Immediately prior to use, whilst on the surface, the probe was ch

Immediately prior to use, whilst on the surface, the probe was checked by reference to a proprietary standard solution (redox potential of 125 mV, Russel pH Ltd). Redox measurements were taken by inserting the probe into the sediment to a depth of 80 mm. The sediment depth of 80 mm was chosen for four reasons: (1) previous research had indicated that the pre-deployment (baseline) sediment at the reef-site was oxic at this sediment-depth (

Wilding and Sayer, 2002), (2) that achieving very accurate depth penetration by the probe was difficult underwater meaning the errors were proportionately less the greater the sediment-penetration-depth, (3) TAM Receptor inhibitor that at 80 mm the probe could be left standing, unassisted, in the sediment until the reading had stabilised thus eliminating diver-caused probe shake and (4) as per the recommendation given in Pearson and Stanley (1979) for between-station comparisons. Between measurements, on the same dive, the probe was cleaned by shaking it in the surrounding seawater until a highly positive reading was observed. Where necessary any phytodetrital material was moved to one side prior to inserting the probe. Reported probe readings were adjusted to the hydrogen scale by the addition of 198 mV ( Zobell, 1946) and adjusted for temperature

( SEPA, 2005). Water current speed data were generated over the entire reef site during August 2004 (spring tides, 4.0 m range) using a research vessel-mounted

acoustic Doppler oxyclozanide current profiler (RD Instruments, Mariner, 300 kHz) set to record at 60 Hz. selleck chemicals The survey vessel’s course ran approximately NE–SW, parallel to the shore of Lismore, at a speed of 6–8 knots. The survey consisted of four survey tracks, each approximately 150 m apart. Each survey track ran over, or in close proximity to, the reef groups and each was surveyed 9 times during the 12.5 h survey period (one complete tidal cycle). The current speed data from within 75 m of the centre of each reef group was extracted. ADCP measure current speeds throughout the water column, however, in this case only the current data for the lowest measurable depth (10% of water depth above the seabed) were used to more closely reflect the current environment around the reef modules on the seabed. Outliers were removed by excluding the highest 1% of recorded currents prior to the calculation of median values and the first and third quartiles. The response variable was redox. The distance effect was the main factor of interest. Distances of 0, 1 and 4 m from the reef edge were chosen on the basis of prior observations (Wilding, 2006) and Distance was, therefore, considered fixed. The effect of location (Reef Group) on the distance effect was also of interest. The reef groups were chosen on the basis of their differing characteristics (current exposed or unexposed) and were, therefore, considered fixed.

Two studies were reanalyses of a prior publication; these were no

Two studies were reanalyses of a prior publication; these were not classified as new studies but were evaluated

and the findings are discussed. We fully reviewed and evaluated 112 studies. For these 112 studies, the level of evidence was determined based on criteria used in our prior reviews.1 and 2 Well-designed, prospective, RCTs were considered class I evidence; studies using SCH727965 order a prospective design with quasi-randomized assignment to treatment conditions were designated as class Ia studies. Given the inherent difficulty in blinding rehabilitation interventions, we did not consider this as criterion for class I or Ia studies, Linsitinib molecular weight consistent with our prior reviews. Class II studies consisted of prospective, nonrandomized cohort studies; retrospective,

nonrandomized case-control studies; or multiple-baseline studies that permitted a direct comparison of treatment conditions. Clinical series without concurrent controls, or single-subject designs with adequate quantification and analysis were considered class III evidence. Studies that were designed as comparative effectiveness studies but did not include a direct statistical comparison of treatment conditions were considered class III; this occurred for 4 articles. Disagreements between the 2 primary reviewers (as occurred for 3 articles) were first addressed by discussion between reviewers to correct minor sources of disagreement,

and then by obtaining a third review. Of the 112 studies, 14 were rated as class I, 5 as class Ia, 11 as class II, and 82 as class III. The overall evidence within each predefined Carnitine palmitoyltransferase II area of intervention was synthesized and recommendations were derived from the relative strengths of the evidence. The level of evidence required to determine Practice Standards, Practice Guidelines, or Practice Options was based on the decision rules applied in our initial review ( table 1). All recommendations were reviewed for consensus by the entire task force through face-to-face discussion. We reviewed 2 class I studies9 and 10 and 6 class III studies11, 12, 13, 14, 15 and 16 addressing remediation of attention. A class I study9 investigated the effectiveness of cognitive remediation and cognitive-behavioral psychotherapy for participants with persisting complaints after mild or moderate TBI. The cognitive remediation consisted of direct attention training along with training in use of a memory notebook and problem-solving strategies. Cognitive-behavioral therapy was used to increase coping behaviors and reduce stress.

