e., 48% Europe, 20% America, 15% Africa, 8.5% in Asia-Oceania,

and 6.6% in the Near and Middle East).7 The repatriation of French patients from foreign hospitals, but also health care provided to foreigners traveling in France, whatever their nationality, then expose the French population to highly resistant bacteria acquired in high resistance prevalent areas. The risk of the emergence and spread of highly resistant bacteria from migration has been recently evaluated in France because sporadic or limited epidemic situations have occurred in the recent past with pathogens such as Clostridium difficile ribotype 027,8,9 carbapenemase-producing Enterobacteriaceae (CPE),10–12 vancomycin-resistant Enterococcus (VRE),13,14 or multidrug-resistant Acinetobacter baumannii.15 French guidelines Fostamatinib ic50 to control the hospital spread of CPE and VRE from patients repatriated and travelers hospitalized in French hospitals were published in August 2010.16 They are so far available in French only but an official translation into English is under consideration. This article reviews the highly resistant bacteria at risk of importation from high prevalence foreign countries, having only spread to France mTOR inhibitor on sporadic or limited epidemic situations, and describes the recent French guidelines to control their

spread. The emergence of CPE since the early 1990s is alarming, and carries the risk for therapeutic failures.17 The carbapenems are now often used for the treatment of severe infections caused by Enterobacteriaceae producing extended-spectrum β-lactamases (ESBL). The large increase of ESBL prevalence and the exposure Obatoclax Mesylate (GX15-070) of hospitalized population

to carbapenems appear to be a major factor favoring the emergence of carbapenem-resistant bacteria via selective pressure, particularly in Klebsiella pneumoniae species, also in other species such as Escherichia coli.18 Resistance is due to carbapenemases, of which there are three types: K pneumoniae carbapenemases (KPC), metallo-β-lactamases, and oxacillinases.19 The production of metallo-β-lactamases has mostly been associated with Pseudomonas aeruginosa and Acinetobacter spp. and is rare in Enterobacteriaceae, except in isolates from Mediterranean Europe.20 New Delhi metallo-β-lactamase (NDM) 1 was identified in K pneumoniae and E coli recovered from a Swedish patient who was admitted in a hospital in New Delhi, India.21 The first CPE strain described was a Klebsiella isolate recovered in North Carolina, United States in 1996, and the enzyme was called KPC-1.22 Subsequently, other KPC-type enzymes have been described throughout the United States (KPC-2 to KPC-7) by sporadic or epidemic spread.23 The first outbreak of KPC outside the United States was reported in Israel, from passengers and/or patients having traveled between the two countries.24 Since then, many continents, such as South America and Asia, have reported the emergence of CPE.

[9] At 4559 m, inhalation of NO led to a marked decrease in PAP and an increase in arterial oxygen saturation especially in subjects susceptible to HAPE.[10] In addition, decreased pulmonary NO production during acute hypoxia was suggested to contribute among other EPZ-6438 nmr factors to the enhanced hypoxic pulmonary vascular response in HAPE-susceptible subjects[11] and therefore might contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.[12] As

it is an NOS inhibitor, ADMA should cause an increase in PAP and raise the risk of developing altitude sickness and HAPE. By measuring ADMA serum levels during standardized altitude exposure, we were able to assess this approach both from a principal therapeutic perspective as described in the aforementioned studies and from a diagnostic perspective. This prospective comparative study was conducted to test the hypothesis that there is a relationship between Δ-ADMA in blood and a hypoxia-induced increase in PAP and AMS and that ADMA could be a predictive value for the development of AMS or a PAP > 40 mmHg. The tests

were performed in the altitude and climate chamber of the German Air Force Institute of Aviation Medicine in Koenigsbrueck, Germany (134 m). This hypobaric PD-0332991 in vitro chamber has a capacity of six individuals for an overnight stay. Two tests were performed and 12 subjects could be investigated. Each trial consisted of two overnight stays in the chamber. The subjects were allowed to sleep. For intraindividual comparison, both nights followed the same protocol. Altitude conditions, however, were simulated only during the second night, when the

