The aerial mycelia of the PDC1 deletion mutant adhered too tightly to the media, however, and we instead used the back of the surgical blade. Mycelia formed just above and below the agar surface were much denser in PDC1 deletion mutant. Although perithecia maturation in the PDC1 deletion mutant was

variable and dependant on induction conditions, PDC1 deletion mutants produced many immature perithecia compared with the wild-type and complemented strains (Fig. 1a). Mature perithecia of wild-type and complemented strains contained viable ascospores and discharged them normally, but most of the immature perithecia of the PDC1 deletion mutants were barren (Fig. 1b). The PDC2 and PDC3 deletion mutants displayed wild-type-like vegetative growth, conidiation, sexual learn more reproduction, virulence, and toxin production (Table S3 and Fig. S3). Perithecia maturation is defective in ACS1 deletion mutants because of reduced lipid production (Lee et al., 2011). Thus, we analyzed lipid

production in PDC1 mutants and found that total lipid production in the PDC1 deletion mutant was not significantly different compared with the wild-type and complemented strains. We also observed that POL production was unaffected in the PDC1 deletion mutant Antiinfection Compound Library (Fig. S4). Cell surface hydrophobicity tests demonstrated that aerial mycelia of PDC1 deletion mutants were highly wettable by water (Fig. 2). Lipid bodies were not observed to accumulate in aerial mycelia of PDC1 deletion mutants, although wild-type and complemented strains were observed to contain a large amount of lipids in their hyphae. Mycelia of PDC1 deletion mutants embedded in agar, however, possessed more lipid bodies than the embedded mycelia of wild-type and complemented strains. The lipid content of the mycelia in the PDC1 deletion mutants did not change when potassium acetate was added to the agar media (Fig. 2). We examined the expression of PDC1-GFP and ACS1-GFP in both aerial and embedded mycelia and found that PDC1-GFP was highly expressed in both of types of mycelia (Fig. 3). ACS1-GFP, however, was highly expressed Farnesyltransferase only in aerial mycelia (Fig. 4). Deletion of the PDC1 gene results in suppression of ACS1-GFP expression

(Fig. 4). When acetate was added to induce ACS1 expression, ACS1-GFP was not detected in the mycelia of the PDC1 deletion mutant (Fig. 4). As previously reported, the ACS1 deletion mutant exhibited defective perithecia development (Lee et al., 2011). However, it was observed that all of the ACS1 mutant phenotypes, including POL production, are masked in the ∆pdc1 ∆acs1 double mutant (Fig. 5). Thus, the PDC1 gene is epistatic to the ACS1 gene. Five-day-old carrot agar incubations were sliced into 2-mm-wide sections and evaluated by dissection and optical microscopy. Embedded mycelia of the wild-type and complemented strains penetrated into the agar to depths of more than 8 mm, whereas embedded mycelia of the PDC1 deletion mutant penetrated to depths of only 1 mm (Fig. 6).

However, the measured values of TPP+ distribution also indicated that ionophores had only a minor influence on membrane potential. Some acidification of the cytoplasm occurred, but the total protonmotive force was

only decreased by about 20%. In contrast, the ATP pool fell by 75%. It should be noted that the experiments were performed with late-exponential or stationary-phase cells to reflect the conditions that pertain predominantly in the rumen (Hobson & Wallace, 1982). It seems improbable that the mechanisms differ in more active bacteria, as in mid-exponential phase, although the magnitude of the gradients and pools may be different. Russell and his colleagues INCB024360 price have made similar observations with other species of ruminal bacteria. The high apparent intracellular concentrations of Na+ and K+ were similar to those measured in S. bovis (Russell, 1987). Ruminal bacteria have been described as mildly halophilic, based on their requirements of Na+ for growth (Caldwell et al., 1973; Caldwell & Hudson, 1974). The membrane potential fell by < 10% when monensin

was added to S. bovis, although intracellular pH was affected to a greater extent (Russell, 1987). The protonmotive force of a ruminal Peptostreptococcus was unaffected by monensin, yet the ATP pool fell by two-thirds (Chen & Russell, 1989). It therefore appears that it is not the collapse of transmembrane ion gradients that causes the toxic effect of ionophores on intact bacteria, but the energy expenditure required to support the increased energy demand of homoeostatic C59 wnt in vitro mechanisms maintaining the gradients. Any extra demands induced by adding different cations may therefore have an influence on the efficacy of an ionophore, even if the ion is not translocated by the ionophore. In conclusion,

