J. Int J Clin Pharm. 2013 Oct; 35: 813–820. S Corlett, Rapamycin P Goel, S Kothari, L Dodds Medway School of Pharmacy, Anson Building, Chatham Maritime ME4 4TB The study investigated the relationship between hospital pharmacy referral activity and provision of discharge Medicines Use Reviews (dMURs) by community pharmacists 2 years after the dMUR service was commissioned. Hospital pharmacy referral activity was minimal in 50% of trusts contacted and absent in the remainder, while over 50% of community pharmacists contacted had never undertaken a dMUR, citing not knowing a patient had been discharged as the key barrier to service provision. It appears hospital

pharmacy teams could do more to encourage discharged patients to access the dMUR service, in particular, by reminding them to tell their community pharmacist they had recently been in hospital. Medication errors can occur on transfer of care.1 dMURs were commissioned

in 2011 to enable community pharmacists to support recently discharged patients by ensuring no unintentional changes in treatment had occurred, provide medicines information and encourage adherence.2 At the time, hospital pharmacy teams were encouraged to refer find more patients into this service. This study aimed to establish the provision of dMURs by community pharmacists and the practices of hospital pharmacy

teams in referring patients into the service over an area covered by eight Clinical Commissioning Groups and served by four acute hospital trusts. Four hospital pharmacy trusts serving an area covered by eight CCGs were contacted for by e-mail and asked to provide details of how they promote the dMUR service. All community pharmacies (n = 340) within the eight CCGs were asked by letter to participate in a short telephone interview. The structured telephone interviews lasted less than 10 minutes and explored participant uptake of, and perceived barriers to, dMURs using both open and closed questions. Data were analysed thematically and using SPSS version 21, respectively. University research ethics approval was obtained. Community pharmacists in 170 (50%) of pharmacies contacted took part in the survey. Of these, 53% (n = 90) had never conducted a dMUR despite 82% (n = 139) being the regular pharmacist. The main barrier to performing a dMUR was reported as not knowing a patient had been recently discharged. Participants were asked to estimate how many dMURs they performed each month (Table 1). Hospitals A and C reported they had prepared leaflets to promote the dMUR to patients. However, Hospital A reported they were rarely used and Hospital C that they had only been issued regularly for a few months after the initiation of the new service.

The results of brushing for children aged 8–12 years could benefit from

increasing tooth-brushing time. Children could be given an increasing responsibility from 7 to 8 year of age but parental help is motivated up to 10 years of age. “
“International Journal of Paediatric Dentistry 2013; 23: 101–109 Background.  Malnutrition has been consistently associated with caries in primary teeth, although an effect on permanent teeth has not been established because of the few longitudinal studies. Aim.  To explore the association between stunting and caries increment in permanent teeth over 3.5 years. Design.  In 2003, 121 children aged 7–9 years were randomly selected from nine underserved communities in Lima (Peru). Parents provided demographic information and a food diary for Ibrutinib chemical structure their children. Clinical examinations included assessments of height, weight, oral hygiene, learn more and dental caries. Stunting was defined using the 2000 CDC and 2007 WHO standards. In 2006, 83 children were re-examined, and the 3.5-year net DMFS increment was calculated. The association between stunting and net DMFS increment was assessed using negative binomial regression. Results.  Stunting was related to net DMFS increment after adjustment

for sex and age, oral hygiene, sugary snacks between meals, and caries experience in primary and permanent teeth. Consistent results were found when using either the 2000 CDC (incidence rate ratio: 1.61; 95%CI: 1.07, 2.44) or 2007 WHO standards (IRR: 1.79; 95%CI: 1.28, 2.51). Conclusion.  Stunting was a significant risk factor for caries increment in permanent teeth over a 3.5-year period, independent of other well-known risk factors for caries development. “
“International Journal of Paediatric Dentistry 2013; 23: 39–47 Background.  Caries in preschool children remains an important public health issue. Aim.  To determine (i) which teeth and tooth surfaces are most susceptible to dental caries by age 3, (ii) where do caries lesions Liothyronine Sodium develop during 2-year follow-up, and (iii) to

evaluate the impact of caries onset on the distribution of new caries experience. Design.  One thousand and fifty seven consecutively born children were recruited in Flanders (Belgium). Parents completed validated questionnaires on oral health-related behaviour and trained dentists examined the children at ages 3 and 5. Results.  Children with visible caries experience at age 3 were significantly more vulnerable in developing additional caries during follow-up. In this group, new caries experience developed primarily in the occlusal and distal surfaces of the mandibular first molars and the occlusal surfaces of the maxillary second and first molars, whereas in the caries-free group, the occlusal surfaces of both mandibular and maxillary second molars ranked first. Conclusions.  This paper confirms the higher vulnerability for further caries development in those children with caries experience at age 3.