subjects were decompressed over a period of 53 minutes to a pressure equivalent to an altitude see more of 4000 m. The subjects spent 12 hours in the chamber under these altitude conditions. At all time points, the subjects could have been rapidly recompressed or could have left the chamber through an airlock. An emergency physician with expertise in altitude medicine was continuously present. The study design had been approved by the ethics committee of the Society of Physicians of the state of Baden-Wuerttemberg, Stuttgart, Germany. All participants had given their written informed consent to take part in the study. Twelve male subjects (median age: 23 years, range: 18–33 years; median height: 182.5 cm, range: 169–194 cm; median weight: 76 kg, range: 55–100 kg; median body mass index: 22.5 kg/m2, range: 19–29 kg/m2) without altitude exposure higher than 1500 m in the last month prior to this study showed a minor tricuspid valve insufficiency found incidentally in the context of this study and were otherwise healthy. Prior to the tests, the subjects received an echocardiogram (ECG). Blood tests (HBG, HCT, RBC, MCH, MCV, PLT) and a 12-channel ECG were performed immediately before the trial. All results were unremarkable.

[9] At 4559 m, inhalation of NO led to a marked decrease in PAP and an increase in arterial oxygen saturation especially in subjects susceptible to HAPE.[10] In addition, decreased pulmonary NO production during acute hypoxia was suggested to contribute among other BTK inhibitors high throughput screening factors to the enhanced hypoxic pulmonary vascular response in HAPE-susceptible subjects[11] and therefore might contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.[12] As

it is an NOS inhibitor, ADMA should cause an increase in PAP and raise the risk of developing altitude sickness and HAPE. By measuring ADMA serum levels during standardized altitude exposure, we were able to assess this approach both from a principal therapeutic perspective as described in the aforementioned studies and from a diagnostic perspective. This prospective comparative study was conducted to test the hypothesis that there is a relationship between Δ-ADMA in blood and a hypoxia-induced increase in PAP and AMS and that ADMA could be a predictive value for the development of AMS or a PAP > 40 mmHg. The tests

were performed in the altitude and climate chamber of the German Air Force Institute of Aviation Medicine in Koenigsbrueck, Germany (134 m). This hypobaric SAHA HDAC datasheet chamber has a capacity of six individuals for an overnight stay. Two tests were performed and 12 subjects could be investigated. Each trial consisted of two overnight stays in the chamber. The subjects were allowed to sleep. For intraindividual comparison, both nights followed the same protocol. Altitude conditions, however, were simulated only during the second night, when the

subjects were decompressed over a period of 53 minutes to a pressure equivalent to an altitude Thymidylate synthase of 4000 m. The subjects spent 12 hours in the chamber under these altitude conditions. At all time points, the subjects could have been rapidly recompressed or could have left the chamber through an airlock. An emergency physician with expertise in altitude medicine was continuously present. The study design had been approved by the ethics committee of the Society of Physicians of the state of Baden-Wuerttemberg, Stuttgart, Germany. All participants had given their written informed consent to take part in the study. Twelve male subjects (median age: 23 years, range: 18–33 years; median height: 182.5 cm, range: 169–194 cm; median weight: 76 kg, range: 55–100 kg; median body mass index: 22.5 kg/m2, range: 19–29 kg/m2) without altitude exposure higher than 1500 m in the last month prior to this study showed a minor tricuspid valve insufficiency found incidentally in the context of this study and were otherwise healthy. Prior to the tests, the subjects received an echocardiogram (ECG). Blood tests (HBG, HCT, RBC, MCH, MCV, PLT) and a 12-channel ECG were performed immediately before the trial. All results were unremarkable.

The mean age of victims was 38.1 (range 10–72). Most of the victims were diving at sea, while one diver died in fresh water during a speleological expedition (2.1%). N (%) N (%) N (%) The information on the type of diving was isocitrate dehydrogenase inhibitor review missing for one victim. The number of victims in scuba diving and free-diving does not differ [23 (50%) vs 23 (50%)]. Out of 22 scuba diving fatalities,

3 (6.7% of the total diving accidents) occurred while performing a technical dive (at depths greater than 60 m or during occupational and/or speleological diving). In the group of free-divers, two cases (4.3%) involved snorkelers and included the youngest (a 10-year-old girl) and the oldest (a 72-year-old man) victim. The age groups of victims in the two categories differ in that the majority of scuba divers belong to the age group of 30 to 49 years