17 and 50 In this study, it was found that the lowest values in C

17 and 50 In this study, it was found that the lowest values in Ca/P ratios were obtained in groups with dietary control (Ovx/alc, Ovx/iso, Sham/alc and Sham/iso), and were higher in groups with the ad libitum diet (Ovx/ad libitum/Sham/ad libitum). These findings suggest that diet may play an important role in the variations of the stoichiometric hydroxyapatite. However, further studies are necessary to validate this statement with greater statistical

reliability. Within the alcohol groups of the present study, an average of 37.83% of total calories came from alcohol, similar to previous studies, in which alcohol was responsible for 35–40% of calories in the rats’ diet.28, 52 and 53 This is considered a high dosage of alcohol consumption,28, 52 and 53 resulting in elevated blood ethanol concetrations.52 selleck screening library In another study35 with rats treated with 20% ethanol (in drinking water), similarly to that undertaken in our study, blood SGI-1776 alcohol levels were eight times higher in the treated rats (0.869 g l−1) than those in the control group (0.11 g l−1). The 20% concentration was administered for 15 days which was considered a chronic intake.35 In our study the rats received alcohol for eight weeks. A comparison of results suggests that our rats were subjected

to an excessive and chronic consumption of alcohol. This is an important factor, as most researchers seem to believe that the harmful effects of alcohol on bone is observed with abusive alcohol consumption and not with moderate consumption.54 and 55 The methodology for the treatment of the animals

is based on previous studies21, 22 and 23 that have used similar experimental groups, concentration of alcohol (20% in drinking water) and time of ovariectomy. The standardization of the treatment facilitated the comparison of our results with other studies.21, 22 and 23 However, potential confounding effects pertaining to the type of diet used in our experiment should be considered when interpreting the results. Lieber et al.56 criticized the delivery of alcohol in drinking water, as it reduces water intake and makes it difficult to control nutrients. Since nutritional changes could interfere with the host’s response to the progression of periodontal disease,17 and 50 other studies could verify if the results of this experiment would be similar if other forms of Phosphatidylinositol diacylglycerol-lyase administration of alcohol could be considered, for example, using a nutritionally adequate liquid diet containing alcohol (Lieber–DeCarli liquid diet),28, 37, 53 and 56 the administration of alcohol by intraperitonial injections27 and 32 or by intubation.57 The present study has some limitations. One of the limitations was that of not being able to control the isocaloric group ingesting exactly the same amount of calories as those of the alcohol group (when considering the liquid diet). To minimize this problem, other ways of administrating the liquid diet could be considered.

Our experimental design focused primarily on separately comparing

Our experimental design focused primarily on separately comparing S2 TMS to sham vertex TMS, and S1 TMS to sham vertex TMS. Because of the possibility that both S1 and S2 TMS are involved in pain perception, we did not have strong predictions about the differences buy XL184 between S1 and S2 conditions. Interestingly, however, we found that judgements of intensity were significantly disrupted not only when comparing S2 to vertex TMS, but also when comparing S2 to S1 TMS. This result points

to distinct roles for S1 and S2 in pain perception, even though they are co-activated in parallel (Liang et al., 2011; Ploner et al., 2009) by nociceptive stimuli. A previous study investigating the role of S1 and S2 in pain intensity discrimination observed that whilst S1 responses were able to gradually encode the intensity of a painful stimulus S2 responses had a more categorical or binary form, showing a sharp increase in amplitude at intensities above the pain threshold (Timmermann et al., 2001). Our results extend these findings by providing evidence that S2 plays a causal role in discrimination of nociceptive stimulus intensity. Kanda et al. (2003) found that TMS over S1 applied 150 msec and 200 msec post-stimulus increased reports of pain, while TMS over S2 had no effect. However,

Kanda et al.’s (2003) task focused on pain detection, rather than coding for graded levels of pain intensity. Indeed, their stimuli remained constant, and they relied on (presumably random) variations in perceived intensity. In the present study we used a two-alternative PARP inhibitor forced choice pain intensity judgement, which may be more sensitive to the neural encoding of pain levels. Our TMS did not affect participants’ ability to localise noxious stimuli. This result is consistent with the findings of Kanda et al. (2003) but at odds with those of Porro et al. (2007). These last authors observed that TMS over S1 significantly disrupted localisation of painful much stimuli. Nevertheless, the role of S1 in pain localisation is still controversial (Apkarian et al., 2005; Bushnell et al., 1999), and several reasons could explain the discrepant results.