it may be possible to enhance the efficacy of ionophores by adding salts of mineral cations to the diet. However, the spectrum of antibacterial activity against different species, upon which ionophore depends for its nutritional effects, may well be different Adenosine when the added cations are present, depending on the ion gradients present in different species. Thus, the nutritional effects of the ionophores (Chen & Russell, 1989) may not be the same at different cation concentrations. The present results also have implications for mechanisms by which ruminal bacteria may become resistant to ionophores. Adaptive resistance to ionophores involves changes in the permeability of the cell envelope (Newbold et al., 1992; Callaway & Russell, 1999), which may well affect changes in transmembrane ion gradients. One of the fears concerning the use of antimicrobials in livestock production is that transmissible resistance factors will arise and by transfer to human pathogens will render antibiotic therapy ineffective (Goodrich et al., 1984). However, there is no evidence that such resistance arises by exposure to ionophores such as monensin (Russell & Houlihan, 2003; Phillips, 2007).

This sequence is also a preferential DNR-intercalating site where a mutually exclusive competitive binding of DNR and DnrN occurs. This may be the mechanism that senses the intracellular DNR level to either turn on or turn off the expression of DnrI, which is the key activator for DNR biosynthesis. This study shows the circular nature of regulation, where three elements namely the DnrI activator, the DrrA–DrrB efflux pump and DNR are acting in sequence. At a steady-state level of antibiotic production, DnrI activates the drrA–drrB operon as

well as major biosynthetic operons. The efflux system maintains the intracellular DNR at an optimum concentration, and a micro increase in the intracellular DNR level leads to preferential intercalation at the DnrN-binding selleck site that shuts down dnrI transcription temporarily. The intercalated drug must leave the site before DnrN can bind and reactivate dnrI, which is possibly affected by DrrC (Lomovskaya et al., 1996). Yet

Dactolisib mouse another regulation is by the control of DnrN expression, which is dictated by its activator DnrO that binds at the upstream element near the dnrN promoter. This site is also a preferential intercalating site for DNR (Otten et al., 2000). These combined factors possibly fine tune the feedback regulation of drug biosynthesis. We analyzed the effect of the drrAB mutation on the three regulatory genes dnrN, dnrO and dnrI along with the structural gene dpsA, which is essential for polyketide biosynthesis (Grimm et al., 1994). qRT-PCR results show that both dnrI and dpsA are downregulated to 1/8th and 1/16th, respectively,

when compared with the WT (Fig. 4b). The melting-curve analysis shows a single peak for the respective amplicons and the amplification efficiency plot had a slope <0.1 (Fig. 4a). This finding confirms the hypothesis that an increase in the DNR level is sensed and the key activator of drug biosynthesis DnrI is downregulated. This results in a decline of dpsA expression, which is essential for polyketide biosynthesis. In the null mutant, DnrN has MycoClean Mycoplasma Removal Kit failed to activate dnrI transcription in spite of a 2.2-fold increase in the dnrN transcript relative to WT as seen in qRT-PCR results. The DnrN-binding site at the dnrI promoter region is a high-affinity site for DNR intercalation (Furuya & Hutchinson, 1996). Therefore, a small increase in the DNR level within the cell is sufficient to exclude DnrN from its activation site. It is intriguing that dnrN/O has an upstream element that is intercalated by DNR in competition with DnrO, which is an activator protein of dnrN transcription (Otten et al., 2000). The possible reason for the increase in the dnrN transcript is that DnrO possibly binds to a second activation site indicated in a previous report (Jiang & Hutchinson, 2006). Nevertheless, the slight increase in the dnrN transcript in the mutant remains unexplained. qRT-PCR shows that the DnrO transcript level increases by 3.4-fold in the mutant relative to WT.

