, enzyme induction pattern and heat stability studies suggested the existence of two different enzymes, 1-hydroxy-2-naphthoic acid hydroxylase MRIP and salicylate-1-hydroxylase, responsible for the conversion of 1-H2NA to 1,2-DHN and salicylic acid to catechol, respectively. The enzyme responsible for the hydroxylation of 1-H2NA has not been reported so far. This is the first study reporting the existence of 1-hydroxy-2-naphthoic acid hydroxylase. The property of heat stability helped to resolve 1-hydroxy-2-naphthoic acid hydroxylase from salicylate hydroxylase and was exploited to partially purify the protein (Table 3). The enzyme was yellow in color and showed characteristic flavoprotein absorption spectrum (Fig. 2), as observed for several other hydroxylases (Yamamoto et al., 1965; Hesp & Calvin, 1969; White-Stevens & Kamin, 1972).

The Km for the substrate 1-H2NA remained unaltered

in the presence of NADPH or NADH (Table 5). The enzyme showed similar Km for NADPH and NADH (Table 5). The saturation plot for FAD was hyperbolic and Km was determined to be 4.7 μM (Table 5). Alcaligenes sp. strain PPH degrades phenanthrene, hydroxybenzoates (o-, m- and p-) and o-phthalate (Deveryshetty et al., 2007). Based on metabolic analysis, the proposed pathway for phenanthrene degradation is: phenanthrene 1-H2NA 1,2-DHN salicylaldehyde salicylic acid catechol. The steps involved in the metabolism of 1-H2NA to salicylic acid are similar to that involved in naphthalene degradation and hence referred to as the ‘naphthalene click here route’. The generated catechol enters the central carbon cycle via the meta ring-cleavage pathway. Organisms capable of degrading phenanthrene via the ‘naphthalene route’ have the ability to degrade naphthalene (Davies & Evans, 1964; Evans et al., 1965; Menn et al., 1993; Sanseverino et al., 1993; Kiyohara et al., 1994; Takizawa et al., 1994; Yang et al., 1994). Interestingly, strain PPH failed to metabolize naphthalene as the carbon source; this could be due to lack of naphthalene dioxygenase or the presence of highly specific phenanthrene dioxygenase in this strain. Compared to salicylate,

phenanthrene-grown cells showed higher specific activity of 1-hydroxy-2-naphthoic acid hydroxylase (Table 2). As observed for several aromatic degradative pathways (Grund et al., 1990; Gescher et al., 2002; Phale et al., 2007; Swetha et al., Selleck Pembrolizumab 2007; Deveryshetty & Phale, 2009), enzymes of phenanthrene

degradation in strain PPH were also found to be inducible in nature. The upper-pathway enzymes of naphthalene degradation (naphthalene to salicylic acid) have been proposed to be involved in the conversion of phenanthrene to 1-H2NA and anthracene to 2-hydroxy-1-naphthoic acid (Menn et al., 1993). Further, 1-H2NA was metabolized to 1,2-DHN by salicylate-1-hydroxylase and reported to have broad substrate specificity (Balashova et al., 2001). In Alcaligenes sp. strain PPH, enzyme induction pattern and heat stability studies suggested the existence of two different enzymes, 1-hydroxy-2-naphthoic acid hydroxylase Janus kinase (JAK) and salicylate-1-hydroxylase, responsible for the conversion of 1-H2NA to 1,2-DHN and salicylic acid to catechol, respectively. The enzyme responsible for the hydroxylation of 1-H2NA has not been reported so far. This is the first study reporting the existence of 1-hydroxy-2-naphthoic acid hydroxylase. The property of heat stability helped to resolve 1-hydroxy-2-naphthoic acid hydroxylase from salicylate hydroxylase and was exploited to partially purify the protein (Table 3). The enzyme was yellow in color and showed characteristic flavoprotein absorption spectrum (Fig. 2), as observed for several other hydroxylases (Yamamoto et al., 1965; Hesp & Calvin, 1969; White-Stevens & Kamin, 1972).

, 2003; Aine et al.,2006). The congruence between available resources and maintaining the level of performance can be considered as the optimal use of limited resources in alternative ways (recruiting different brain areas). In accordance with the compensation hypothesis, preservation of receptive language abilities in aging has been confirmed by different studies (Wingfield & Grossman, 2006; Tyler et al., 2010). However, evidence of age-related neurofunctional changes sustaining expressive

word retrieval abilities remain scarce. One specific aim of this study was to describe buy GSI-IX the age-related changes in the neurofunctional patterns of activation for some of the basic and strategic processes in VF. With regards to expressive language abilities in aging, only a few neuroimaging studies have investigated semantic and orthographic Selleckchem Venetoclax and phonemic processing of words at the spoken level. This can be performed within the framework of a VF task requiring participants to generate as many words as possible under specific search conditions (e.g. animals’

names) and a limited amount of time. Using fMRI and a response pacing paradigm, Meinzer et al. (2009, 2012a) reported similar performances for the total number of words correctly produced and left-lateralized patterns of cerebral activations (e.g. inferior frontal gyri) between younger and older adults during the phonemic condition, while a significant age-related drop in semantic performances was accompanied by additional right-hemisphere activations. Moreover, Meinzer et al. (2012a,2012b) showed that bilateral activity in the ventral inferior frontal gyri was crucially mediated by task difficulty rather than solely by age. However, the VF task involves a number of cognitive components and the simple assessment of the total number of words produced is unlikely to fully describe their interactions with age. Considering that word retrieval becomes more effortful in time within a category, this task can be used to explore the temporal progression of the processes involved by analysing performances

at different period (e.g. MG-132 mouse Crowe, 1998). In addition, Troyer et al. (1997) proposed assessing clustering and switching components of fluency performances, which respectively correspond to the number of words produced within semantic or phonemic subcategories (or clusters) and the ability to shift between these subcategories. However, to the best of our knowledge, the age-related changes in the brain activation for strategic processes have never been explored. Age-related differences in patterns of brain activity during different production times (0–30 s, 31–60 s and 61–90 s) and retrieval processes (clustering and switching) were looked at using a self-paced overt semantic and orthographic VF task (Marsolais et al.