The results of brushing for children aged 8–12 years could benefit from

increasing tooth-brushing time. Children could be given an increasing responsibility from 7 to 8 year of age but parental help is motivated up to 10 years of age. “
“International Journal of Paediatric Dentistry 2013; 23: 101–109 Background.  Malnutrition has been consistently associated with caries in primary teeth, although an effect on permanent teeth has not been established because of the few longitudinal studies. Aim.  To explore the association between stunting and caries increment in permanent teeth over 3.5 years. Design.  In 2003, 121 children aged 7–9 years were randomly selected from nine underserved communities in Lima (Peru). Parents provided demographic information and a food diary for learn more their children. Clinical examinations included assessments of height, weight, oral hygiene, selleck screening library and dental caries. Stunting was defined using the 2000 CDC and 2007 WHO standards. In 2006, 83 children were re-examined, and the 3.5-year net DMFS increment was calculated. The association between stunting and net DMFS increment was assessed using negative binomial regression. Results.  Stunting was related to net DMFS increment after adjustment

for sex and age, oral hygiene, sugary snacks between meals, and caries experience in primary and permanent teeth. Consistent results were found when using either the 2000 CDC (incidence rate ratio: 1.61; 95%CI: 1.07, 2.44) or 2007 WHO standards (IRR: 1.79; 95%CI: 1.28, 2.51). Conclusion.  Stunting was a significant risk factor for caries increment in permanent teeth over a 3.5-year period, independent of other well-known risk factors for caries development. “
“International Journal of Paediatric Dentistry 2013; 23: 39–47 Background.  Caries in preschool children remains an important public health issue. Aim.  To determine (i) which teeth and tooth surfaces are most susceptible to dental caries by age 3, (ii) where do caries lesions Inositol monophosphatase 1 develop during 2-year follow-up, and (iii) to

evaluate the impact of caries onset on the distribution of new caries experience. Design.  One thousand and fifty seven consecutively born children were recruited in Flanders (Belgium). Parents completed validated questionnaires on oral health-related behaviour and trained dentists examined the children at ages 3 and 5. Results.  Children with visible caries experience at age 3 were significantly more vulnerable in developing additional caries during follow-up. In this group, new caries experience developed primarily in the occlusal and distal surfaces of the mandibular first molars and the occlusal surfaces of the maxillary second and first molars, whereas in the caries-free group, the occlusal surfaces of both mandibular and maxillary second molars ranked first. Conclusions.  This paper confirms the higher vulnerability for further caries development in those children with caries experience at age 3.

, 2001, 2003). FlhD by itself, independent of FlhC, has also been reported to regulate cell division in E. coli (Prüß

& Matsumura, 1996). Cells in flhD mutant cultures were observed to continue dividing for several generations after cells in the flhD+ parental culture had stopped growing and entered the stationary click here phase. This work is frequently cited as evidence that FlhD regulates cell division (Kaper & Sperandio, 2005; Umehara et al., 2007; Cui et al., 2008; Hatt & Rather, 2008; Isalan et al., 2008); however, our data indicate that this is not the case. We re-examined the effects of flhD mutations on entry to the stationary phase and found that the previously observed phenotype is not due to the flhD locus. Here, we show that the difference in the final cell number is due to the thyA mutation in the parental flhD+ strain, which had apparently reverted in the flhD− mutant strain used in the study. When the strains being compared have the same thyA allele (wild type or mutant), flhD mutations have no effect on growth. The E. coli K-12 strains and phage used in this study are listed in Table 1. λWM7 (Mao & Siegele, 1998) is a derivative of λRS45 (Simons et al., 1987) that carries an operon fusion between the mcb operon promoter (positions

