The micromanipulator

was cemented to the skull and a copp

The micromanipulator

was cemented to the skull and a copper mesh cone was built around the entire assembly, to both protect and electrically shield the headgear. During the post-surgery recovery period of 1 week, the probe was lowered gradually until it reached the CA1 pyramidal layer. The animals were then recorded in the maze for ∼30-min sessions, one or two sessions per day. During the recording sessions, a preamplifier (Plexon, Dallas, TX, USA) was connected to the probe’s output connector. For tracking the position of the animals, two small light-emitting diodes (5 cm separation) mounted selleck above the headstage were recorded by a digital video camera. A blue laser (473 nm; 60 mW; Aixiz) controlled by an analog input was used for ChR2 activation. The laser was collimated into a 6-m-long single-mode optical fiber (Thorlabs custom patch cable) using a fiberport (Thorlabs no. PAF-X-11-A). The other end of the optical fiber terminated in an LC connector, and connected to the optrode’s LC connector via an LC-to-LC adapter (Thorlabs no. ADALC1). Androgen Receptor Antagonist datasheet Before implantation,

the power of the laser at the tip of the optrode was measured with a power meter (no. 13PEM001; Melles Griot). The eNpHR (version 2.0)-GFP fusion protein was cloned into an AAV cassette containing the mouse synapsin promoter, a woodchuck post-transcriptional regulatory element (WPRE), SV40 polyadenylation sequence and two inverted terminal repeats. rAAV-FLEX-rev-eNpHR-GFP (Atasoy et al., 2008) was assembled using a modified helper-free system (Stratagene) as a serotype 2/7 (rep/cap genes) AAV, and harvested and purified over sequential cesium chloride gradients as previously described (Grieger et al., 2006). Using the same procedure as described for rats, the dorsal hippocampus of parvalbumin (PV)-Cre (Hippenmeyer et al., 2005) transgenic mice (3–5 weeks old) were injected (Fig. 3) at three sets of coordinates: 2.2, 2.4 and 2.7 mm posterior to bregma, and 2.1 mm from midline. Virus

(10–20 nL) was injected every 150 μm from 1.55 to 0.95 mm below pia. The pipette was held at 0.95 mm for 3 min before being completely retracted from the brain. Mice were prepared for chronic recordings Molecular motor and trained to run for water reward with their heads fixed via a mounted head-plate into a stereotaxic device. Under isofluorane anesthesia two small watch-screws were driven into the bone above the cerebellum to serve as reference and ground electrodes. A custom-fabricated platinum head-plate with a window opening above the left hippocampus was cemented to the skull with dental acrylic. After this surgery, the mice were trained for 3 days to be head-fixed, and then for 2 weeks to run on a custom-built treadmill with their head fixed (one 40-min session per day). A water reward was delivered through a licking port after every completed belt rotation. The recordings were performed 3–6 weeks after the virus injection.

In monkeys, only studies relevant to the issue of directional mot

In monkeys, only studies relevant to the issue of directional motor components of neglect will be discussed here. Both inactivation (Stein, 1976) and unilateral lesion (Faugier-Grimaud et al., 1985) of area 7 lead to increased inaccuracy of reaching and to longer reaction times for reaches to contralateral visual targets. In the first study, this effect was reported for both arms. In the latter, it was observed for monkeys using the contralesional

arm, and was more severe for movements toward contralateral rather than ipsilateral space. In one animal, an increase in RT was also observed for the ipsilesional arm, especially for movements directed to targets in the contralateral space. In this latter study (Faugier-Grimaud et al., 1985) the two limbs were tested each in GDC-0449 only one direction of movement, i.e., the right arm for leftward movements and the left arm for rightward ones. Therefore, it is difficult to conclude whether the prolongation of reaction time was related to the arm used or to the GDC-0068 in vivo direction of movement (toward or away from the side of the lesion). In any case, the impaired movements were mainly those directed to the target located in the contralesional space. An additional study (LaMotte & Acuña, 1978) reported a directional impairment of reaches to visual targets performed with the contralesional arm, in either

the presence or absence of visual guidance of movement. In fact, reaches towards targets in contralesional space were consistently hypometric as they were systematically misdirected toward the midline, as if the contralateral space was somehow ‘compressed’ or under-represented.

