All subjects gave written informed consent before participation in the study. Genomic DNA was extracted from circulating leucocytes. The 4b4a genotype was identified directly after a polymerase chain reaction (PCR) amplification protocol,10 and the −786T>C and 894G>T genotypes were identified by PCR, followed by restriction fragment length polymorphism. Quality control for these assays was assessed by randomly selecting samples to be re-genotyped by 2 independent researchers. No misgenotyping was observed. Haplotypes for each subject were inferred using the software PHASE version 2.1 (University of Washington, Seatle,

Wash).21 The volunteers and researchers were blinded to the genotypes and haplotypes during the study. The PCR was performed using the following

Selleck Cabozantinib primers: sense 5’-AGG CCC TAT GGT AGT GCC TTT-3’ and antisense 5’-TCT CTT AGT GCT GTG GTC AC-3’. DNA was amplified for 35 cycles consisted of denaturing at 94°C GSK-3 beta phosphorylation for 30 seconds, annealing at 51°C for 40 seconds, and extension at 72°C for 40 seconds. The PCR products were digested by incubation with a restriction endonuclease, NgoMIV (New England Biolabs, Ipswich, MA), at 37°C for 16 hours and visualized by gel electrophoresis. The PCR was performed using the following primers: sense 5’-AGG CCC TAT GGTAGT GCC TTT-3′ and antisense 5′-TCT CTT TAG TGC TGT GGT CAC-3′. DNA was amplified for 35 cycles, and each cycle was composed of denaturing at 94°C for 1 minute, annealing at 49°C for 40 seconds, and

extension at 72°C for 40 seconds. The PCR products ID-8 were visualized by gel electrophoresis. The PCR was performed using the following primers: sense 5’ AAG GCA GGA GAC AGT GGA TGG A-3’ and antisense 5’ CCC AGT CAA TCC CTT TGG TGC TCA-3’. DNA was amplified for 35 cycles consisted of denaturing at 94°C for 1 minute, annealing at 58°C for 1 minute, and extension at 72°C for 1 minute. The PCR products were digested by incubation with Ban II (New England Biolabs, Ipswich, Mass) at 37°C for 16 hours and visualized by gel electrophoresis. Blood was drawn in the morning after 12 hours of fasting. Cholesterol and its subfractions (high-density lipoprotein [HDL] and LDL], as well as triglycerides, were determined by the dry chemistry method. Plasma glucose was measured by enzymatic in vitro test. The experimental protocol was conducted in the morning, 1 hour after a standardized light breakfast. The evaluation was performed from the first to the 12th day after the onset of menstruation. Subjects did not drink alcohol or caffeinated beverages and did not perform intense physical activities for at least 24 hours before the experimental visit. During the study, subjects were placed in a supine position in a quiet air-conditioned room (≈24°C), and they rested quietly for 10 minutes before any measurement.

Apoptosis measured employing semi-quantitative and quantitative assays, and parameters showed good agreement in direction and extent of change that appears to be one of the major contributors in disappearance of BPDE-DNA adducts in tissues studied. Quantitative analysis and comparison of IHC staining measuring BPDE-DNA adducts and apoptosis in tissue sections have the advantage that preceding or subsequent paraffin-embedded sections from the same portion of the tissue are

compared, and this comparison is likely to be relevant and meaningful. Curcumin-mediated enhancement of apoptosis in B(a)P-treated (normal liver and lung tissues) cells has some similarity with its effects in terms of apoptosis observed in transformed or immortalized cells in culture [23], [24] and [25]. To our knowledge, this is an initial in vivo report demonstrating that dietary curcumin augmented the expression of caspase-3 APO866 cost and increased the Bax/Bcl-2

www.selleckchem.com/products/Everolimus(RAD001).html ratio and a apoptotic index in normal cells in response to B(a)P-induced DNA damage. This in turn probably accounts for the enhanced disappearance of adduct containing nuclei although the degree of responses varied. The other potential contributor in observed relative decrease in BPDE-DNA adducts is cell proliferation, and its role was assessed by comparing the levels of PCNA by western blot analysis. It was seen from experiment 1 that levels of PCNA were enhanced post B(a)P-treatment especially most at later time points [subgroups BP(+96h) and BP(+144h)], and B(a)P-mediated

