AMS is generally not related to gender, training, alcohol intake, or cigarette smoking.[31] Smoking may represent some kind of acclimatization to hypoxia and is associated with a slightly decreased risk to develop AMS.[34] However, in addition to all the well-known negative health effects, smoking will also impair long-term altitude acclimatization and

lung function.[34] Persons suffering from hypertension, coronary artery disease, and diabetes do not appear to be more prone to AMS than healthy persons.[11, 35] Richalet and colleagues recently documented in a large sample of mountaineers that a low selleck chemicals llc ventilatory response to hypoxia at exercise and marked desaturation at exercise in hypoxia are strong risk factors for high-altitude illness.[29] Similarly, Epigenetics inhibitor pronounced arterial oxygen desaturation during sleep has been suggested to be an important risk factor for the development of AMS.[10] Periodic breathing typically occurs during sleeping at high altitudes and may be advantageous up to about 3,000 to 3,500 m because oxygen saturation is stabilized at a relatively high level.[36] At altitudes up to 5,000 m, periodic breathing even appears to override the negative feedback loop in patients with risk of sleep-disordered breathing leading

to revolving sleep apneas. Between 4,500 and 5,500 m altitudes, periodic breathing is replaced by high-frequency breathing driven directly by hypoxia-sensitive neurons in the brain stem.[20] However, at Adenylyl cyclase higher altitudes,

frequent arousals cause total sleep deprivation and mental and physical impairments.[36] Patients with AMS can develop HACE when SaO2 further drops, for example, by further ascent or when additionally HAPE occurs.[37] Therefore, further ascending with AMS or existing HAPE are risk factors for HACE, which is thought to be a progression of AMS representing the final encephalopathic, life-threatening stage of cerebral altitude effects.[7, 11, 37] One risk for the development of HAPE relates to individual susceptibility.[3] A genetic predisposition may lead to an exaggerated pulmonary vascular response to hypoxia and as a consequence to pulmonary hypertension.[3, 12] Pulmonary hypertension is the hallmark in the development of the disease,[12] but also other genetic defects might contribute to the pathogenesis (eg, defect of the transepithelial sodium transport[12]). Additionally, a large patent foramen ovale in the heart may contribute to exaggerated arterial hypoxemia and facilitate HAPE at high altitude.[38] Other individual risk factors include hypothermia as well as anatomical or functional abnormalities (eg, having only one lung) facilitating pulmonary hypertension.[12] Finally, men may be more susceptible to HAPE than women, although the mechanisms are probably multifactorial.

6.3.4.2 Serology. Commercial tests that use complement fixation are not type-specific. Seroconversion from a zero baseline is usually diagnostic of a primary infection. In the case of recurrent infection, an immune response from a non-zero baseline may be detected. However, these tests cannot distinguish between initial and recurrent infections and have been replaced by sensitive tests such as ELISAs and RIAs. Type-specific serology tests (TSSTs) that detect HSV-specific glycoprotein G2, which is specific to HSV-2, and glycoprotein G1, which is specific to selleck chemical HSV-1 infection, are the only commercially available diagnostic tools to identify individuals with asymptomatic HSV infection, and can effectively

distinguish HSV-1 and HSV-2 with high sensitivities (80–98%) and specificities (≥96%) [58]. Case-controlled studies have shown that there are certain clinical situations where these tests may provide an aid to the diagnosis of HSV infection [59,60]. The clinical diagnosis of genital HSV infection has a low sensitivity and specificity; laboratory confirmation of infection and typing of HSV is essential as it influences

the management, prognosis and counselling of patients. 6.3.4.3 CNS disease. In patients with HSV encephalitis or meningitis, typical CSF findings include a lymphocytosis and mildly selleck compound elevated protein [61,62]. Low CSF glucose levels may also occur. Abnormal findings on magnetic resonance imaging and electroencephalogram are supportive of a diagnosis of HSV encephalitis but not diagnostic. For both HSV meningitis and encephalitis, PCR detection of HSV DNA in the CSF is the diagnostic method of choice and has a high specificity and sensitivity [62,63]. For HSV encephalitis, false-negative results for PCR may occur within the first 72 h of the illness and then