(34.8%), while most free-divers are young adults [20–29 years (19.6%)] (Table 1). However, there is no significant difference between the mean ages of the victims belonging to the two groups. Data about the organization of the diving were available in 40 cases. Most free-divers were diving alone at the time of death (16/20, 80%), while scuba divers were always diving in pairs or in a group (20/20, 100%). Out of 47 CHIR-99021 mw victims, 28 were tourists (59.6%), mostly coming from Germany (7 victims), Austria (4 victims), Czech Republic (3 victims), France (3 victims), and Italy (3 victims). A significant difference (p = 0.002) in diving styles was discovered

between foreign and local divers: while foreign divers were most commonly victims of scuba diving (19/27, 70.4%), residents died during free-diving (15/19, 78.9%) (Table 1). Only four deaths of Croatian Montelukast Sodium scuba divers were recorded and of these, three (15.8%) were casualties of technical and occupational dives. A significant difference (p < 0.001) in age was observed between tourists and local victims, tourists being older than Croatian victims (mean age of tourists was 44 years, while for residents it was 29.3 years). Most of the fatal diving incidents occurred in the summer months (38.9% locals vs 60.7% tourists). All female victims in the sample were tourist divers. The number of diving-related deaths has grown with every decade. From 1981 to 1990 there were 8 causalities, from 1991 to 2000 17 casualties, and from 2001 to 2010 22 diving casualties (Figure 1). While the number of casualties due to scuba diving shows stagnation during the last decade, the number of free-diving casualties has continued to rise (Figure 1). During the last three decades, the number of tourist casualties has risen faster than the number of Croatian diver casualties (Figure 2). The difference is most notable when examining the number of diving-related deaths before and after 1996. After 1996, the rise of tourist casualties (5 tourists before 1996 and 23 tourists after 1996) is greater than that of local divers (6 Croatian divers before 1996 and 13 after 1996).

Efavirenz CNS toxicity during the initial phase of treatment may be related to Cmax, regardless of the sampling time. A plasma therapeutic range of 1–4 µg/mL has been established for the nonnucleoside reverse transcriptase inhibitor efavirenz [1,2], and great variation in the pharmacokinetics of the drug exists within and between patients, causing variation in drug concentrations [3–6]. Factors reported to be associated with interpatient variability in efavirenz concentration

include gender, ethnicity and genetic polymorphisms [3,4,7,8,36], while autoinduction and adherence [8,9] may contribute to both inter- and intrapatient variability. Female gender has been reported to be associated with higher efavirenz concentrations and a larger volume of distribution [3,4,7], while Black patients have

been reported to exhibit lower CT99021 rates of clearance of the drug and hence higher plasma concentrations [10]. A recent study comparing 24-h efavirenz pharmacokinetics between HIV-infected patients and healthy volunteers after a C59 wnt clinical trial single dose showed patients with HIV/AIDS to have lower efavirenz oral bioavailability compared with healthy volunteers when genetics and gender were controlled for [11]. Certain polymorphisms of the gene encoding the major enzyme responsible for efavirenz metabolism, CYP2B6 (an enzyme belonging to the cytochrome P450 group of liver enzymes), have been found to be associated with low clearance of the drug, resulting in high plasma concentrations [3,12–14], and adverse reactions to efavirenz [15]. These polymorphisms, notably CYP2B6*6 and CYP2B6*11, are present at high frequencies however in Black populations, causing slower clearance of the drug in a large proportion of individuals in these populations

[4,7]. A study conducted in the Netherlands with predominantly Caucasian participants reported 18.9% of participants with concentrations above the therapeutic range [3], while a study conducted among Zimbabweans in Africa showed that 50% of the study population exhibited efavirenz plasma concentrations above the therapeutic range [4]. Caucasians have subsequently been reported to have an average intrinsic hepatic clearance rate 28% higher than that of Africans and Hispanics [10]. In addition, other factors, including autoinduction, contribute to inter- and intraindividual variability in efavirenz pharmacokinetics. The clearance of efavirenz has been shown to increase from the baseline value as a result of autoinduction [8], although the timing and the extent to which efavirenz induces its own metabolism differ among studies. While Zhu et al. [8] observed a 2-fold increase in efavirenz clearance at steady state from baseline values, Kappelhoff et al.