increases were significantly decreased by dietary curcumin when compared to time-matched B(a)P-treated controls in liver [subgroups BP(+96 h) + C 72 h, BP(+144 h) + C 120 h] and lungs [BP(+144 h) + C 120 h]. In experiment 2, levels of PCNA were not altered significantly at 8-28 days post B(a)P [BP(+8d), BP(+15d), BP(+29d)] both in the liver and lungs while curcumin treatment resulted in significant increase in the levels of PCNA in liver [subgroups BP(+8d) + C 7d, BP(+29d) + C 28d] and lungs [BP(+15d) + C 14d, BP(+29d) + C 28d]. It may be noted that exposure to dietary curcumin alone does not alter the levels of PCNA in liver and lungs of mice. After considering and comparing the slope of time-related and curcumin-mediated changes in BPDE-DNA adducts and numbers of cells undergoing apoptosis and cell proliferation, it is seen that the observed decrease in BPDE-DNA adducts in experiment 1 is mainly attributed to curcumin-mediated enhanced apoptosis. In experiment 2 dilution of BPDE-DNA adducts by newly synthesized non-adducted DNA due to cell proliferation appears to be the reason (Figure 3, Figure 5 and Figure 8). In both these experiments, apoptosis (experiment 1) and cell proliferation (experiment 2) alone may not be sufficient to result in the extent of decrease as potential contribution of DNA-repair may also be included.

Interestingly, we have found that apoptotic

and autophagic cell death induced by DQQ was caspase-dependent. A universal caspase inhibitor, Z-VAD-FMK, revert back the entire key event associated with DQQ mediated MOLT-4 cell death. Caspase inhibitor reversed cell growth inhibition and key protein expression of PARP-1, caspase-3, beclin1 and ATG7, which were induced by DQQ (Fig. 5A, B). These findings put forward the key role of caspases in the induction of apoptosis and autophagy. Therefore, HIF-1 pathway we can say that DQQ induce caspase dependant autophagy and intrinsic and extrinsic apoptosis in human leukemic MOLT-4 cells. Furthermore, cytochrome c inhibition through siRNA, very significantly blocked the activity of DQQ in terms of viability, apoptosis and autophagy (Fig. 6A-C). However, we did not get such type of significant reversal effect by silencing the MOLT-4 cells through beclin1 siRNA (Fig. 7A, B). The MOLT-4 cell viability reversal effect of DQQ via cytochrome c siRNA was much higher than the caspase inhibitor and beclin1 siRNA. Interestingly, our study first time portrays the negative feedback control role of cytochrome c in the activation of autophagy. Thousands of publications revealed the role of cytochrome c in apoptosis induction, but none has described its role in autophagy induction, although there are evidences

see more suggesting the inhibitory role of cytochrome c on autophagy [12]. Furthermore, the crosstalk between autophagy and apoptosis was confirmed by silencing of beclin1 through siRNA. The results of the experiments revealed that beclin1 inhibition partially reversed the viability and the PARP-1 cleavage inhibition induced by DQQ; indicating the partial role of beclin1 in apoptosis. The experiment also confirmed the notion that autophagy and apoptosis induced by DQQ in MOLT-4 cells were interdependent. Much of the work has been done in the field of apoptosis and autophagy; however the relation between the two is still controversial and unexplored to some extent. In conclusion, the present Abiraterone molecular weight study briefly describes the crosstalk between autophagy and apoptosis induced by a novel

quinazolinone derivative, DQQ, in human leukemia MOLT-4 cells. It induces extrinsic and intrinsic apoptosis, confirmed by apoptotic bodies’ formation, PS exposure, enhance sub-G0 population and induction of various apoptotic proteins like Bcl-2/Bax, PARP and caspase. We for the first time elucidated the negative feedback role of cytochrome c in autophagy induction. Hence, our discovery of this novel mechanism not only further insight the interdependent role of apoptosis and autophagy, but also disclose the clinical significance of agent like DQQ, that simultaneously induce apoptosis and autophagy. All authors declare that there are no conflicts of interest in this study. ASP, SKG and AK thanks Council of Scientific and Industrial Research (CSIR), New Delhi, India for their research fellowships.