10–14 days after the onset of symptoms. Incidence of false-positive PCR is extremely low. Culture of the CSF for HSV is of little value in HSV encephalitis and not recommended. PCR for HSV DNA in the CSF is the diagnostic method of choice for diagnosis of HSV encephalitis or meningitis (category III recommendation). First episode or severe recurrent orolabial herpes infection should be treated with antiviral therapy. Aciclovir 200–400 mg orally five times a day for 7–10 days is recommended (category either II recommendation), Alternative treatments are valaciclovir or famciclovir. For severe oral mucocutaneous disease treatment should be initiated with aciclovir intravenously 5–10 mg/kg every 8 h (category III recommendation). Most episodes of recurrent orolabial herpes are mild and self limiting. Episodic or suppressive antiviral therapy may be considered for those with severe or frequent recurrences. A study has shown equivalent efficacy of famciclovir 500 mg orally bd in comparison to aciclovir 400 mg orally five times a day in a mixed group of HIV-seropositive individuals with either orolabial (38%) or genital HSV [64].

6.3.4.2 Serology. Commercial tests that use complement fixation are not type-specific. Seroconversion from a zero baseline is usually diagnostic of a primary infection. In the case of recurrent infection, an immune response from a non-zero baseline may be detected. However, these tests cannot distinguish between initial and recurrent infections and have been replaced by sensitive tests such as ELISAs and RIAs. Type-specific serology tests (TSSTs) that detect HSV-specific glycoprotein G2, which is specific to HSV-2, and glycoprotein G1, which is specific to ABT 888 HSV-1 infection, are the only commercially available diagnostic tools to identify individuals with asymptomatic HSV infection, and can effectively

distinguish HSV-1 and HSV-2 with high sensitivities (80–98%) and specificities (≥96%) [58]. Case-controlled studies have shown that there are certain clinical situations where these tests may provide an aid to the diagnosis of HSV infection [59,60]. The clinical diagnosis of genital HSV infection has a low sensitivity and specificity; laboratory confirmation of infection and typing of HSV is essential as it influences

the management, prognosis and counselling of patients. 6.3.4.3 CNS disease. In patients with HSV encephalitis or meningitis, typical CSF findings include a lymphocytosis and mildly find more elevated protein [61,62]. Low CSF glucose levels may also occur. Abnormal findings on magnetic resonance imaging and electroencephalogram are supportive of a diagnosis of HSV encephalitis but not diagnostic. For both HSV meningitis and encephalitis, PCR detection of HSV DNA in the CSF is the diagnostic method of choice and has a high specificity and sensitivity [62,63]. For HSV encephalitis, false-negative results for PCR may occur within the first 72 h of the illness and then

10–14 days after the onset of symptoms. Incidence of false-positive PCR is extremely low. Culture of the CSF for HSV is of little value in HSV encephalitis and not recommended. PCR for HSV DNA in the CSF is the diagnostic method of choice for diagnosis of HSV encephalitis or meningitis (category III recommendation). First episode or severe recurrent orolabial herpes infection should be treated with antiviral therapy. Aciclovir 200–400 mg orally five times a day for 7–10 days is recommended (category many II recommendation), Alternative treatments are valaciclovir or famciclovir. For severe oral mucocutaneous disease treatment should be initiated with aciclovir intravenously 5–10 mg/kg every 8 h (category III recommendation). Most episodes of recurrent orolabial herpes are mild and self limiting. Episodic or suppressive antiviral therapy may be considered for those with severe or frequent recurrences. A study has shown equivalent efficacy of famciclovir 500 mg orally bd in comparison to aciclovir 400 mg orally five times a day in a mixed group of HIV-seropositive individuals with either orolabial (38%) or genital HSV [64].

Plates were then incubated anaerobically at 37 °C for 48–72 h. Transformants were cultivated on cMRS

supplemented with chloramphenicol at a final concentration of 3 μg mL−1. DNA was extracted from colonies using GeneReleaser (BioVentures), and the AZD8055 ic50 presence of pNZ8048 in transformants was confirmed by PCR using the primers pNZFw (5′-TTTGCAGCGAAGATGTTGTC-3′) and pNZRv (5′-CTATAGCTAACGCCGCAACC-3′) targeting DNA regions on this plasmid. The transformation efficiency was calculated according to the following formula: Transformation experiments were performed in triplicate. Transformants were inoculated into fresh broth in the presence of chloramphenicol and grown for 24 h. These cultures were then screened for plasmid Selleckchem BI 6727 content prior to the start of the experiment to ensure that plasmid pNZ8048 was present.