In a French study, transmission rates with dual therapy (zidovudine and lamivudine) to both the neonate and mother (1.6%) were lower than zidovudine monotherapy reported in historical controls (6.8%; OR 0.22; 95% CI 0.2–0.5) [259]. The strength of recommendation is proportionate to the estimated risk of transmission. Thus, benefit of additional neonatal DNA Damage inhibitor therapy is anticipated at higher VLs, in circumstances

where resistance is suspected or confirmed and where VL is increasing despite treatment. As with the recommendations regarding PLCS at VLs <400 HIV RNA copies/mL, favourable trends can be considered in the risk assessment. Despite the lack of evidence for its use, NSHPC data indicate a trend towards increasing use of triple-neonatal PEP. When an infant has been started on triple-combination PEP because find more the maternal VL is >50 HIV RNA copies/mL at 36 weeks and subsequently a delivery maternal VL is <50 HIV RNA copies/mL, then it is reasonable to simplify the infant PEP to monotherapy. Most neonates born in the UK to mothers known to have HIV will be exposed to ART in utero, during delivery and

after birth for the first 4 weeks of life. The range of cARTs to which neonates are being exposed in utero continues to increase. Neonatal drug metabolism is generally slower than that of older infants or children and premature neonates have even less efficient metabolism. Owing to a lack of neonatal pharmacokinetic and efficacy studies and suitable formulations, ART dosing regimens remain restricted to a small proportion of the ARV drugs currently manufactured (Table 1). Small pharmacokinetic studies have been performed (zidovudine [260], lamivudine [261],[262], tenofovir [139], emtricitabine [263]) and dosing regimens are available for most of the nucleoside analogues and for abacavir from age 1 month [264], while limited study of didanosine in neonates suggests that the pharmacokinetics are highly variable [108]. The pharmacokinetics of nevirapine in neonates has been

described in more ASK1 detail [72],[74],[265-267]. Pharmacokinetic-supported dosing is available for the PIs nelfinavir [261] and ritonavir-boosted lopinavir (based on HIV-1 infected infants initiating therapy in the first 6 weeks of life) [268-270] and a study that included some infants treated from birth [271]. However, evidence of adrenal suppression has been documented in some neonates treated with lopinavir/ritonavir, particularly when preterm [272], in addition to case reports of cardiac, renal and neurological toxicity, especially in, but not restricted to, premature infants, and including one death during PEP with lopinavir/ritonavir [273]. No effects have been observed with maternal lopinavir/ritonavir in the absence of neonatal dosing. It remains unclear whether these effects are related to lopinavir/ritonavir specifically or could be seen with other ritonavir-boosted PIs.

15 Antibodies in breast milk inhibited newborns’ seroconversion following polio immunization. 16 This effect was temporary and it was considered unnecessary to withhold breastfeeding when administering oral polio vaccines to infants >6 weeks of age. 17 Moreover, antibody response following rubella vaccine in breastfed infants whose mothers received rubella vaccine postpartum was similar to those in formula-fed infants and infants of naturally immune mothers. 18 Hence, immunization

with rubella in breastfeeding women does not Palbociclib cell line suppress the immune response to rubella vaccine in the infant. Antibody persistence in breast milk may vary depending on antibody type. Women vaccinated during pregnancy with pneumococcal and meningococcal

polysaccharide vaccines had specific IgA type 6B antibodies in colostrum that fell to undetectable levels by 2 weeks, whereas type 19F antibodies were found in breast milk up to 5 months. 19 Because an insignificant amount of antibodies in breast milk pass from the GI tract into infant circulation, these antibodies do not suppress the infant immune response. 20,21 CHIR-99021 in vivo Preservatives and other components of vaccines have caused concern over their potential effect on infants. Studies have assessed the effect of vaccine components (adjuvants, chemicals, preservatives, and additives) on infants, particularly that of thimerosol. Research has repeatedly refuted the association of adverse effects from thimerosol in vaccines administered directly to infants, 22 and the minute amounts that may possibly pass through breast milk should further reduce concern. Unfortunately, such concerns may lead to interruption of breastfeeding when the mother is immunized. The common Food and Drug Administration label “because many drugs are excreted

in human milk, caution should be exercised when administering vaccine Morin Hydrate to a nursing woman” does little to reassure. Nonetheless, with the exception of smallpox vaccine, breastfeeding is not a contraindication to vaccination (Table 1). Drugs that breastfeeding travelers may encounter include anti-infectives, antimalarials, high-altitude medications, analgesics, antimotility drugs, and topical preparations. The following section will review available data regarding their safety in breastfeeding infants. The most commonly prescribed anti-infectives in the pre-travel consultation are quinolones, macrolides, and occasionally sulfonamides, usually for self-treatment of travelers’ diarrhea. Doxycycline, a tetracycline prescribed for chemoprophylaxis of malaria, is also frequently considered in the United States but the World Health Organization (WHO) considers it contraindicated for prophylaxis and treatment for breastfeeding women.