−344 to +79) and the lac operon. Strains lysogenic for λWM7 were isolated by infecting YK410 and YK4131 with λWM7 and screening survivors on medium containing X-Gal selleck compound where lysogens form blue colonies. Monolysogens were identified by measuring β-galactosidase activity in several independent Dehydratase isolates of

each lysogen. Transductions with P1vir were performed as described by Miller (1972). Hfr mapping was performed as described (Singer et al., 1989) using the Hfr strains described in that paper as donors. To facilitate the exchange of flhD alleles, derivatives of YK410 (λPmcb-lacZ) and YK4131 (λPmcb-lacZ) were constructed that carry the linked uvrC279∷Tn10 mutation and retain their original flhD allele. These are strains DS507 and DS511, respectively, which were used as the donor strains in all subsequent strain constructions. Motility assays (described below) were used to determine whether transductants carried the wild type or the mutant flhD allele. Introduction of the uvrC279∷Tn10 mutation did not affect the expression of the Pmcb-lacZ fusion (Table 2 and data not shown). For β-galactosidase assays, cultures were grown in TB medium [1% Bacto tryptone, 0.5% NaCl (Arber et al., 1983)] supplemented with MgSO4 (10 mM), thymidine (10 μg mL−1), and thiamine (2 μg mL−1). For plates, 1.3% Bacto agar (Difco Laboratories) was included.

, 2001, 2003). FlhD by itself, independent of FlhC, has also been reported to regulate cell division in E. coli (Prüß

& Matsumura, 1996). Cells in flhD mutant cultures were observed to continue dividing for several generations after cells in the flhD+ parental culture had stopped growing and entered the stationary Selleck EGFR inhibitor phase. This work is frequently cited as evidence that FlhD regulates cell division (Kaper & Sperandio, 2005; Umehara et al., 2007; Cui et al., 2008; Hatt & Rather, 2008; Isalan et al., 2008); however, our data indicate that this is not the case. We re-examined the effects of flhD mutations on entry to the stationary phase and found that the previously observed phenotype is not due to the flhD locus. Here, we show that the difference in the final cell number is due to the thyA mutation in the parental flhD+ strain, which had apparently reverted in the flhD− mutant strain used in the study. When the strains being compared have the same thyA allele (wild type or mutant), flhD mutations have no effect on growth. The E. coli K-12 strains and phage used in this study are listed in Table 1. λWM7 (Mao & Siegele, 1998) is a derivative of λRS45 (Simons et al., 1987) that carries an operon fusion between the mcb operon promoter (positions

−344 to +79) and the lac operon. Strains lysogenic for λWM7 were isolated by infecting YK410 and YK4131 with λWM7 and screening survivors on medium containing X-Gal SB203580 molecular weight where lysogens form blue colonies. Monolysogens were identified by measuring β-galactosidase activity in several independent 5-FU manufacturer isolates of

each lysogen. Transductions with P1vir were performed as described by Miller (1972). Hfr mapping was performed as described (Singer et al., 1989) using the Hfr strains described in that paper as donors. To facilitate the exchange of flhD alleles, derivatives of YK410 (λPmcb-lacZ) and YK4131 (λPmcb-lacZ) were constructed that carry the linked uvrC279∷Tn10 mutation and retain their original flhD allele. These are strains DS507 and DS511, respectively, which were used as the donor strains in all subsequent strain constructions. Motility assays (described below) were used to determine whether transductants carried the wild type or the mutant flhD allele. Introduction of the uvrC279∷Tn10 mutation did not affect the expression of the Pmcb-lacZ fusion (Table 2 and data not shown). For β-galactosidase assays, cultures were grown in TB medium [1% Bacto tryptone, 0.5% NaCl (Arber et al., 1983)] supplemented with MgSO4 (10 mM), thymidine (10 μg mL−1), and thiamine (2 μg mL−1). For plates, 1.3% Bacto agar (Difco Laboratories) was included.