Since the concentration of oxyhemoglobin in the

infarct core was increased in the 100% oxygen group, a better tissue delivery of oxygen due to a higher CBF might explain the results [7]. On the other hand, increased blood flow might cause reperfusion damage or hypertensive hemorrhage in the infarction area during reperfusion. DZNeP Before studying any neuroprotective effect of helium in acute ischemic stroke in humans, it is necessary to know if helium influences cerebral blood flow in healthy people. In order to investigate this, we performed a n = 1 trial measuring cerebral blood flow parameters by means of transcranial Doppler (TCD) in a healthy young women alternatingly inhaling air or helium. To measure cerebral blood flow TCD was performed with a pulsed Doppler transducer (Pioneer TC4040, EME Überlingen, Germany), gated at a focal depth of 50 mm. Our female 29-year-old healthy volunteer was positioned laying on the back and the transducer (2 MHz) was placed at the right temporal bone. When the main stem of the right middle cerebral artery was found, the transducer was fixed with a head strap. The mean flow velocity (MFV), peak systolic velocity selleck chemicals (PSV), and pulsatility index (PI) were measured continuously and recorded every

minute. Furthermore, heart rate frequency and blood oxygen saturation were measured with a fingertip monitor (pulse oximetry) in order to exclude possible confounding factors. At baseline all parameters were measured during 3 min while breathing normal room air. After baseline measurement, Heliox (helium 79%, oxygen 21%) was administrated for 5 min using an oral nasal mask. This intervention was followed by a washout of 5 min breathing room air. This block of 5 min Heliox intervention and 5 min

washout was repeated four times. At the end, all measurements were performed during another period of 5 min breathing room air. The null hypothesis was that there would not be any difference in the hemodynamic parameters during helium inhalation or room air inhalation. For analysis Resminostat we used a one tailed Student’s t-test. We considered a P-value of less than 0.05 as statistically significant. No adverse events occurred during helium administration except for temporary changes in voice pitch. Median baseline values were: MFV 50 cm/s, PSV 79 cm/s, PI 0.92, heart rate 77 min−1 and oxygen saturation 99%. Heart rate frequency and blood oxygen saturation were stable and did not differ significantly between the periods of breathing helium and room air. MFV in the right middle cerebral artery as well as the PSV did also not differ significantly in the two test conditions (Table 1). The PI had a mean of 0.95 in Heliox compared to 0.91 in room air inhalation; this difference was significant with a P-value of 0.01.

The Medical Research Council National Survey of Health and Development (NSHD) comprises participants sampled PD332991 from all births in a week in March 1946 and followed up since. In 1999, at age 53 years, men and women were visited by a research nurse and consent for DNA extraction was given by approximately 2900 members of the cohort. Details of the data collected and the several phases of the study are available on the cohort’s website (www.nshd.mrc.ac.uk) and elsewhere [41]. The English Longitudinal Study of Ageing (ELSA) comprises men and women aged 50 years and over who originally participated in the Health Survey for England

in 1998, 1999 or 2001. Fieldwork began in 2002–03 (Phase I) with two-yearly follow-ups and in 2004–05 (Phase II) blood samples were provided by 6231 participants. Details of the cohort have been published [42]. The Hertfordshire Cohort Study (HCS) consists of 2997 participants born 1931–39 and registered with a General Practitioner in East, North or West Hertfordshire who attended a clinic in 1994–2004 (Phase I). A second assessment took place in 2004–05 for participants in East Hertfordshire (Phase II). Further details of study design, data collected and summaries of participant characteristics

have been published [43] and are available on its website (www.mrc.soton.ac.uk/herts). The Boyd Orr cohort is a historical cohort study based on children surveyed in 1937–39 in English and Scottish districts. Participants were followed-up for vital status via Osimertinib in vivo the NHS Medical Information Arachidonate 15-lipoxygenase Research Service (MIRS) since 1948, with questionnaire administration to survivors in 1997–98 (Phase II) and a research clinic visit in 2002–03 (Phase III), during which DNA was extracted from 728 adults, of which 385 had at least one physical capability measure and one relevant genotype called for this analysis. Details of the study design and the data collected have been described on its website (www.epi.bris.ac.uk/boydorr) and elsewhere [44]. The Caerphilly Prospective Study

(CaPS) recruited 2512 men aged between 45 and 59 years in 1979–83 from the town of Caerphilly, South Wales, and its surrounding villages. Blood samples were collected at baseline and at each of the four follow-ups (Phase II: 1984–88, Phase III: 1989–93, Phase IV: 1993–97 and Phase V: 2002–04.) Further details are available on the cohort’s website (www.epi.bris.ac.uk/caerphilly/caerphillyprospectivestudy.htm). The Lothian Birth Cohort 1921 (LBC1921) participants were all born in 1921 and most completed a cognitive ability assessment at age 11 years. In 1999–2001 (Wave I), at approximately 79 years old, 550 participants living in and around Edinburgh, underwent a series of cognitive and physical tests. Details of the recruitment into the study are available on its website (www.lothianbirthcohort.ed.ac.