Cultures were then diluted (1%) in fresh broth without chloramphenicol, followed by continuous subcultivation for 15 days by dilution into fresh broth every 24 h in the absence of antibiotic selection. To determine plasmid stability, at least 50 colonies from each tested transformant were transferred to cMRS agar plates with or without chloramphenicol (3 μg mL−1). Growth of these colonies was monitored following 24 h of incubation, and plasmid extractions were performed where relevant. All animals used in this study were cared for in compliance with guidelines established by the Italian Ministry of Health. All procedures were approved by the University of Parma, as executed by the Institutional Animal Care and Use Committee (Dipartimento per la Sanità Pubblica Veterinaria, la Nutrizione e la Sicurezza degli Alimenti Direzione Generale della Sanità Animale e del Farmaco Veterinario). Two groups, each containing six animals of 3-month-old

female BALB/c mice, were orally inoculated with bacteria or with water. Bacterial colonization was established by five consecutive daily administrations whereby each animal received 20 μL of 109 mL−1 of cells using a micropipette AMP deaminase tip placed immediately behind the incisors (Sleator et al., 2001). Bifidobacterial inocula were prepared by growing B. bifidum PRL2010 containing pNZ8048 anaerobically overnight at 37 °C in cMRS broth containing 3 μg mL−1 chloramphenicol. Cultures were harvested by centrifugation (950 g for 8 min), washed, and resuspended in 100 μL of water. The viable count of each inoculum was determined by retrospective plating on cMRS containing the antibiotic. To estimate the number of B. bifidum PRL2010 cells per gram of feces, individual fecal samples were weighed and followed by serial dilution and culturing on selective cMRS agar with chloramphenicol. Following enumeration of B.

44, p = 0.001). The increases in the maximum temperature had no significant effect on the attack rate. In contrast to the rates for ETEC, the rates of EAEC-associated diarrhea remained relatively constant despite seasonal temperature variations (p = 0.1). TD is caused by a variety of bacterial agents of which ETEC and EAEC are the most common identifiable pathogens.1

In agreement with the previously published studies on TD acquired in Guadalajara, Mexico from 1986 to 19899, this see more study found that the rates of TD were higher during summertime when compared to wintertime in central Mexico. This second study was conducted in Cuernavaca, Mexico, which is called “the city of eternal springtime” where temperature variations are milder. The warmer and wetter summer months are associated with an increased occurrence of diarrhea.12 Warmer climates may encourage propagation of enteric bacterial pathogens in food13 and water14 explaining the increase in bacterial diarrhea during Volasertib molecular weight the summertime. Furthermore, in the case of ETEC, seasonality also appears to influence the rates of identified toxin phenotypes. It has previously been suggested that in Egypt, ST (heat-stable toxin)-producing ETEC strains are more commonly identified in the stools of children with diarrhea in the summer, whereas LT

(heat-labile toxin)-producing ETEC strains are identified all year around.15 In our study, the rates of LT- and ST-producing ETEC did not appear to vary according to seasonality. In this study, we found that minimum and average temperatures are positively associated to higher rates of ETEC-associated diarrhea. We hypothesize that since weekly maximum temperatures do not fluctuate as much as minimum temperatures, Fossariinae the analysis failed to show a statistical correlation with maximum temperatures. When studied in the univariate analysis, the identification of STEC as defined by the

presence of stx1 or stx2 in stools also showed a positive correlation with warmer temperature and summertime diarrhea, however only ETEC showed a significant correlation when an adjusted multivariate analysis was performed. An important observation in this study is that in contrast to ETEC, the rates for EAEC, the second most common bacterial cause of TD, remained similar in both seasons. This is consistent with a previous study carried out in Korea that failed to find a seasonal pattern for EAEC infection16 and contrasts with a 12-month study in a US pediatric population, where Cohen and colleagues reported a seasonal peak of EAEC in children during March to April months; However, a confounding variable in that study was that many of the EAEC cases were coinfected with Rotavirus.4 Although EIEC was only identified in the summer, additional studies are needed to determine if the occurrence of EIEC infection is also seasonal.