6.5 at 20 °C. The alkali tolerance of this strain extends the pH range of highly adaptable Fe(III)-reducing Serratia species from mildly acidic pH values associated with acid mine drainage conditions to alkali conditions representative of subsurface sediments stimulated for extensive denitrification and metal reduction. Dissimilatory Fe(III)-reducing

bacteria are widely distributed in freshwater and marine environments and have the ability to utilize a wide range of compounds as electron donors (Lovley et al., 2004; Weber et al., SCH727965 clinical trial 2006). Dissimilatory Fe(III) reduction has been shown to occur over a wide pH range from acid mine drainage sites to alkaline soda lakes (Johnson, 1995; Straub et al., 2001; Pollock et al., 2007). Although Fe(III) reduction at low (< pH 3) and circumneutral pH is well documented, few studies exist showing Fe(III) reduction above pH 9 (Gorlenko et al., 2004; Pollock et al., 2007), despite the potential significance of these reactions in a range of natural and engineered environments. Alkaline pH is challenging for microbial metabolism as microorganisms must maintain their optimum intracellular pH and possess a mechanism for

creating an electron motive force capable learn more of driving solutes across the cell membrane against a proton counter gradient (Krulwich et al., 2001; Detkova & Pusheva, 2006; Stewart et al., 2010). It is suggested that in extreme alkaline environments, Na+ may replace H+ to create an electron motive force in some alkaliphilic microorganisms (Kevbrin et al., 1998; Krulwich et al., 2001; Detkova & Pusheva, 2006). Fe(III) reduction at a pH

> 9 has been observed by several species isolated from natural alkaline soda lakes, including Anaerobranca californiensis (Gorlenko et al., 2004), Alkaliphilus metaliredigens (Ye et al., 2004), Tindallia magadii (Kevbrin et al., 1998) and species most similar to (96%) Bacillus agaradhaerens (Pollock et al., 2007). In addition to natural high pH environments, such ID-8 as soda lakes, there is interest in the biogeochemistry of engineered high pH sediments, for example those resulting from industrial contamination and the use of alkaline cements as a building material. Alkaline sediment geomicrobiology is of particular current interest to the nuclear industry owing to the proposed use of cement containment for deep geological disposal of radioactive wastes and for remediation scenarios for existing contaminated land (NDA, 2011). It is important to understand how changes in pH may affect the microbial community and therefore the biogeochemical processes occurring in the subsurface. Microbial processes are a key to predicting the mobility of problematic radionuclides in the subsurface (Lloyd, 2003).

L.). H.O.-K. was supported PF-2341066 by a grant from the West Virginia Graduate Student Fellowships in Science, Technology, Engineering and Mathematics program. C.C.C. and H.O.-K. contributed equally to this work. “
“Biosynthesis

in fungal cultures of 27 Fusarium graminearum isolates of three different chemotypes (3AcDON, 15AcDON and NIV) grown on yeast extract sucrose agar medium was examined in this study. Volatile organic compound (VOC) analysis performed by headspace solid phase microextraction GC-MS allowed for determination of various concentrations of six alcohols, 14 aldehydes and ketones, 10 benzene derivatives, one furane, five hydrocarbons and three terpenes. In general, the determined VOC profile in fungal cultures