Thus, it is suspected that augmenting the GH axis in patients with HIV-associated lipodystrophy results in improved utilization of fat stores and subsequent redistribution of adipose tissue [9]. GH axis drugs investigated for the treatment of HIV-associated lipodystrophy include recombinant growth hormone (GH), growth Opaganib solubility dmso hormone releasing hormone (GHRH), tesamorelin, also known as growth hormone releasing factor (GHRF), and insulin-like growth factor-1 (IGF-1). There are some concerns with this class of drug. GH, the most studied GH axis drug, costs approximately $52 per milligram, and is estimated to cost approximately US$10 000–US$30 000

per year of treatment [10]. Significant treatment-associated side effects of these drugs include arthralgias, myalgias, peripheral oedema,

insulin resistance and diabetes [11]. Considering the expense and side effects associated with these drugs, it is important to evaluate the evidence regarding the efficacies of these treatments to allow the patient and health care provider to make informed decisions. In the present systematic review, we evaluate randomized controlled trials comparing the effects of GH axis treatments with those of placebo in changing VAT, subcutaneous adipose tissue (SAT) and lean body mass (LBM) in patients with BMS-777607 price HIV-associated lipodystrophy. A detailed protocol was written prior to conducting the review. The protocol and documentation of all changes made after construction of the protocol are available upon request. Inclusion criteria were as follows (all were required to be met): (1) the study design must be a randomized controlled trial; (2) study participants were adult patients with HIV-associated lipodystrophy;

(3) the intervention was a GH axis drug (GH, GHRH, tesamorelin or IGF-1); (4) the comparison group was treated with placebo; and (5) the study included one of the primary outcomes. There were no exclusion criteria. Our primary outcomes of interest included changes in VAT mass, SAT mass or LBM. The secondary Beta adrenergic receptor kinase outcomes included changes in extremity fat, levels of fasting plasma glucose, high-density lipoprotein (HDL) cholesterol and triglycerides, and waist circumference. Potential harms of treatment were also evaluated. The following databases were searched for studies: OVID MEDLINE (1996 to present; accessed 6 June 2010), The Cochrane Library [Cochrane Central Register of Controlled Trials and Cochrane Database of Randomized Controlled Trials (CENTRAL); accessed 11 October 2009], Web of Science (accessed 11 October 2009), Summons (accessed 13 October 2009), Google Scholar (accessed 11 October 2009) and PubMed (accessed 5 June 2010). Search terms included: HIV, AIDS, growth hormone, Serostim, GH releasing hormone, tesamorelin, IGF-1, HIV-associated lipodystrophy, adipose tissue and body composition. A comprehensive list of all search terms is available upon request.

Thus, it is suspected that augmenting the GH axis in patients with HIV-associated lipodystrophy results in improved utilization of fat stores and subsequent redistribution of adipose tissue [9]. GH axis drugs investigated for the treatment of HIV-associated lipodystrophy include recombinant growth hormone (GH), growth Selinexor hormone releasing hormone (GHRH), tesamorelin, also known as growth hormone releasing factor (GHRF), and insulin-like growth factor-1 (IGF-1). There are some concerns with this class of drug. GH, the most studied GH axis drug, costs approximately $52 per milligram, and is estimated to cost approximately US$10 000–US$30 000

per year of treatment [10]. Significant treatment-associated side effects of these drugs include arthralgias, myalgias, peripheral oedema,

insulin resistance and diabetes [11]. Considering the expense and side effects associated with these drugs, it is important to evaluate the evidence regarding the efficacies of these treatments to allow the patient and health care provider to make informed decisions. In the present systematic review, we evaluate randomized controlled trials comparing the effects of GH axis treatments with those of placebo in changing VAT, subcutaneous adipose tissue (SAT) and lean body mass (LBM) in patients with Tyrosine Kinase Inhibitor Library cost HIV-associated lipodystrophy. A detailed protocol was written prior to conducting the review. The protocol and documentation of all changes made after construction of the protocol are available upon request. Inclusion criteria were as follows (all were required to be met): (1) the study design must be a randomized controlled trial; (2) study participants were adult patients with HIV-associated lipodystrophy;

(3) the intervention was a GH axis drug (GH, GHRH, tesamorelin or IGF-1); (4) the comparison group was treated with placebo; and (5) the study included one of the primary outcomes. There were no exclusion criteria. Our primary outcomes of interest included changes in VAT mass, SAT mass or LBM. The secondary Fossariinae outcomes included changes in extremity fat, levels of fasting plasma glucose, high-density lipoprotein (HDL) cholesterol and triglycerides, and waist circumference. Potential harms of treatment were also evaluated. The following databases were searched for studies: OVID MEDLINE (1996 to present; accessed 6 June 2010), The Cochrane Library [Cochrane Central Register of Controlled Trials and Cochrane Database of Randomized Controlled Trials (CENTRAL); accessed 11 October 2009], Web of Science (accessed 11 October 2009), Summons (accessed 13 October 2009), Google Scholar (accessed 11 October 2009) and PubMed (accessed 5 June 2010). Search terms included: HIV, AIDS, growth hormone, Serostim, GH releasing hormone, tesamorelin, IGF-1, HIV-associated lipodystrophy, adipose tissue and body composition. A comprehensive list of all search terms is available upon request.