Microorganisms eluted from the day 1 samples were spread on Luria–Bertani agar plates and incubated at 25 °C for 5 days to enrich the culturable strains as much as possible. Loopfuls of inoculum from the plates were then grown in shake flasks in 100 mL of MSM with 400 mg L−1 dichlorvos as the sole carbon source. A suitable control was set using the same medium containing 400 mg L−1 of dichlorvos without inoculum. After cultivation for 2 days, 1 mL of the supernatant was collected and analysed for its dichlorvos concentration by HPLC. The isolates of dichlorvos-degrading bacteria are available upon request from the

corresponding author. Total DNA of the microbial pellets from the controls and treated samples of experiment 1 and pure cultures of the

isolates were selleck chemicals selleckchem extracted with the method of Zhou et al. (1996). The PCR universal primer pair PRBA338f and PRUN518r (Øvreås et al., 1997) was used to amplify the bacterial V3 region of the 16S rRNA genes, and PRBA338f with a GC clamp was used for DGGE (Muyzer et al., 1993). The 16S rRNA genes of the pure isolates were amplified by PCR using the universal primers 27F and 1492R (Lillo et al., 2006). All the PCR products were confirmed by agarose gel electrophoresis and staining with ethidium bromide. DGGE was performed with the Dcode™ universal mutation detection system (Bio-Rad). The PCR products (40 μL) were loaded onto a 10% w/v acrylamide gel (acrylamide/bis solution, 37.5 : 1; Amresco) containing a linear chemical gradient ranging from 30% to 60% denaturant (where the 100% denaturing solution contained 7 M urea and 40% v/v formamide). The electrophoresis was run for 16 h at 60 °C at 100 V in 1 × TAE buffer. Aprepitant The gel images

were transformed into digital data using quantity one from Bio-Rad. The DNA isolated in experiment 1 from the control and treated samples on days 0 and 1 were used as the templates to amplify the complete 16S rRNA genes with primers 27F and 1492R, as described above. The products were purified and cloned into the pGEM-T Easy vector (Promega) and then transformed into competent Escherichia coli DH5α cells. The inserts were PCR amplified from randomly selected colonies using the T7 forward and SP6 reverse primers. The resulting library of PCR products was sequenced (Beijing Aoke Biotechnology Co. Ltd) based on different restriction fragment length polymorphism genetic profiles using the RsaI restriction enzyme. The DNA bands of interest were excised from the DGGE gel. The gel slices were placed into microcentrifuge tubes and the DNA was eluted at 37 °C for 2 h in sterile distilled water by allowing it to passively diffuse into the water. The eluted DNA was further amplified using the primers PRBA338f and PRUN518r, as described above.

Following approval from the University’s Malaysia campus ethical committee, a cross sectional survey was designed to capture student views of the dyspepsia module, in particular their experiences selleck kinase inhibitor of the integrated content. The questionnaire

primarily comprised closed questions with attitudes being explored using 5-point Likert scales, together with some open questions about students’ likes and dislikes in the module. The questionnaires were distributed by an MPharm 4 research student during the final module lecture and students were given time to complete the questionnaire in class. Data analysis used SPSS version 20 to determine frequency counts with percentages. A total of 89 completed questionnaires were received (response rate=94%); 79% (n = 70) of respondents were female and 63% (n = 56) were aged 18–20 years. 100% of respondents felt (strongly agreed or agreed) that the module

content linked together effectively and provided an integrated description of dyspepsia and its treatment. 97% (n = 86) felt that the focus in the module on the Drug, Medicine and Patient had facilitated their learning and 90% (n = 80) felt this had enhanced their selleck screening library enjoyment of the module. 85% (n = 76) felt that the integration had helped their understanding of their future role as a pharmacist. A small proportion of students (7%, n = 6) reported that they would prefer to study science Ribonucleotide reductase and practice in separate modules (thus allowing them to integrate the content in their own way) and (21%, n = 19) struggled to understand the links between the content in the module. However 49% (n = 44)

strongly agreed or agreed that they found it challenging to use their science when interacting with patients. Our results show that the novel DMP approach to integration has provided a positive educational experience for students within the dyspepsia module, however these results are limited in that students did not have other experiences of learning at university to compare with this approach. These results support the view that pharmacy educators should not place the burden on students to integrate large volumes of information themselves,1 but instead should design new teaching and curricular approaches to support integrative learning.2 Although integration has been successful in the dyspepsia module, the mechanisms by which students make connections between science and practice still needs further investigation, to enable us to understand the reasons why students found it challenging to use their science when interacting with patients. 1. Ratka A. Integration as a paramount educational strategy in academic pharmacy. Am J Pharm Educ 2012; 76(2): Article 19. 2. Pearson ML, Hubball HT. Curricular integration in pharmacy education. Am J Pharm Educ 2012; 76(10): Article 204. H. Hull, P. S.