Consistent with ITS and β-tubulin phylogenies, molecular clustering based on lac3-1 sequence analysis grouped the P. cinnabarinus and P. puniceus strains into two highly supported specific lineages. The P. sanguineus and P. coccineus strains were distributed through four distinct, well supported clades

and sub-clades. A neotropical sub-clade grouped the P. sanguineus strains from French Guiana and Venezuela – and the reference strain CIRM-BRFM 902 – corresponding to P. sanguineus sensu stricto. A paleotropical sub-clade clustered the strains from Madagascar, Vietnam and New Caledonia, and could be defined as Pycnoporus cf. sanguineus. The Australian clade of P. coccineus, including the reference strain MUCL 39523, corresponded to P. coccineus sensu stricto. This clade also included

LY2835219 the Malesian strain from the Solomon Islands, positioned separately, consistent with the high level of endemic species in that country (Udvardy, 1975). Ribociclib research buy The fourth group was the Eastern Asian region clade, clustering the strains from China, including CIRM-BRFM 542 of unknown origin and the strain MUCL 38527 from Japan. The strains of this last clade shared polymorphism in ITS and β-tubulin sequences with P. coccineus sensu stricto strains, as well as intron length in β-tubulin gene sequences, known to be characteristic of a lineage in basidiomycetes (Begerow et al., 2004). This suggests a misidentification of Chinese specimens, very recently confirmed by macroscopic observation of basidiocarps. The high degree of similarity of the morphological characters between Cepharanthine P. sanguineus and P. coccineus and the high variability of specimens across the season and the geographical area could explain this field misidentification (Nobles & Frew, 1962). Accordingly, the

Eastern Asian region strains of Pycnoporus (from China and Japan), together with the related strain CIRM-BRFM 542 (suspected to be of East Asian descent), formed a P. coccineus-like group defined as Pycnoporus cf. coccineus (Fig. 3). Biogeographic phylogenetic structure was related in polyporoid fungi such as Grifola frondosa, separating Eastern North American strains from Asian strains, and no morphological distinction was detected between them (Shen et al., 2002). In the Ganoderma applanatum/australe species complex, eight distinct clades were strongly correlated with the geographic origin of the strains, and corresponded to mating groups (Moncalvo & Buchanan, 2008). Interestingly, the East Asian clade in our study corresponded to the functional group of Pycnoporus strains previously reported for their high level of laccase production (Lomascolo et al., 2002).

As with the DR task, aged monkeys are slower to learn the task and perform more poorly selleck products as delay intervals are increased (Shamy et al., 2011). Behavioral flexibility is another frontal-dependent cognitive process that is compromised with aging. This has been studied using a variety of tasks, notably extradimensional set-shifting and reversal tasks in humans (Ridderinkhof et al., 2002; Marschner et al., 2005; Weiler et al., 2008), monkeys (Bartus et al., 1979; Lai et al., 1995; Voytko, 1999; Moore et al., 2003) and rats (Stephens et al., 1985; Barense et al., 2002; Schoenbaum et al., 2002; Nicolle & Baxter, 2003; Mizoguchi et al., 2010). Interestingly,

lesions of area 9 in marmoset monkeys affected extradimensional set-shifting performance, whereas lesions of the orbital PFC affected Z-VAD-FMK cost reversal performance (Dias et al., 1996). These data suggest that these tasks rely on different brain structures within the PFC. Extradimensional set-shifting refers to the problem of switching attention between cues that are in different perceptual dimensions in order to perform the task correctly. An example

of this is to train a rat to use light cues to determine which arm to select in a maze, and then shift the relevant cue to an auditory stimulus. When the extradimensional set-shifting occurs, the rat must shift its strategy and follow the sound cue in order to select the correct baited arm (e.g., Insel et al., 2012). In contrast, reversal learning refers to adapting a behavior to the changing contingencies required to reach a goal. For example, a rat can initially learn to press a lever in a ‘light-on’ condition to receive reward. After a reversal, the rat must adapt its behavior to press during the ‘light-off’ condition (e.g., Nomura et al., 2004). In parallel to the age-related cognitive deficits discussed above, aging is also associated with changes in attentional processes (Gazzaley & D’Esposito, 2007; Prakash et al., 2009; Hedden et al., 2012). This is accompanied by a greater susceptibility to distraction or interference during the delay period of a working memory task in humans (Bowles & Salthouse, 2003; Campbell et al., 2012) and monkeys (Bartus & Dean,

1979; Phosphatidylethanolamine N-methyltransferase Prendergast et al., 1998). Additionally, fMRI studies in older adults have reported that there is increased activity in brain regions mediating distraction (Milham et al., 2002; Stevens et al., 2008), and in cases where task-irrelevant stimuli are presented (Gazzaley et al., 2005). One of the most consistent finding in the literature on aging brain is a decline in the volume of the PFC of humans, monkeys and rodents. This decline is one of the earliest changes detected, and for almost fifty years it was thought that the decrease in frontal lobe volume was the result of cell loss (Haug, 1986; Peters, 2002). The early reports of cell loss, however, turned out to be an error resulting from differential shrinkage of young and aged tissue during processing (Haug et al.