was dominated by hexanal (up to 74%), followed by nonanal (18%) and 2-methylbutanal (18%). Principal component analysis and discriminant analysis based on VOCs allowed for unambiguous discrimination of all studied isolates into three different groups in accordance with their trichothecene production (chemotypes). Significant differences were revealed between the levels of aldehydes and ketones, benzene derivatives and hydrocarbons in fungal cultures of three F. graminearum chemotypes. “
“Mesorhizobium loti MAFF303099 has a functional type III secretory system (T3SS) involved in the nodulation process on Lotus tenuis and Lotus japonicus. Four selleck chemicals Carnitine palmitoyltransferase II putative M. loti T3SS effectors (Mlr6358, Mlr6331, Mlr6361, and Mlr6316) have been previously described, and it has been demonstrated that the N-terminal regions of Mlr6361 and Mlr6358 mediate the secretion via a T3SS. Here, we demonstrate the capacity of Mlr6316 and Mlr6331 N-terminal regions to direct the secretion of a translational fusion to a reporter peptide through T3SS. By using single,

double, and triple mutants, we demonstrated the positive and negative participation of some of these proteins in the determination of competitiveness on Lotus spp. Low competitiveness values correlated with low nodulation efficiency for a mutant deficient in three of the putative M. loti effectors. Our data suggest that the net effect of M. loti T3SS function on symbiotic process with Lotus results from a balance between positive and negative effects. Type III secretion systems (T3SSs) are present in several pathogenic bacteria (Cornelis, 2002). These systems are multiprotein complexes through which effector proteins are delivered into the host cell where they can modulate various cellular functions (Galán, 2001; Cornelis, 2002; Alfano & Collmer, 2004). Various rhizobium species also have a T3SS through which several proteins are secreted (Viprey et al., 1998; Krause et al., 2002; Lorio et al., 2004; de Lyra et al., 2006).

It will outline how, to move policy and practice forward, it is important that there is a good understanding of the pharmacy team, which allows working together effectively, for the

benefit of patients. Finally, regulation needs to be fit-for-purpose, supportive of practitioners in all sectors and enabling practice innovation. Research is not a lone activity, and undertaking high quality research which has the potential to inform and impact practice relies on working with a great team, and I have been fortunate to have worked with many truly inspirational Selleckchem Pifithrin-�� colleagues. My research has particularly benefitted from working with not just pharmacists but many social scientists, who have challenged my perspective, approach or way of thinking. Furthermore, none of my research would have been possible without the pharmacists, pharmacy staff, students, and indeed patients who have participated by completing surveys, agreeing to be interviewed, observed or otherwise involved. Their views are what make practice research Regorafenib in vitro rich, insightful and relevant. (1) Schafheutle EI, David TJ, Hall J, Noyce PR, Silverthorne J, Tully MP (2009 January

23). MPharm Student Code of Conduct: A Literature Review. www.rpsgb.org/pdfs/ccpharmstudentslitrev.pdf (accessed 4 January 2011). (2) Schafheutle EI, David TJ, Hall J, Noyce PR, Silverthorne J, Tully MP (2009 January 23). Fitness to Practise Procedures for Pharmacy Students in UK Universities: A Literature Review. www.rpsgb.org/pdfs/studftpsoplitrev.pdf (accessed 11 June 2009 Jun 11). (3) Schafheutle EI, Hassell K, Ashcroft DM, Hall J, Harrison S. How do UK pharmacy students learn professionalism? Int J Pharm Pract 2012; 20: 118–128. (4) Schafheutle EI, Hassell K, Ashcroft triclocarban DM, Harrison S. Organizational philosophy as a new perspective on understanding the learning of professionalism. Am J Pharm Educ 2013; 77: Article 214. (5) Elvey R, Hassell K, Lewis P, Schafheutle E, Willis S, Harrison S.

Patient-centred professionalism in pharmacy: values and behaviours. Journal of Health Organization and Management 2014 (in press). (6) Elvey R, Lewis P, Schafheutle EI, Willis S, Harrison S, Hassell K. Patient-Centred Professionalism Among Newly Registered Pharmacists. London: Pharmacy Practice Research Trust, 2011. (7) Jee S. The process of professional socialisation and development of professionalism during pre-registration training in pharmacy. The University of Manchester, 2014 (PhD Thesis). (8) Schafheutle EI, Jee SJ, Hassell K, Noyce PR. What could the NHS appraisal system contribute to revalidation in pharmacy? Pharm J 2011; 286: 82. (9) Jee SD, Jacobs S, Schafheutle EI, Elvey R, Hassell K, Noyce PR. An exploration of the utility of appraisals for the revalidation of pharmacy professionals in community pharmacy in Great Britain. Res Soc Admin Pharm 2013; 9: 155–165.