781 ln[gamma-glutamyl transpeptidase (GGT) (UI/L)]+3.467 ln[age (years)]−0.014 [cholesterol (mg/dL)]. If the FI is ≥6.9, patients can be considered to have F≥2, with a PPV of 94% according to one study [9] and 100% according to another study [13]. The low cut-off of FI <4.2 was found to be inaccurate to exclude F≥2 [9,13]. Continuous variables are expressed as median (Q1–Q3) and Erastin purchase the categorical variables as numbers (percentage). Continuous variables were compared using the Student’s t-test or the Mann–Whitney U-test when appropriate. Categorical variables were compared using the χ2 test with Yates

correction or Fisher’s test when appropriate. The predictive accuracy of the APRI and Forns index was tested by measuring the areas under the receiver-operating-characteristic curves (AUROCs). The diagnostic accuracy was calculated on the basis of sensitivity (S), specificity (Sp), PPV and negative predictive value (NPV). F≥2 was considered as the disease. The predictive and diagnostic accuracy of the indexes was also tested in the group of patients with larger liver biopsies. The statistical analysis was carried out using the spss 15 statistical software package (SPSS, Chicago, IL, USA). The study was performed according to the Helsinki

declaration and was approved by the Ethics committee of Hospital Germans Trias i Pujol. The GRAFIHCO study recruited 8829 patients. An LB was performed in 1701 selleckchem (19%) of them. Five hundred and nineteen (31%) of the patients with LB fulfilled the inclusion criteria for the present study. The main characteristics of the patients included in this subanalysis compared with the patients included in the GRAFIHCO study are summarized in Table 1. Regarding the 519 individuals selected as the G protein-coupled receptor kinase study group, HCV genotype was one in 300 patients (58%), two in four (1%), three in 105 (20%), four in 101 (20%) and not available in nine (1.7%). Two hundred and sixty-four patients (51%) were staged as F≥2 in the LB (Table 2). Sixty-three patients (12%) were not receiving antiretroviral therapy at their last clinical visit.

The AUROC (95% confidence interval) of the APRI was 0.67 (0.66–0.71) and that of the FI was 0.67 (0.62–0.71). The LB length was recorded in the case report form in 193 patients (37%). One hundred and twenty (62.2%) of them had biopsy specimens ≥15 mm. The characteristics of these patients are displayed in Table 2. The two indexes had similar predictive accuracy in the subgroup of patients with recorded biopsy length ≥15 mm and in the global study group. The AUROC (95% confidence interval) of the APRI was 0.66 (0.56–0.76) and that of the FI was 0.66 (0.56–0.77) for patients with biopsy size ≥15 mm (Fig. 1). Applying the APRI, 111 (44%) of 255 individuals with F0 or F1 in the biopsy were correctly classified using the cut-off value <0.5 (Table 3). Among the 168 patients with APRI<0.5, 57 (34%) showed F≥2.

, 2007). We found that pfm also influences bacterial adherence. As shown in Fig. 1, the number of wild-type PA68 bacteria adhering to the surface of human lung cell line A549 was significantly (P < 0.001) higher than that of mutant strain I69. The I69 complemented with a plasmid pDN18 encoding pfm (strain I69C) recovered much of the lost adherence (P < 0.001). These results indicated that pfm affects bacterial adherence to the host cells. To further test the role of pfm on the bacterial adherence, we performed a microarray assay to obtain transcriptional profiles of wild-type PA68 and the isogenic pfm mutant Dabrafenib price strain I69. Most strikingly, all the genes of the flp-tad-rcp gene cluster were severely

downregulated in the I69 (Table 1). The flp-tad-rcp gene cluster is well known to be required for the assembly of type IVb pili that are responsible for the bacterial adherence (de Bentzmann et al., 2006). Therefore, the dramatic impact of pfm on the flp-tad-rcp gene cluster is the most likely reason for the decreased bacterial adherence of the pfm mutant strain I69. Interestingly, most of genes in the flp-tad-rcp gene