In this experiment, the lesion included both SPL and IPL. Finally, monkeys with unilateral lesions confined to area 7a (Deuel & Farrar, 1993) were observed to be reluctant, slow and inaccurate when reaching to moving targets only in the contralesional space, although they were able to detect and glance at them. Therefore, in both monkeys and humans Racecadotril IPL lesions severely impair the representation of directional motor information concerning action space. Understanding such representations was a necessary step toward understanding the directional movement disorders of neglect from a neurophysiological perspective. To this end, we will refer to recent studies of the dynamic properties of neurons in area 7a of the IPL of monkeys examined during the performance of several tasks aimed at assessing the relationships between neural activity and the direction of visually- and memory-guided eye–hand movements (Battaglia-Mayer et al., 2005, 2007). The tasks adopted in these studies were designed to reproduce in the laboratory set-up the forms of behaviour that are compromised by IPL lesions in neglect patients.

, 1995) or cometabolism of chrysene (Mueller et al, 1990; Boonch

, 1995) or cometabolism of chrysene (Mueller et al., 1990; Boonchan et al., 1998). Recently, Baboshin et al. (2008) reported o-hydroxyphenanthroic acid as the only metabolite

formed during the cometabolism of chrysene by Sphingomonas sp. VKM B-2434. However, their report was confined to cleavage of the first ring of chrysene only. No detailed investigations on chrysene degradation pathways have been reported. In this study, we propose a tentative GDC 0199 catabolic pathway consistent with the complete mineralization of chrysene on the basis of characterization of metabolites by chromatographic and mass spectral analysis as well as enzymatic evidence. Chrysene, 1-hydroxy-2-naphthoic acid, phenanthrene, NADH and NAD+ were purchased from Sigma-Aldrich (Steinheim, Germany). 1,2-Dihydroxynaphthalene, salicylate and catechol were procured from Lancaster Chemicals (UK). All chemicals used were of analytical grade. The bacterial strain capable of degrading chrysene was isolated from soil of the coal-powered Raichur Thermal Power Station, India, by enrichment culture methods. About 1 g of soil was added to 100 mL phosphate-buffered mineral salts (PMS) medium (Nayak et al., 2009) supplemented with 40 mg chrysene [added as R428 supplier a solution in dimethylformamide (DMF)] and 5 mg salicylic acid, and was incubated at 37 °C for 12

days on a rotary shaker at 180 r.p.m. The culture was then transferred to fresh PMS medium containing chrysene and incubated under either similar conditions. After several transfers (2 months) strain PNK-04 was isolated by plating on PMS medium with chrysene (10 mg dissolved in DMF and spread on the plate) as sole carbon source, and subsequent purification in Luria–Bertani agar. The bacterial strain was identified based on morphological and physiological data and 16S rRNA gene sequencing (Nayak et al., 2009). This culture has been deposited in the National Collection of Industrial Microorganisms (NCIM), Pune, India, with accession number NCIM 5309. Chrysene degradation

experiments were carried out by growing the strain in PMS medium with chrysene and monitoring the disappearance of chrysene by quantitative UV analysis. Experiments were conducted in triplicate. To increase the solubility of chrysene, a stock solution of chrysene was prepared in the minimum amount (80 mg mL−1) of DMF. The appropriate amount of filter-sterilized (0.2 μm; Millipore) stock solution of chrysene was introduced into a 250 mL flask containing 100 mL sterilized PMS medium to obtain 40 mg chrysene per flask. Chrysene-grown cells from late exponential growth phase (OD660 nm of 0.6) were used as inoculum (2%, v/v). Controls consisted of uninoculated samples, inoculated samples in the absence of carbon source and inoculated samples containing only DMF. Cultures and controls were incubated on a rotary shaker (180 r.p.m., 37 °C).