First, Porro et al. (2007) used mechanical stimuli that activate tactile as well as nociceptive fibres, whilst we used an Nd:YAP laser that selectively activates A-delta fibres but not A-beta fibres. The additional tactile component in Porro et al.’s (2007) study may have contributed to pain localisation, and it may have been this tactile location information that was disrupted by S1 stimulation. Further, we applied single-pulse TMS at 120 msec after a noxious stimulus, based on previous electrophysiological studies of the N1 LEP component (e.g., Valentini et al., 2012), while Porro et al. (2007) applied TMS trains 150 msec and 300 msec after a painful stimulus. They found a significant increase in localisation errors only for the later stimulation.

The increase in carbonyl formation caused by Orn and Hcit was ful

The increase in carbonyl formation caused by Orn and Hcit was fully prevented by this pre-treatment, as shown in Fig. 2B and C (Orn: [F(3,19) = 5.114; p < 0.01]; Hcit: [F(3,18) = 8.666; p < 0.01]). GSH concentrations measured in cerebral cortex 30 min after Orn and Hcit ICV administration

revealed that Hcit moderately reduced (15%) the concentrations of GSH after Hcit injection, whereas Orn did not alter this parameter [F(2,16) = 6.608; p < 0.01] (nmol/mg protein: n = 6; control: 4.25 ± 0.45; Orn: 3.95 ± 0.17; Hcit: 3.66 ± 0.14). The next set of experiments was carried out to investigate the effect of ICV administration of Orn and Hcit on the activities of the antioxidant enzymes SOD, CAT and GPx. Fig. 3 shows that only Hcit was able to reduce the activities of GPx [F(2,17) = 3.786; APO866 cost p < 0.05] and CAT AZD4547 in vivo [F(2,18) = 8.328; p < 0.01], without affecting SOD activity. We also verified that Orn was not able to change any of these activities. The effect of Orn and Hcit on reactive nitrogen species generation was assessed by measuring nitrate and nitrite production. We observed that this parameter was not altered by Orn and Hcit ICV administration (nmol/mg protein: n = 5; control: 2.88 ± 1.23; Orn: 2.43 ± 0.89; Hcit: 2.15 ± 0.87). We investigated the effect of ICV injection of Orn and Hcit on CO2

production from labeled substrates in cortical homogenates. Fig. 4 shows that CO2 production from [U-14C] glucose was significantly inhibited by Orn (35%) and Hcit (32%)

[F(2,12) = 5.515; p < 0.05] 30 min after ICV treatment. CO2 formation from [1-14C] acetate was also inhibited by Orn (32%) and Hcit (25%) administration [F(2,12) = 11.048; p < 0.01]. These results suggest that the aerobic glycolytic pathway and the CAC activity were compromised by Orn and Hcit. We also evaluated the effect of Orn and Hcit ICV administration on CAC enzyme activities. We found that Branched chain aminotransferase Hcit, significantly inhibited (20%) aconitase activity (μmol NADPH min− 1 mg protein− 1: n = 6; control: 1339.4 ± 82.9; Orn: 1208.4 ± 135.6; Hcit: 1070.4 ± 96.9), [F(2,14) = 8.450, p < 0.01], whereas Orn did not alter this activity. Furthermore, citrate synthase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase activities were not changed by Orn and Hcit administration (results not shown). The next set of experiments was performed to evaluate the effect of ICV injection of Orn and Hcit on the activities of the respiratory chain complexes I–III, II, II–III and IV. We found that complex I–III activity was significantly inhibited by Orn (20%) and Hcit (26%) [F(2,15) = 10.274; p < 0.01], with no significant alteration of the other tested activities of the respiratory chain ( Table 1).