cluster were reported to be quorum-activated genes, including PA4296, PA4297, PA4298, PA4300, PA4302, PA4304, PA4305, and PA4306 (Schuster et al., 2003). Furthermore, focusing Proteasome function on the genes whose transcriptional level had been changed more than twofold with confidence level higher than 99.5%, we found that the majority of those genes had previously been reported as the quorum-controlled genes, including those upregulated genes as well as downregulated genes as shown in Table S1 and Table S2. The results showed that with the exception

of those genes whose confidence degree was < 99.5%, almost all quorum-activated genes reported in the previous report were downregulated Vildagliptin in the pfm mutant (Table S1; Schuster et al., 2003). Conversely, all quorum-repressed genes were upregulated (Table S2). These results suggested that the product of the pfm gene might affect bacterial adherence through the QS system. To further explore whether pfm affects the QS system of P. aeruginosa, we determined the production of AHLs that contain both the signaling molecules 3O-C12-HSL and C4-HSL. The amount of AHLs can be reflected with the biosensor strain JB525, which harbors a plasmid encoding GFP under the control of the AHLs responsive promoter (Wu et al., 2000). Pseudomonas aeruginosa cultures were pelleted, and the supernatants were used as the AHL sources to incubate with the indicator strain JB525. The GFP fluorescence intensity was then determined (‘Materials and methods’). As shown in Fig. 2, the fluorescence intensity of the pfm mutant strain I69 was about twofold lower compared to that of the wild-type strain PA68. The I69C strain, a complemented strain, partially recovered the decreased fluorescence of I69.

60; 95% CI 2.55–12.29) with insignificant differences when comparing pre-travel diarrhea and TD. Experiencing multiple diarrheal attacks raised the IBS risk sixfold (OR 6.01; 95% CI 2.02–17.89) when controlled for gender, age, and an adverse life event. Concordant within all the above analyses, the risk for IBS while having experienced an adverse life event within the past 12 months was about threefold increased. For the sensitivity analysis, the results of the multiple logistic regression conducted on the total study population were compared

with the results conducted on each half and the same independent risk factors were found. For a 3-month post-travel selleck chemicals llc follow-up a lower overall 3-month IBS incidence rate (0.9%; 95% CI 0.5–1.3; n = 22) was detected and the corresponding overall travel-duration-related IBS incidence for any 2-week stay was 0.6% (95% CI 0.3–0.9). The majority of IBS patients were classified as mixed IBS-M (also the majority with TD on index travel, two cases of IBS-D group with TD on

index travel) (31, 81.6%), four patients (10.5%) as diarrhea-predominant IBS-D, and three (7.9%) as constipation-predominant IBS-C. Seventeen (44%) patients sought medical care, 10 of them selected a physician of their choice and the remaining 7 visited the Gastroenterology Outpatient Clinic at the University Hospital. Three of these seven patients were diagnosed with IBS, one patient was diagnosed with lactose intolerance, Blastocystis hominis was found in one patient. One patient experienced prolonged TD and one did not show up. Tofacitinib purchase Two of medroxyprogesterone the three patients who obtained a gastroenterologist’s diagnosis had IBS, while one was infested by Ascaris

lumbricoides. This is the first large prospective cohort study that used the Rome III criteria to evaluate IBS among travelers to resource-limited destinations on various continents. Our data are comparable to the publications which used Rome II criteria, as in these the follow-up period was limited to 6 months, as in Rome III, which uses exactly the same questions. New onset of IBS assessed 6 months post-travel has occurred overall in 1.5% of subjects while 3.0% had TD-related pIBS. Our IBS incidence rates are in the same range as the ones found in general population of 0.2% to 7% per year, but below the pIBS rates of 4% to 36%15,16 or 4% to 14% reported for TD-related pIBS.18–20 The TD attributable risk difference of 2.3% is similar to the 2.6% reported in the smaller initial Ilnickyj study.20 Our lower IBS rates among travelers may be explained by separating pre- from in-travel diarrheal episodes and by the more stringent exclusion criteria, having for instance detected 189 cases with preexisting (un)-diagnosed organic or FGID (Rome III) at recruitment. In addition, the destinations and the study populations differed, eg, we included also senior citizens and not just students.