The authors would like to thank Dr Chris Morley, BVSc BSc (Hons)

The authors would like to thank Dr Chris Morley, BVSc BSc (Hons) MVPHMgt Ministry of Agriculture, New Zealand, for tracing the source of the Trichostrongylus from the sheep manure that was being used as an organic fertilizer in the salad garden. The authors state that they have no conflicts of interest to declare. “
“A Belgian traveler returning from Laos developed acute schistosomiasis. Feces microscopy and polymerase chain reaction (PCR) followed by sequence analysis revealed Schistosoma mekongi. Schistosome antibody test results and real-time PCR in serum were initially negative or not interpretable. A HRP-2 antigen test for Plasmodium falciparum and an

enzyme-linked immunosorbent assay (ELISA) antibody test for Trichinella yielded false-positive results. Schistosoma mekongi infection is exceptional in travelers. Even when diagnosis is suspected, 3-Methyladenine chemical structure confirming early stage infection may be complicated by insufficient sensitivity

of schistosome antibody assays and by (false) positive antigen and antibody assays against other pathogens. A 27-year-old male Belgian traveler developed low grade fever, night sweats, and cough soon after returning from a 4 months’ adventurous travel to Laos, Cambodia, and Yunnan province in south China. He had lost some weight but had neither diarrhea nor anorexia. He was a practicing vegetarian. He had, together with his girlfriend, visited the “Four Thousand Islands” (Si Pan Don) region, a conglomerate of islets situated in the Mekong River straddling the Laos–Cambodian border, 5 weeks prior. He reportedly took a daily swim in the Mekong River for www.selleckchem.com/products/sotrastaurin-aeb071.html 1 week (D0 = first day of exposure), as well as in a sandy old river bend with stagnant water at the southernmost part of Khong Island, called Don Det, on one occasion. He did not report swimming in rivers or ponds elsewhere during his travel. Symptoms started about 6 weeks after exposure (D45). The patient consulted his family physician 10 days later (D55) and was referred at the outpatient clinic of the Institute of Tropical Medicine,

Antwerp, Belgium (ITMA) 5 days thereafter (D60), when symptoms had already subsided. Clinical signs were unremarkable. Nutlin-3 chemical structure Ultrasound revealed a modest spleen enlargement, and the routine laboratory workup showed a marked hypereosinophilia (Table 1). Chest X-ray was normal. Two serum antischistosome antibody tests were performed at the initial and the subsequent visits: an in-house enzyme-linked immunosorbent assay (ELISA) using a Schistosoma mansoni antigen (mixture of egg and adult worm extract), and an indirect hemagglutination inhibition assay (IHA), using a S mansoni adult worm extract (ELI.H.A Schistosoma, ELITech Group, Puteaux, France), with titration and cut-off at 1/80 (positive at ≥1/160). Up to 15 weeks after exposure (D105), the IHA could not be interpreted because of the presence of antibodies reacting with sheep RBC in the patient’s serum.

7, P < 00001) This finding is contrary to our expectation of ha

7, P < 0.0001). This finding is contrary to our expectation of having the A allele associated with high trait values and is addressed further in the Discussion. Because age and body weight are identified as covariates

and sex has previously been found to influence hippocampal neurogenesis (Tanapat et al., 1999), we regressed the RMS linear density for each animal against these three variables and calculated the average residuals per strain. QTL mapping of variation in the adjusted Selleck Pexidartinib RMS linear densities generated a whole-genome scan LRS plot that resembled the plot produced from mapping with the unadjusted trait data (Fig. 6B). A prominent QTL is mapped to the distal end of chromosome 11 (Rmspq1) and the genetic markers, D11Mit103 and gnf11.125.992, are again associated with the highest LRS score (Fig. 6E). The B allele in this QTL interval increases trait value by ∼24 BrdU+ cells/mm,

suggesting that the removal of covariates could unmask an even greater genetic effect on phenotype. In additional to Rmspq1, another QTL is seen at the proximal end of Chr 2 at 25 ± 5Mb (genome-wide P < 0.63; LRS = 10.56; LOD = 4.61; Fig. 6B). Strains Erastin price having a B allele in this Chr 2 QTL interval is associated with an increase in linear density of ∼22 BrdU+ cells/mm compared with strains carrying the A allele (Fig. 6E). To further explore the robustness of Rmspq1 and determine whether