, 2006) We have confirmed that the N450 is most

, 2006). We have confirmed that the N450 is most E7080 ic50 representative of general conflict detection (Szucs and Soltész, 2010a, Szucs and Soltész, 2010b, West et al., 2004 and West and Schwarb, 2006). Previously the N450 had been ambiguously related to both response conflict (Liotti, Woldorff, Perez, & Mayberg, 2000) and semantic conflict (Rebai et al., 1997). As we found no significant differences in the mean amplitude of the N450 in the SC and RC conditions we conclude that the N450 is

most sensitive to general conflict (Szucs and Soltesz, 2012, Szucs et al., 2009b and West et al., 2004). Our second objective was to map maturational changes in the N450. There were no differences between the adolescent and young adult groups in the topography of the N450 during congruent and SC conditions. However during the RC condition the topography of the N450 was focused on the right scalp in adolescents

and on the left scalp in young adults. In adults a similar left hemisphere effect during the N450 has been found in previous Stroop studies (Chen et al., 2011, Jongen and Jonkman, 2008 and Lansbergen et al., 2007). Adleman et al. (2002) found increased left hemisphere activation in adults when compared to adolescents specifically in the left middle frontal gyrus during colour word Stroop conflict. The left middle frontal gyrus has been associated with both word generation (Thompson-Schill, D’Esposito, Aguirre, & Farah, 1997) and generating colour names (Martin, Haxby, Lalonde, Wiggs, & Ungerleider, 1995). The left scalp activation found Nutlin-3a manufacturer in adults could represent the increased use of a verbal strategy to resolve conflict. In adolescents the topography of the N450 was focused on the right scalp. Right scalp activity has also been observed in adolescence during a Stop task and a Go-No/go task (Rubia et al., 2000 and Stevens et al., 2007) as well as during a Stroop task in children (previously unrecorded in adolescence) (Jongen & Jonkman, 2008). These authors have concluded that this right scalp activity is indicative of improved performance

strategy. Thymidylate synthase For example Stevens et al. (2007) found that in adolescents increased frontal–parietal circuit activity was related to good performance however this was not found in adults. Therefore increased right scalp activation may recruit frontal–parietal circuitry and allow for improved performance. In terms of middle age adults a stimulus conflict deficit was expected. However there were no differences in the topography of the N450 during stimulus conflict detection for young adults and middle age adults. Nevertheless topographical examination of the N450 during the RC condition reveals dispersed and increased negative amplitude with a right scalp shift. In a middle age group (41–61-year olds) Mager et al. (2007) similarly found increased amplitude of the N450. Mathis et al.

5% The most prevalent specific causative agent noted in the

5%. The most prevalent specific causative agent noted in the Selleckchem VE821 cultures was Staphylococcus aureus (25.8%). The least prevalent agents among the reported causative microorganisms were Enterobacter cloacae and Acinetobacter anitratus (0.9% each) ( Table 2). Of the total confirmed positive cultures, 13% had not been tested for resistance to antibiotics. Of the remaining 385 cultures, 87% were resistant to at least one type of antibiotic. The most commonly

reported resistance was to ampicillin (19.2%), followed by ticarcillin/clavulanic acid resistance (15.1%). Of the 445 total infected patients, 125 (28.1%) were matched with a comparison group of uninfected patients. Although the matching was perfect for gender, in 9 of 125 pairs, the patients fell into adjacent age groups. For these 9 pairs, the differences in actual age ranged between 2 and 12 years (M = 7.89, SD = 3.69). Of the 125 pairs, 56.8% were male (n = 142); of the total matched pairs, 45% were over

60 years of age, and of 125 pairs, 63.2% (n = 46) were matched based on the same admission unit. Nearly 42% of the infected patients had at least one cardiovascular disorder (e.g., hypertension, heart failure, or coronary artery disease) compared to 32% of the uninfected group. More than one-fourth of the infected patients had undergone at least one type of invasive procedures (e.g., endoscopy, bronchoscopy, nasogastric intubation, endotracheal intubation, colonoscopy, endoscopy, abdominal paracentesis, and/or bone marrow biopsy). The