This study describes the complications associated with health in traumatized permanent teeth (TPT) over a 12-month period and assesses the relationships between TDI, involved tissues, and BIBW2992 cost root development (RD). The study enrolled 294 patients with 548 TPT. Data were collected on the TDI, RD, and the healing complication (HC) and when they were examined (03, 06, and 12 months). Frequencies are described and analyzed using the chi-squared test, relative risk (RR), and Mantel–Haenszel analysis (P ≤ 0.05). Healing complications were present in

201 (36.68%) teeth and were more frequently diagnosed 3 months (63.68%) after the TDI. Pulp necrosis was the most common HC (38.3%), and it was significantly associated with avulsion (P = 0.023). Teeth with complete RD showed a tendency of developing HC over time, independent of TDI (P = 0.05). HC in teeth with complete RD related to support tissue trauma (P = 0.005) and avulsion (P < 0.001) appeared more frequently after 3 months. Healing complications are more common in teeth that have suffered trauma in supporting tissues and avulsion, especially in teeth with complete

RD. The HC occur more frequently in the first 3 months, and a necrotic AG 14699 pulp was the most common complication. “
“Amelogenesis imperfecta (AI) is an inherited dental condition affecting enamel, which can result in significant tooth discolouration and enamel breakdown, requiring lifelong dental care. The possible impact of this condition on children and adolescents from their perspectives is not fully understood. The aim of the study was

to explore the impact of AI on children and adolescents through in-depth interviewing. The information derived from this was then used to construct a questionnaire to distribute to a larger cohort of AI patients. This research involved semistructured in-depth interviews with seven AI patients, and common themes and concepts were then identified using framework analysis. A questionnaire Cediranib (AZD2171) was developed based on the themes and subthemes identified, and completed by 40 AI patients at various stages of treatment. Children and adolescents with AI exhibited concerns regarding aesthetics and function. Patients also expressed a high level of concern regarding comments by other people and self-consciousness associated with this. A small number of AI patients highlighted the effect of their dental treatment and health on their personal life. The results indicate that there are marked impacts on children and adolescents as a result of AI, including aesthetics, function, and psychosocial. “
“International Journal of Paediatric Dentistry 2013; 23: 64–71 Background.  The abuse and neglect of children constitutes a social phenomenon that unfortunately is widespread irrespective of geographic, ethnic, or social background.

Patients regularly followed at the Department of Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy, with known HIV-1 infection since before 1988, no previous diagnosis of DM, and available HCV and HBV serology data were contacted between February and June 2008 and asked: (i) to undergo a complete physical examination,

including blood pressure Epigenetics inhibitor and anthropometry; (ii) to complete a questionnaire to evaluate their family history of DM, their current smoking history, and their use of lipid-lowering agents and antihypertensive medications; (iii) to provide a fasting blood sample for the measurement of glucose, insulin, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides; and (iv) to undergo an OGTT on a different day within a month of the first blood sample. All of the study participants gave their informed consent to take part in the study. Blood samples were collected after an overnight fast (defined as at least 12 h), which was always rigorously verified. All of the parameters were tested by means of routine standard procedures (Diagnostic Unit, San Raffaele Scientific Institute, Laboraf). The homeostatic model assessment for insulin resistance (HOMA-IR) index was calculated according to Matthews et al. as [fasting glucose (mg/dL) × baseline insulin (mIU/L)]/405 [28]. A standard 75-g OGTT was used to assess