the mapping of this locus is confounded by differences in age, we mapped RMS linear density from animals that were 60–100 days old (n = 98). Mapping with a narrowed age Carbohydrate parameter located the same Chr 11 QTL on the distal end at 116.75 ± 0.75 Mb (see supplementary Fig. S3; Trait ID: 10157). We also mapped RMS linear density using only adult female mice (n = 83) and revealed a significant QTL mapped to the same Chr 11 region (see supplementary Fig. S3; Trait ID: 10155). These results provide additional evidence that age and sex do not significantly alter the identification of Rmspq1. The SGZ of the DG is another well-studied proliferative zone in the adult mammalian brain that contains a mixture of progenitors with limited self-renewal capacity (Seaberg & van der Kooy, 2002). We also examined the genetic architecture underlying the proliferative potential of these SGZ cells in comparison with the RMS. The average total number of BrdU+ cells was calculated in the SGZ of 27 AXB/BXA RI strains as described in the Materials and methods. After exposing to BrdU for 1 h, the C57BL/6J SGZ had higher numbers of BrdU-immunoreactive cells (52 ± 2) than that of A/J (29 ± 2.5) (Fig. 7A). This reversal in phenotypic direction was intriguing and suggested different alleles are regulating the proliferative potential of RMS and SGZ cell populations.

In conclusion, low CRF-R activation during lactation is an essent

In conclusion, low CRF-R activation during lactation is an essential prerequisite for the adequate occurrence of maternal behaviour. “
“Neuropeptide

S (NPS) regulates various biological functions by selectively activating the NPS receptor (NPSR). Recently, epidemiological studies revealed an association between NPSR single nucleotide polymorphisms and susceptibility to panic disorders. Here we investigated the effects of NPS in mice subjected to the elevated T maze (ETM), an assay which has been proposed to model anxiety and panic. Diazepam [1 mg/kg, BYL719 in vitro intraperitoneally (i.p.)] elicited clear anxiolytic effects reducing the latency to emerge from the closed to the open (CO) arm without modifying the latencies from the open to the closed (OC) arm. By contrast, chronic fluoxetine (10 mg/kg i.p., once a day for 21 days) selectively increased OC latency, suggesting a panicolytic-like effect. NPS given intracerebroventricularly at 0.001–1 nmol elicited both anxiolytic- and panicolytic-like effects. However, although the NPS anxiolytic dose–response curve displayed the classical sigmoidal shape, the dose–response Vemurafenib concentration curve of the putative panicolytic-like effect was bell shaped with

peak effect at 0.01 nmol. The behaviour of wild-type [NPSR(+/+)] and receptor knock out [NPSR(−/−)] mice in the ETM task was superimposable. NPS at 0.01 nmol elicited anxiolytic- and panicolytic-like effects in NPSR(+/+) but not in NPSR(−/−) mice. In conclusion, this study demonstrated that NPS, via selective activation of the NPSR, promotes both anxiolytic- and panicolytic-like actions in the mouse ETM. “
“The role for phosphorylated p38 mitogen-activated protein kinase [p-p38(MAPK)] in β-amyloid plaque deposition [a hallmark of Alzheimer’s

disease (AD) pathology] remains ambiguous. We combined immunohistochemistry and stereological sampling to quantify the distribution of plaques and p-p38(MAPK)-immunoreactive (IR) cells in the sensorimotor cortex of 3-, 6- and 10-month-old TgCRND8 mice. The Gefitinib ic50 aggressive nature of the AD-related human amyloid-β protein precursor expressed in these mice was confirmed by the appearance of both dense-core (thioflavin-S-positive) and diffuse plaques, even in the youngest mice. p-p38(MAPK)-IR cells of the sensorimotor cortex were predominantly co-immunoreactive for the Macrophage-1 (CD11b/CD18) microglial marker. These p-p38(MAPK)-IR microglia were associated with both dense-core and diffuse plaques, but the expected age-dependent increase in the density of plaque-associated p-p38(MAPK)-IR microglia was restricted to dense-core plaques. Furthermore, the density of dense-core plaque-associated p-p38(MAPK)-IR microglia was inversely correlated with the size of the core within the given plaque, which supports a role for these microglia in restricting core growth.

[5] In 2011, a national plan on integrated human surveillance of

[5] In 2011, a national plan on integrated human surveillance of imported and autochthonous vector-borne disease (CHIKV, DENV, and West Nile disease) was issued.[10] Integrated human and entomological surveillance is crucial to monitor the spread of emerging vector-borne diseases and to implement public health measures in order to avoid transmission and control such diseases in humans.