During the study period, no clinical signs, ophthalmological abnormalities, or deaths were observed in either the control or the treatment groups (data not shown). The animals showed no significant

differences in body weight and food consumption between the control and treatment groups. Body weight increased gradually throughout the study period in males and females of all groups (Fig. 1). At the end of the study, all animals were euthanized selleck chemicals llc and subjected to a necropsy. Data in Table 4 indicate that there were no significant differences in hematological parameters between the control and Vigiis 101-treated groups. Data in Table 5 show some statistically significant differences (p < 0.05) in clinical chemistry Selleckchem CX 5461 parameters between the control and Vigiis 101-treated groups. In male rats, blood chemistry parameters, including potassium (K), aspartate aminotransferase (AST), and triglyceride (TG) were significantly different but were within the physiologically acceptable range (K: 3.82∼5.55 mg/dl; AST: 74∼143 U/l; TG: 20∼114 mg/dl) in the treatment groups. In Vigiis 101-treated female rats, statistically significant changes in AST also resulted in the values that was within

the acceptable range (AST: 65∼203 U/l). The data in Table 6 and Table 7 indicate that no significant organ weight and relative organ weight changes were noted in either the male or female rats. Fig. 2 and Fig. 3 demonstrate the results of histopathological examination

of the rats. The results showed that no significant lesions were present in Baricitinib the liver, kidneys, heart, spleen, adrenal glands, epididymis, testes, uterus, and ovaries of the control or high-dose Vigiis 101 groups. Probiotic products fermented by L. paracasei subsp. paracasei NTU 101 have been shown to have various beneficial effects on humans and animals, such as hypolipidemic, immunomodulatory, osteoprotective, and antiobesity effects. In the literature, there are no available classical toxicology data on Vigiis 101. To our knowledge, there are no published studies on traditional genotoxicity or mutagenicity of L. paracasei subsp. paracasei NTU 101 or L. paracasei subsp. paracasei strains in general. Hence, we decided to evaluate the safety of Vigiis 101 powder made from L. paracasei subsp. paracasei NTU 101 provided by SunWay Biotech Co., Ltd. (fermentation by means of typical industrial equipment). We used two in vitro genotoxicity tests of Vigiis 101, one in vivo genotoxicity test, and a 28-day oral toxicity assay in Wistar rats. The Ames test in Salmonella strains TA98, TA100, TA102, TA1535, and TA1537 showed that Vigiis 101 does not induce a greater than two-fold increase in the number of reverse mutations at the doses 0.3–5.0 mg/plate. Nor does metabolically activated Vigiis 101 (with an S9 mix) exhibit mutagenicity.

Inorganic Se compounds account for only a small fraction of total Se naturally occurring in foods. Far more abundant are organic compounds such as selenomethionine and Se-methylselenocysteine (SMSC). In the Selenium and Vitamin E Cancer Prevention Trial (SELECT), a high dose of selenomethionine was given to subjects, most of whom began the study with high Se status

[14]. Such supplementation resulted in a minimal but statistically significant increase in risk of type II diabetes [14]. The choice of SMSC for use in this study is based on (a) its significant contribution to total Se in foods, particularly in those foods of high total Se content; (b) its high biological availability; (c) its demonstrated ability to induce selenoenzyme activity and increase other markers of Se status; (d) chemopreventive efficacy, Alectinib which is superior to that of selenomethionine; (e) its low toxicity in comparison with other Se forms; (f) its noninvolvement in protein synthesis, unlike selenomethionine, which is incorporated nonspecifically into proteins in place of methionine and thus diverted from Se metabolic pathways;

and (g) the paucity of data concerning effects on glucose metabolism of this Se form, which is demonstrably relevant and significant in human nutrition. Dasatinib price Elucidating the mechanisms through which supplemental Se affects glucose metabolism, particularly Janus kinase (JAK) forms of Se that are commonly found in food, is an important step in understanding the associated risk of Se supplementation. Recent work by Misu et al [15] has shown that Se-induced

changes in glucose metabolism may occur by reducing basal activation of AMPK. If Se is to be useful as an anticancer supplement without increasing the risk of metabolic diseases associated with IR, it may be necessary to couple it with other factors that limit these potential complications. Isoflavones (IF) are estrogen-like compounds found primarily in soy. Increased dietary IF cause favorable adaptations in glucose metabolism [16]. Interestingly, there is growing evidence that these changes may be facilitated via increased AMPK activation [17]. Isoflavones are also reported to cause a reduction in body fat that is likely mediated by increased energy metabolism [18]. Thus, increasing IF consumption may be an effective approach to help prevent or limit the potentially negative impact of Se supplementation on glucose management. Therefore, due to differences in metabolic responses to increased IF and Se, we hypothesized that (1) a chronic increase in SMSC consumption would lead to impaired glucose control, (2) a high IF (HIF) diet would improve glucose control, and (3) if HIF diet was consumed with high SMSC, the negative effects on glucose management associated with Se supplementation would be attenuated.