2-h post-load glucose levels. Glucose values were interpreted on the basis of the criteria recommended by the American Diabetes Association [1]: FPG<100 mg/dL (<5.6 mmol/L)=normal fasting glucose; FPG 100–125 mg/dL (5.6–6.9 mmol/L)=impaired NVP-BKM120 order fasting glucose; FPG≥126 (≥7 mmol/L)=provisional diagnosis of diabetes; 2-h post-load glucose <140 mg/dL (<7.8 mmol/L) =normal glucose tolerance; 2-h post-load glucose 140–199 mg/dL (7.8–11 mmol/L)=IGT; 2-h post-load glucose ≥200 mg/dL (≥11.1 mmol/L)=provisional diagnosis of diabetes. The subjects' family history of DM was evaluated by means of a self-administered questionnaire and was considered positive if at least one first-degree relative was/had been diabetic. Waist circumference was classified as normal

or abnormal on the basis of see more the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) criteria (abnormal for males: ≥102 cm; abnormal for females: ≥88 cm) [29]. Sitting blood pressure was determined using a sphygmomanometer after a >5-min rest. Coinfection with hepatitis B virus (HBV) and hepatitis C virus (HCV) was defined as the presence of HBV surface antigen and HCV antibodies, respectively. The characteristics of the patients are described using median values and quartiles (Q1–Q3) or frequencies and percentages (%), as appropriate. The differences between subjects with IGT or DM and those with normal OGTT results were assessed for significance using Wilcoxon’s two-sample rank sum test for nonparametric data.

columnare at 5 min postexposure to the mucus. However, when F. columnare cells were pretreated with 50 mM d-mannose, the catfish skin mucus failed to induce the upregulation of gldH, suggesting that gldH might play an important role in the chemotactic

response of F. columnare to catfish skin mucus and that pretreatment of F. columnare with d-mannose might be able to block the chemotactic response of F. columnare to catfish. Whether pretreatment of F. columnare with d-mannose will affect the virulence of F. columnare to catfish merits further study. In summary, using a different pretreatment of F. columnare cells and an in vitro chemotaxis assay, we found Dorsomorphin that at least two major components were involved in the chemotactic responses of F. columnare

to catfish skin mucus. Firstly, the capsule of F. columnare plays an important role in recognizing the extracellular chemoattractants from the catfish mucus through lectin-like receptors. Secondly, one or more gliding motility proteins are involved in the chemotactic response of F. columnare to catfish skin mucus. These components might play important roles in the cell-to-cell communication necessary for gliding the chemotaxis of F. columnare toward catfish skin mucus. However, the exact roles of F. columnare gliding motility proteins in chemotaxis and the identities of the lectin-like receptors on the capsule of F. columnare receptors and the chemoattractants of the catfish skin mucus remain to be further studied. We thank Drs Benjamin LaFrentz (USDA-ARS) and Victor Panangala (USDA collaborator) for critical reviews of the manuscript. Tofacitinib order We thank Beth Peterman and Stacey LaFrentz (USDA-ARS) for their excellent technical support. We also thank the management team of the Aquatic Animal Health Research Unit for daily care and management of the fish. This study of was supported by the USDA/ARS CRIS project #6420-32000-024-00D. The use of trade, firm or corporate names in this publication is for the information and convenience of the reader. Such use does

not constitute an official endorsement or approval by the United States Department of Agriculture or the Agricultural Research Service of any product or service to the exclusion of others that may be suitable. “
“National Institute of Vegetable and Tea Science, Mie, Japan University of Tsukuba, Tsukuba, Japan Fusarium oxysporum produces three kinds of asexual spores: microconidia, macroconidia and chlamydospores. We previously analysed expressed sequence tags during vegetative growth and conidiation in F. oxysporum and found 42 genes that were markedly upregulated during conidiation compared to vegetative growth. One of the genes, FVS1, encodes a protein with a sterile alpha motif (SAM) domain, which functions in protein–protein interactions that are involved in transcriptional or post-transcriptional regulation and signal transduction.

The sex ratio was 9/1 (6/1 in the armed forces as a whole); median age was 33 years (range: 19–56). (per 1000 person-years) Symptoms and clinical signs were

myalgia (95%), fever (94%), headache (90%), retro-orbital pain (56%), rash (25%), and digestive symptoms (21%). Twenty-five patients LY294002 were hospitalized for observation, but their condition was not serious. Surveillance results highlighted dengue circulation in the West Indies, French Polynesia, Africa (Djibouti, Ivory Coast, Mayotte, Tanzania), French Guiana, and Indonesia. More exactly, laboratory results enabled the serotype to be identified: DENV-1 in Guadeloupe, Martinique, French Guiana, New Caledonia, and Djibouti; DENV-3 in Mayotte and Djibouti; and DENV-4 in French Guiana. Incidence rates of dengue according to location are presented in Table 1. The incidence rate was highest in the French West Indies, immediately followed by French Guiana (p < 10−9). The risk was high in the French West Indian islands where an outbreak occurred among the local population during the summer of 2010. No dengue cases occurred in the French military in the Central African Republic, Chad, Gabon, Uganda, Reunion Island, and Senegal. The limits of epidemiological surveillance have to be taken