Moreover, establishing an integrated surveillance could be valuable also to rapidly identify the risk of introduction of new vector-borne diseases in Europe, with the most obvious candidates being CHIKV[16] and DENV,[17] not forgetting also malaria.[18] The authors thank all colleagues from the regional and local Health Services for providing data on Chikungunya/Dengue click here imported cases: Finarelli A (Emilia Romagna); Gallo L (Friuli Venezia Giulia); Vitagliano A (Lazio); Palumbo A, Gramegna M (Lombardia); Audenino M XL184 datasheet (Piemonte); Prato R, Quarto M (Puglia); Palermo M (Sicilia); Balocchini E, Pecori L (Toscana); Sudano L (Valle D’Aosta); Russo F, Zanella F (Veneto). We also thank Dott.ssa Flavia Riccardo for her support with Capstats database management and the Italian Ministry of Health Special Surveillance project (Grant no. 1M61) for

funding. The authors state they have no conflicts of interest to declare. “
“In most years varicella is the vaccine-preventable disease most frequently reported to Centers for Disease Control and Prevention (CDC) by cruise ships. Since 2005, CDC has received numerous isolated case reports of varicella among crew members and has investigated varicella outbreaks aboard vessels sailing into and from US seaports. CDC investigators reviewed electronic varicella case reports from 2005 to 2009 and outbreak reports from 2009 to characterize the response and control efforts implemented by cruise ships in accordance with CDC protocols. Outbreak reports from 2009 were manually reviewed for details of case identification, contact investigations, isolation VAV2 and restriction of cases and contacts, respectively, and number of contacts administered varicella

vaccine post-exposure by cruise lines. During 2005 to 2009, cruise ships reported 278 cases of varicella to CDC among predominantly male (80%) crew members, three-quarters of whom were residents of Caribbean countries, Indonesia, the Philippines, or India, and whose median age was 29 years. Cases were more commonly reported during spring and winter months. During 2009, cruise ships reported 94 varicella cases among crew members of which 66 (70%) were associated with 18 reported varicella outbreaks. Outbreak response included isolation of 66 (100%) of 66 cases, restriction of 66 (26%) of 255 crew-contacts, and administration of post-exposure vaccine to 522 close contacts and other susceptible crew members per standard CDC recommendations.

Similarly, SC glucose sensors which have become part of some inte

Similarly, SC glucose sensors which have become part of some integrated CSII systems rely on the difference between SC glucose and BG being proportional to the rate of change taking

place in BG;9 this time lag limits the sensitivity of continuous glucose monitors to detect hypoglycaemia; algorithms can be produced to mitigate this where there are sufficient data from sequential readings to give the BG/time gradient. Intraperitoneal insulin infusion offers a more physiological route for insulin delivery RG7422 datasheet devices, producing greater porto-systemic and hepatic insulin gradients, and controls hepatic glucose metabolism more efficiently. Recent research10,11 in our laboratory has focused on producing an implantable insulin delivery device (INSmart) which would deliver insulin to the peritoneum in an automated fashion linked to changing glucose levels (Figures 1a and b). INSmart delivers insulin via a glucose-sensitive gel which acts as

both a sensor selleck compound and controller of the amount of insulin released (Figure 1c). The glucose-sensitive gel comprises polymerised derivatives of dextran and a glucose-sensitive lectin, concanavalin A. The highly viscous gel that forms due to the equilibrium binding between the dextran and the lectin binding sites impedes insulin release. This changes in the presence of glucose as the binding sites are disrupted resulting in a reduction in the viscosity of the gel that facilitates insulin MRIP release. This process is both reversible and repeatable, being sensitive to the changes in glucose levels that occur in the peritoneal cavity. The gel layer is therefore both the sensor and the delivery port in this design and contains no electronics or moving parts. The benefits of an INSmart device for the treatment of diabetes are that it could provide automated control preventing hypoglycaemia and also the long-term harm from hyperglycaemia. However,

the associated risks from an implantable device could arise from surgery, leakage of the insulin reservoir and infection. A prototype design was used to demonstrate the feasibility of this novel approach by restoring normoglycaemia in diabetic rats12 and pigs13 for up to five weeks but would require some redesign to provide it with biocompatibility, reliability and security to be optimal for clinical use. In designing a clinically-testable prototype it is important to understand the needs of the market, i.e. potential users, and to assess their reaction to it. To gain these insights it was decided to conduct a survey of current users of CSII. We surveyed CSII users to determine their current approach to glucose management and their appreciation of its importance, and to understand the practical difficulties of achieving desired control with their current pump therapy.