At least 500 cells per well were examined, which enabled the determination of the LC50 value (the peptide concentration at which a 50% reduction in cellular viability was observed). In addition, uninfected mouse peritoneal macrophages were seeded in 96-well plates (Nunc Inc.), maintained in RPMI media and treated or not with 1 and 5 μg/ml melittin at 37 °C for 48 h. After this period, the cytotoxic effects were examined using a MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, buy Belnacasan inner salt) assay, in which a reduction of MTS in soluble

formazan by mitochondrial dehydrogenase occurs only in healthy and metabolically active cells (Berridge et al., 2005). Briefly, at the end of the incubation period, the cells were washed with sterile PBS (pH 7.2), and the wells were filled with RPMI media (without a pH indicator color), 10 mM glucose and 20 μl MTS/PMS reagent (20:1), for which the stock solution consisted of 2 mg/ml MTS and 0.92 mg/ml PMS prepared in DPBS (Promega, Madison, WI, USA). Following 3 h of incubation, the absorbance

was evaluated in a microplate reader spectrophotometer at 490 nm Pifithrin-�� cell line to measure the toxicity. All of the animal experimental protocols were submitted to and approved by the Commission of Evaluation for the Use of Research Animals (Comissão de Avaliação do Uso de Animais em Pesquisa (CAUAP) of the Biophysics Institute Carlos Chagas Filho). Both experiments were carried out in triplicate. To investigate the effect of the melittin peptide on the intracellular cycle of the parasite, LLC-MK2 cells were seeded in 24-well plates containing glass coverslips, cultivated in RPMI supplemented with 10% FCS, and maintained at 37 °C in a 5% CO2 humidified atmosphere for 24 h, as previously described (Adade et al., 2011). The

cultures were then washed and infected with tissue culture trypomastigotes (parasite:host cell ratio of 10:1). After 24 h of infection, the non-internalized parasites were removed by repeated washes with PBS, and the cells were cultivated in fresh RPMI media containing 2% FCS with or without the melittin peptide (0.07–0.56 μg/ml). The media was changed every two days. The coverslips were collected daily up to 96 h, rinsed in PBS, fixed in Bouin’s solution, stained with Giemsa and mounted on glass selleck inhibitor slides with Permount (Fisher Scientific, New Jersey, USA). The parasite infection was quantified using a Zeiss Axioplan 2 light microscope (Oberkochen, Germany) equipped with a Color View XS digital video camera. The number of intracellular amastigotes per 100 cells was evaluated by counting a total of 500 cells in three independent experiments. The IC50 was estimated as the dose that reduced the number of amastigotes per infected cell by 50%. The epimastigotes treated with 2.44 μg/ml of melittin and the tissue culture trypomastigotes treated with 0.

These results suggest that fluoxetine may have a direct bearing on the improvement of major depression. Further studies will begin to address these issues. The authors have declared that no competing interests exist. This study is supported by grants 81025025, 81001671 and 81373788 from the National Natural Science Foundation of China. “
“Amyloid-β (Aβ)-peptides, the primary components of neuritic plaques

found in brains of Alzheimer’s disease (AD), are generated by the proteolytic processing of the β-amyloid precursor protein (APP) (Selkoe, 2011 and De Strooper et al., 2012). Beneath the β- and γ-secretases, several other proteases, such as meprin-β, caspase and aminopeptidase A, seem to be involved in this process (Takeda et al., 2004, Sevalle et al., PARP activation 2009 and Bien et al., 2012). Thereby more than 40 different N- and C-terminally truncated and modified variants of the Aβ-peptides are generated (Maler et al., 2007). APP is also present in the immune cells of the central nervous system (CNS) and the periphery, particularly microglia and monocytes (Ledoux, 1993, Bitting et al., 1996, Jung et al., 1999 and Spitzer et al., 2010). The induction of APP and Aβ-peptide secretion in activated mononuclear phagocytes suggests