into account when considering these results. The actual number of cases is usually underestimated, this website resulting from failure to declare cases:[8] In French overseas departments and territories, patients have access to civilian health care and can thus be missed by military surveillance, whereas when stationed in foreign countries, they do not have that choice, but diagnostic capabilities are not always available. To detect

early warning signals for an outbreak, we chose to use a sensitive case definition.[9] That is why possible dengue cases (without biological confirmation but in an epidemic context) and serologically confirmed dengue cases were included. However, serology could create confusion with other flaviviruses due to cross-reactive antibodies. In fact, only confirmed cases using culture, RT-PCR, or Ag NS1 methods were actual dengue cases. Locations where the French armed forces’ epidemiological surveillance system identified dengue circulation in 2010 to 2011 (French West Indies, French Polynesia, French Guiana, Africa, and Indonesia) were well known for dengue virus circulation.[10] Dynein In the French West Indies, the serotype was not the same as during the previous outbreak in 2007.[11] DENV-1 and DENV-4 circulated in 2010, whereas DENV-2 circulated in 2007. This type of situation is usually responsible for intense virus circulation and therefore for outbreaks. Serotype identification is very important to highlight epidemic risk. Our circulation results were complementary to WHO global surveillance results, and could serve to improve knowledge about serotype circulation, that is, detection of DENV-1 circulation in New Caledonia,[12] and DENV-3 in Djibouti.

While the successes achieved in decreasing MTCT are extraordinary, there is still a concern that in utero ART causes mitochondrial toxicity [20]. Many of the NRTIs used in reducing MTCT are NRTIs, including ZDV, which are well known to cause mitochondrial toxicity in adults [21], especially with prolonged exposure [22]. Because NRTIs cross the placenta [23], mitochondrial toxicity is a concern in infants

who have been exposed to them in utero. While studies have shown that clinically apparent disease is rare [4–6,24], many human and primate studies have shown biochemical and histological changes suggestive of mitochondrial toxicity in ART-exposed infants [2–10,12,13,17,20,23,25–27]. However, the exact changes observed, especially in mtDNA content and mitochondrial enzyme expression, vary significantly depending selleck inhibitor on the tissue and cell types analysed, the methods used, and the timing of the collection of samples. In our study, we systematically evaluated mtDNA content in placenta, umbilical cord blood and peripheral infant blood, which had not been previously done, and evaluated mitochondrial enzyme expression level (as an indirect measure of mitochondrial function) in cord blood and infant peripheral blood in HIV-positive/HIV-exposed maternal–infant pairs compared with uninfected controls.

We also evaluated placental oxidative stress levels for the first time. Interestingly, while placental Selleckchem PF-562271 measurements were all similar between Dolichyl-phosphate-mannose-protein mannosyltransferase groups, umbilical cord blood and peripheral infant blood showed significant differences between groups. In umbilical cord blood, mtDNA content was similar between groups but mitochondrial enzyme expression level was significantly decreased in

the HIV-positive/HIV-exposed group. In contrast, infant mitochondrial enzyme expression level was similar between groups, but mtDNA content was significantly increased in the peripheral blood of the HIV-exposed infants. In regression analyses, the significant changes in enzyme expression and mtDNA in the cord and infant blood, respectively, were most associated with HIV/ART exposure. Increased mtDNA content in the infants was also associated with increasing maternal age. While it may seem counterintuitive to observe increased mtDNA content in HIV/ART-exposed infants, these findings may suggest an in utero compensatory mechanism to overcome HIV/ART-associated mitochondrial toxicity. Specifically, the quantity of mtDNA may increase in the infant as HIV/ART exposure has caused a decrease in mitochondrial enzyme expression in the umbilical cord blood. This concept of in utero mtDNA proliferation in HIV/ART-exposed and HIV-infected infants is consistent with the findings of a few other studies [8,12,13,25,26]. Côté et al.