leading comorbidity that was associated with an increased risk of selleck chemical HCABSIs was “renal failure” (RR = 2.9, 95% CI: 1.6, 5.4). Blood products recipients experienced the greatest risk for HCABSIs (RR = 17.9, 95% CI: 4.2, 77.2) ( Table 3). Using a conditional logistic PD184352 (CI-1040) regression analysis, three models were examined (Table 4). Model 1 represented the Odds Ratios (OR), which are adjusted for matching factors but not for other risk factors. The four retained factors were “Blood Products”, “Invasive Procedures”, “Renal Failure”, and “Other Infections”. Model 2 adjusted for matching factors and all other factors in the full model. In Model 3, we dropped “other infections” as the four-factor, which was associated with a wide 95% confidence interval (1.9–243.9). The pseudo R2 for Models 2 and 3 were 0.40 and 0.33, respectively. This study is the first to provide insight into the epidemiology of HCABSIs in a large Jordanian hospital. The study estimated that the overall incidence for HCABSIs among adult hospitalized patients was 8.1 infections per 1000 admissions. This rate was similar to the incidence (8.5 infections per 1000 admissions) reported in Saudi Arabia [33] and much lower than the rate reported in an Egyptian study (76 per 1000 ICU admissions) [34].

A estratégia de pesquisa

incluiu também recolha de inform

A estratégia de pesquisa

incluiu também recolha de informação em websites de organizações nacionais e internacionais (por exemplo, NVP-LDE225 cost normas orientadoras da prática clínica) 3 and 4. Após revisão da literatura, foi conduzido, em janeiro de 2013, um painel de peritos para recolha de estimativas e validação de dados extraídos da literatura sobre a infeção por VHC em Portugal. Seis peritos com experiência na área do VHC, provenientes de diferentes zonas geográficas do país (Norte, Centro e Sul) estiveram reunidos, tendo o painel decorrido segundo o método de Delbecq na presença de um moderador5 and 6. Para analisar as implicações económicas da infeção por VHC em Portugal, recorremos à estimativa dos custos diretos e indiretos decorrentes desta doença. Os custos foram estimados em euros, segundo a perspetiva da sociedade e calculados para o ano de 2013. Após a identificação e quantificação dos

recursos pelo painel de peritos, procedeu‐se à alocação dos respetivos custos unitários, com base em preços/tarifas obtidos a partir de fontes oficiais e literatura, nomeadamente: Catálogo da Administração Central do Sistema de Saúde (ACSS)7 DNA Damage inhibitor para custos da medicação reservada a utilização em meio hospitalar; base de dados INFOMED8 para custos da medicação dispensada em ambulatório; Relatório de Contabilidade Analítica dos Hospitais9 para custos das consultas de especialidade; tabelas de GDH10 and 11 para custos de hospitalizações e exames complementares de diagnóstico e terapêutica; estudo de Elbasha et al. para custos da medicação Sirolimus research buy nos doentes transplantados 12. Os custos indiretos mensurados foram os associados à perda de produtividade de trabalhadores vivos (absentismo)13. Os dados existentes sobre a incidência de hepatite C em Portugal são escassos e resultam do número de notificações efetuadas, estando por isso associados a um baixo nível de evidência científica. Dado

o perfil assintomático da infeção aguda, é reconhecido que nem todos os novos casos são notificados e que muitos dos notificados correspondem a novos diagnósticos de infeção crónica. A partir de uma revisão sistemática da literatura, Muhlberger et al. estimaram para a região europeia da Organização Mundial de Saúde (OMS), uma taxa média anual de incidência de hepatite C de 6,19 casos por 100.000 habitantes (intervalo de confiança (IC) a 95%: 4,90‐7,48), no período de 1997‐200414. Neste período, os dados publicados relativos à incidência da hepatite C em Portugal indicam um valor máximo de 6,9 novos casos/100.000 habitantes em 199815 and 16. Os dados bibliográficos disponíveis para Portugal refletem ainda uma tendência decrescente na taxa de incidência entre 1998 (6,9 casos/100.000 habitantes) e 2010 (0,37 casos/100.000 habitantes)15, 16 and 17. No entanto, a validade desta análise é limitada pelos motivos supramencionados.