a role for APP in the initiation of immune responses (Monning et al., 1990 and Sondag and Combs, 2004). Both, the expression of surface receptors and cytokine secretion by macrophages and microglia are context sensitive. Thus, proinflammatory M1- and anti-inflammatory M2-polarized mononuclear phagocytes BYL719 price represent the extremes of a heterogeneous continuum (Mantovani et al., 2004 and Varnum

and Ikezu, 2012). Although helpful as a model for investigating the basic functions of mononuclear phagocytes, recent research has identified several intermediate stages and cells that express M1 and M2 markers simultaneously (Xue et al., 2014). In brain sections from AD patients, microglia predominately presented markers of M1 polarization (Michelucci et al., 2009, Varnum and Ikezu, 2012 and Sudduth et al., 2013). The selleck kinase inhibitor proinflammatory polarization of microglia was shown to inhibit the clearance of Aβ-peptides and might therefore favor the accumulation of Aβ-peptides and consequent neuronal cell death, finally leading to cognitive deterioration and behavioral disturbances (Yamamoto, 2008). Several studies have investigated the phagocytosis of Aβ-peptides as a means to eliminate them from the organism, but data on a potential physiological role for Aβ-peptides in the process of phagocytosis are scarce. Reduced levels of Aβ-peptides in CSF are found not only in AD but also in several other neuroinflammatory diseases, such as borreliosis, herpes encephalitis and bacterial meningitis, with normalization after successful treatment (Sjogren et al., 2001 and Krut et al., 2013).

All results from this CRM fell within the acceptable range (8.82–13.2 μg/L). The results of the prepared QC saliva samples were used to calculate percentage recoveries for the 10 μg/L spiked sample, corrected for the lead level present in the blank, for both the

“Fresh” SGI-1776 and “Device” QCs. For the “Fresh” QCs, recovery of 107.7% was observed. For the “device” QCs, recovery was 65.9%. Descriptive statistics of the sample cohort are provided in Table 1. The cohort comprised 105 paired blood and saliva samples. All participants were male (this was not an intentional discrimination by the authors, but due to the presence of very few female workers in the industries studied). There were 53 samples provided by smokers and 52 by non-smokers. The age range of participants was 18–65 years, with a mean age of 37 years old and a median Selleck Anti-diabetic Compound Library age of 35 years old. Forty of the individuals sampled were categorised as having “no sample history”. History category 1 (Δ = ± 1 μg/dL) included 27 samples; category 2 (Δ = ± 2 μg/dL) included 42 samples; and category 3 (Δ = ±3 μg/dL) included 44 samples. The remaining 21 samples had Δ > ± 3 μg/dL and were

classified as “fluctuating history”. Summary statistics of the lead levels observed in both the blood and in the saliva samples are presented in Table 2. There were no significant differences in blood lead values between the history categories 1–3 (mean: 5.59 μg/dL, 5.40 μg/dL and 5.91 μg/dL respectively; median: all 4.00 μg/dL). Variability was also very similar for the three categories (standard deviation: 4.16 μg/dL, 3.72 μg/dL and 4.32 μg/dL, respectively). However, the blood lead values for the “fluctuating history” category were much higher (mean: 17.62 μg/dL; median: 15.00 μg/dL). Variability was also much greater in this category (standard deviation: 11.31 μg/dL). For the saliva lead values, the MycoClean Mycoplasma Removal Kit mean and 75th percentile values are substantially lower for history category 1 than for categories 2 and 3 (mean: 19.8 μg/L, 27.8 μg/L and 29.0 μg/L, respectively; 75th percentile: 23.8 μg/L, 29.1 μg/L and 30.6 μg/L, respectively). The variability is also lower in category

1 than the other two categories (standard deviation: 14.2 μg/L, 31.9 μg/L and 32.2 μg/L respectively). However the median values do not demonstrate any significant difference (15.5 μg/L, 15.7 μg/L and 15.9 μg/L, respectively). Similarly to the results in blood, the salivary lead values for the “fluctuating history” category were much higher (mean: 66.2 μg/L; median 48.8 μg/L). Variability was also much higher (standard deviation: 66.3 μg/L) than for categories 1, 2 or 3. There were no substantial differences in the blood lead values between smokers and non-smokers. For the saliva lead values, the mean and 75th percentile values were higher (not statistically significant) in smokers than non-smokers (mean: 43.5 μg/L and 36.