Thus, it is suspected that augmenting the GH axis in patients with HIV-associated lipodystrophy results in improved utilization of fat stores and subsequent redistribution of adipose tissue [9]. GH axis drugs investigated for the treatment of HIV-associated lipodystrophy include recombinant growth hormone (GH), growth Talazoparib cost hormone releasing hormone (GHRH), tesamorelin, also known as growth hormone releasing factor (GHRF), and insulin-like growth factor-1 (IGF-1). There are some concerns with this class of drug. GH, the most studied GH axis drug, costs approximately $52 per milligram, and is estimated to cost approximately US$10 000–US$30 000

per year of treatment [10]. Significant treatment-associated side effects of these drugs include arthralgias, myalgias, peripheral oedema,

insulin resistance and diabetes [11]. Considering the expense and side effects associated with these drugs, it is important to evaluate the evidence regarding the efficacies of these treatments to allow the patient and health care provider to make informed decisions. In the present systematic review, we evaluate randomized controlled trials comparing the effects of GH axis treatments with those of placebo in changing VAT, subcutaneous adipose tissue (SAT) and lean body mass (LBM) in patients with Selleck Vadimezan HIV-associated lipodystrophy. A detailed protocol was written prior to conducting the review. The protocol and documentation of all changes made after construction of the protocol are available upon request. Inclusion criteria were as follows (all were required to be met): (1) the study design must be a randomized controlled trial; (2) study participants were adult patients with HIV-associated lipodystrophy;

(3) the intervention was a GH axis drug (GH, GHRH, tesamorelin or IGF-1); (4) the comparison group was treated with placebo; and (5) the study included one of the primary outcomes. There were no exclusion criteria. Our primary outcomes of interest included changes in VAT mass, SAT mass or LBM. The secondary Hydroxychloroquine ic50 outcomes included changes in extremity fat, levels of fasting plasma glucose, high-density lipoprotein (HDL) cholesterol and triglycerides, and waist circumference. Potential harms of treatment were also evaluated. The following databases were searched for studies: OVID MEDLINE (1996 to present; accessed 6 June 2010), The Cochrane Library [Cochrane Central Register of Controlled Trials and Cochrane Database of Randomized Controlled Trials (CENTRAL); accessed 11 October 2009], Web of Science (accessed 11 October 2009), Summons (accessed 13 October 2009), Google Scholar (accessed 11 October 2009) and PubMed (accessed 5 June 2010). Search terms included: HIV, AIDS, growth hormone, Serostim, GH releasing hormone, tesamorelin, IGF-1, HIV-associated lipodystrophy, adipose tissue and body composition. A comprehensive list of all search terms is available upon request.

maritimum NCIMB2154T obtained at 24 and 48 h using the

three E. coli JM109 lux-based biosensor strains carrying pSB536, pSB401 or pSB1075 to detect a wide range of AHLs differing in the length of their acyl chain. TLC analysis revealed the presence of short-chain AHLs using the E. coli JM109 pSB536 biosensor (Fig. 1). A search for AHL-type QS signals in extracts obtained from the culture media of another eight representative isolates of T. maritimum using the same technique revealed the presence of short-chain AHL activity in all of them, although differences were recorded in relation to their peak in activity (Table 1). LC-MS analysis confirmed the presence of N-butyryl-l-homoserine lactone (C4-HSL) in the culture media of T. maritimum NCIMB2154T grown in both FMM (Fig. 2) and MB (data not shown). This AHL was unequivocally identified by comparison www.selleckchem.com/products/abc294640.html Lumacaftor research buy of its mass spectra with those of pure standards (Fig. 3). As this is the