This cross-reactivity

This cross-reactivity http://www.selleckchem.com/products/pexidartinib-plx3397.html may result in difficulties to correctly identify infections in swine with H1N1v influenza strains by serology. Infections with swine H1N1 influenza strains are very common in many European countries, with seroprevalences

in sows up to 80%, and herd prevalences up to more than 95% [24]. On the other hand, due to this high prevalence of H1N1 antibodies, it may be more difficult for the H1N1v influenza virus to become endemic in the swine population. Currently no reports can be found that suggest a wide spread of H1N1v influenza virus in swine populations where other H1N1 strains are endemic. It remains to be seen how the epidemiology of H1N1v will develop, whether it will be able to co-circulate

with current H1N1 strains or whether one strains will eventually predominating the other. Furthermore, recombination with current swine strains in Europe could occur, as happened before with the European swine H3N2 [25] and H1N2 strain [26]. This could increase the potential of the H1N1v influenza strain to become endemic in the swine population. The authors thank the animal caretakers who took care of the animals and collected all the samples. Ralph Kok, Rob Zwart, Eline Verheij and Sjaak Quak are thanked for their outstanding assistance in the pathology, selleck chemicals llc histopathology and other laboratory tests. “
“Streptococcus pneumoniae is a major cause of diseases such as meningitis, bacteremia, sinusitis, acute otitis media and pneumonia [1]. Pneumococcal diseases are responsible for millions of deaths every year, especially in developing countries [2]. The current pneumococcal vaccines are based on capsular polysaccharides. The 23-valent polysaccharide vaccine

is poorly immunogenic in infants, offering clinical protection rates of about 60% in adults [3]. The 7-valent conjugate vaccine elicits protection in young children, but only against the seven included serotypes [4], [5], [6] and [7]. Thiamet G Recently, 10-valent and 13-valent vaccines have been licensed [8] and [9], but the potential replacement by non-vaccine serotypes and the high cost reinforce the need for cost-effective strategies, such as a protein-based pneumococcal vaccine. Several proteins have been investigated as vaccine candidates against pneumococcus, including the Pneumococcal surface protein A (PspA). This is an important virulence factor, expressed on the surface of all pneumococcal strains [10], able to inhibit complement activation by the classic and alternative pathways [11]. PspA displays variability at the level of DNA sequence, although there are many sequence similarities and serologically cross-reactive epitopes [12]. The N-terminus of PspA contains the majority of protection-eliciting epitopes [13], and has been divided into three regions, A, B and C [12].

In literature, specific causes of prostate cancer were not mentio

In literature, specific causes of prostate cancer were not mentioned but the possible factors could be: age, genetics, lifestyle, and other factors. The

prostate cancer is uncommon in men in their 40s and becomes more common in their 70s. In United States, the African men are having high risk of developing prostate cancer than European men due to genetic factor,3 and 4 though the mortality rate remains controversial.5 and 6 The primary objective of any microarray data is to obtain differentially expressed genes in different conditions. In the present study, microarray data was used for identifying differentially expressed genes that distinguish

the tumor-groups of African–American and European–American men and to obtain biological Crizotinib clinical trial information based on differentially MDV3100 supplier expressed genes. For this, a simple and meaningful approach of moderated t-statistic was used, 7 on both normalized dataset and simulated datasets that were generated based on univariate simulation at gene level, in order to detect the true significant genes that can separate African–American and European–American prostate tumors. The prostate cancer study contains 89 human samples, of which, 34 were African–American prostate tumor samples, 35 were European–American prostate tumor samples Interleukin-3 receptor and 20 were cancer-free samples. The processed data, multi-array suite (MAS) expressions, were downloaded from ArrayExpress using Exp ID: E-GEOD-6956. All these samples were hybridized to Affymetrix GeneChip

HG-U133A 2.0 arrays, with 22,283 probe sets. The intensity data requires an appropriate transformation and normalization. The data was log transformed and normalized with the median centering. The median absolute deviation scaling was also performed across samples in order to reduce the variation across samples. The moderated t-statistics was used on the normalized data to detect the differentially expressed genes between gene expressions profiles of 34 African–American and 35 European–American patients. In the present analysis, the p- value of moderated t-statistics was chosen to be δ0 = (0.05 > 0.1 × 10−5) and univariate simulated data was generated, nearly, 100 times. In each simulated data, the moderated t-statistics were obtained the significant genes at p-value threshold to detect the true significant genes. The univariate simulation procedure is given in detail in the following section. The univariate normal distribution is determined by two parameters: mean and standard deviation.