[6] Hanlon et al[7]

in the UK have made a case for a ‘fi

[6] Hanlon et al.[7]

in the UK have made a case for a ‘fifth wave’ check details in public health concerned with the problems of obesity, social inequalities, and loss of well-being. The first wave of public health responses improved public health after the industrial revolution; the second wave impacted public health based upon the scientific method and subsequent discoveries; the third wave emanated from the implementation of the UK National Health Service and the fourth wave was influenced by medical care interventions affecting mortality.[7] Hanlon et al.[7] view obesity as something that can be treated by impacting the secondary clinical consequences of obesity, a task that they view as very expensive and not dealing with an underlying problem. Hanlon et al.[7] view the impact upon the unhealthy, societal acceptance of obesity as ‘normal’ as the key focal point for change. Changing the view of obesity will entail a complete shift in how societies view the issue of obesity to one examining root causes that have commercial and social impacts.[7] George et al.[8] suggest that there are opportunities to extend weight management Screening Library research buy services from community pharmacies, but findings from a study they conducted in 2010 indicate that expectations on the part of the public will need to be altered for acceptance. Pharmacists can play a

much more active role in dealing with the public health problem of obesity and overweight. There remains a need to produce evidence ADAMTS5 from pharmacy practice research for the benefit of pharmacists’ involvement in directed obesity and overweight patient counselling, pharmacist-directed weight management protocols and the impact of these research endeavours on patient outcomes. Research can inform practice and provide for a much more proactive involvement for pharmacists’ interventions. Pharmacists can serve as a public health resource providing information and referrals for help for patients. Pharmacists can, at every

visit, calculate BMIs and counsel patients with elevated BMIs regarding the continuing and potentials risks associated with high BMIs and the negative influence elevated BMIs has upon the therapeutic options provided by medications to treat chronic conditions.[9] Pharmacists can collaborate with other health professionals within a medical home[10] and/or primary care practice to share information with other providers and the patients on means to help patients take advantage of self-help options available. Within professional societies and organizations, pharmacists can collaborate locally, regionally, nationally and internationally to focus other professional and the pharmacy profession’s attention towards the problem of obesity and overweight and keep this dramatic public health concern in the spotlight.

[6] Hanlon et al[7]

in the UK have made a case for a ‘fi

[6] Hanlon et al.[7]

in the UK have made a case for a ‘fifth wave’ selleck compound in public health concerned with the problems of obesity, social inequalities, and loss of well-being. The first wave of public health responses improved public health after the industrial revolution; the second wave impacted public health based upon the scientific method and subsequent discoveries; the third wave emanated from the implementation of the UK National Health Service and the fourth wave was influenced by medical care interventions affecting mortality.[7] Hanlon et al.[7] view obesity as something that can be treated by impacting the secondary clinical consequences of obesity, a task that they view as very expensive and not dealing with an underlying problem. Hanlon et al.[7] view the impact upon the unhealthy, societal acceptance of obesity as ‘normal’ as the key focal point for change. Changing the view of obesity will entail a complete shift in how societies view the issue of obesity to one examining root causes that have commercial and social impacts.[7] George et al.[8] suggest that there are opportunities to extend weight management GSK2118436 datasheet services from community pharmacies, but findings from a study they conducted in 2010 indicate that expectations on the part of the public will need to be altered for acceptance. Pharmacists can play a

much more active role in dealing with the public health problem of obesity and overweight. There remains a need to produce evidence MYO10 from pharmacy practice research for the benefit of pharmacists’ involvement in directed obesity and overweight patient counselling, pharmacist-directed weight management protocols and the impact of these research endeavours on patient outcomes. Research can inform practice and provide for a much more proactive involvement for pharmacists’ interventions. Pharmacists can serve as a public health resource providing information and referrals for help for patients. Pharmacists can, at every

visit, calculate BMIs and counsel patients with elevated BMIs regarding the continuing and potentials risks associated with high BMIs and the negative influence elevated BMIs has upon the therapeutic options provided by medications to treat chronic conditions.[9] Pharmacists can collaborate with other health professionals within a medical home[10] and/or primary care practice to share information with other providers and the patients on means to help patients take advantage of self-help options available. Within professional societies and organizations, pharmacists can collaborate locally, regionally, nationally and internationally to focus other professional and the pharmacy profession’s attention towards the problem of obesity and overweight and keep this dramatic public health concern in the spotlight.