first description of the production of AHLs by a pathogenic member of the CFB cluster, the analyses were carried out simultaneously in both laboratories using different chromatographic conditions. The results confirmed unequivocally the presence of the C4-HSL. So far, no physiological role other than as QS signals has been assigned to AHLs, except as a chelator, for tetramic acid (a derivative of 3-oxo-C12) or antibiotic activity for both 3-oxo-C12-HSL and tetramic acid (Kaufmann et al., 2005; Schertzer et al., 2009). In addition, a role as biosurfactant has been attributed to long-chain AHLs (Daniels et al., 2006). Therefore, even though the physiological features under the control of these molecules in T. maritimum remain to be investigated, the production of C4-HSL by T. maritimum strains extends the paradigm of AHL-mediated QS beyond the Proteobacteria. Amino acid As the physiological processes under the control of AHL-mediated QS have so far been described for a limited number of genera of the Alpha-, Beta- and Gammaproteobacteria, many

of them human or plant pathogens (Williams et al., 2007), the ecological significance of AHL-mediated QS has been questioned as a key switch controlling gene expression within bacterial populations in nature (Manefield & Turner, 2002). The fact that genera outside the Proteobacteria produce the same signal molecules, and that AHL-degrading activity has been found in Gram-positive, Gram-negative and Cyanobacteria (Dong & Zhang, 2005; Romero et al., 2008) and in mammalian cells (Chun et al., 2004), reinforces the ecological significance of AHL-mediated QS processes. The presence of AHL-mediated QS beyond the Proteobacteria is not surprising, as a phylogenetic study based on the LuxI/LuxR genes suggested that QS mechanisms were established very early in the evolution of bacteria, although horizontal transfer may have also played an important role in the distribution of QS genes, at least within this group (Lerat & Moran, 2004).

maritimum NCIMB2154T obtained at 24 and 48 h using the

three E. coli JM109 lux-based biosensor strains carrying pSB536, pSB401 or pSB1075 to detect a wide range of AHLs differing in the length of their acyl chain. TLC analysis revealed the presence of short-chain AHLs using the E. coli JM109 pSB536 biosensor (Fig. 1). A search for AHL-type QS signals in extracts obtained from the culture media of another eight representative isolates of T. maritimum using the same technique revealed the presence of short-chain AHL activity in all of them, although differences were recorded in relation to their peak in activity (Table 1). LC-MS analysis confirmed the presence of N-butyryl-l-homoserine lactone (C4-HSL) in the culture media of T. maritimum NCIMB2154T grown in both FMM (Fig. 2) and MB (data not shown). This AHL was unequivocally identified by comparison LDE225 NVP-BGJ398 of its mass spectra with those of pure standards (Fig. 3). As this is the

first description of the production of AHLs by a pathogenic member of the CFB cluster, the analyses were carried out simultaneously in both laboratories using different chromatographic conditions. The results confirmed unequivocally the presence of the C4-HSL. So far, no physiological role other than as QS signals has been assigned to AHLs, except as a chelator, for tetramic acid (a derivative of 3-oxo-C12) or antibiotic activity for both 3-oxo-C12-HSL and tetramic acid (Kaufmann et al., 2005; Schertzer et al., 2009). In addition, a role as biosurfactant has been attributed to long-chain AHLs (Daniels et al., 2006). Therefore, even though the physiological features under the control of these molecules in T. maritimum remain to be investigated, the production of C4-HSL by T. maritimum strains extends the paradigm of AHL-mediated QS beyond the Proteobacteria. GBA3 As the physiological processes under the control of AHL-mediated QS have so far been described for a limited number of genera of the Alpha-, Beta- and Gammaproteobacteria, many

of them human or plant pathogens (Williams et al., 2007), the ecological significance of AHL-mediated QS has been questioned as a key switch controlling gene expression within bacterial populations in nature (Manefield & Turner, 2002). The fact that genera outside the Proteobacteria produce the same signal molecules, and that AHL-degrading activity has been found in Gram-positive, Gram-negative and Cyanobacteria (Dong & Zhang, 2005; Romero et al., 2008) and in mammalian cells (Chun et al., 2004), reinforces the ecological significance of AHL-mediated QS processes. The presence of AHL-mediated QS beyond the Proteobacteria is not surprising, as a phylogenetic study based on the LuxI/LuxR genes suggested that QS mechanisms were established very early in the evolution of bacteria, although horizontal transfer may have also played an important role in the distribution of QS genes, at least within this group (Lerat & Moran, 2004).