29 [95% confidence interval (CI) 092–180] Rebound risks increa

29 [95% confidence interval (CI) 0.92–1.80]. Rebound risks increased with decreasing levels of coverage: patients with 80–95% adherence had a 2.69% risk of rebound

(compared with 100% adherence: RR=1.62; 95% CI 1.23–2.14), patients with 60–80% adherence had a 3.15% risk of rebound (RR=1.90; 95% CI 1.39–2.61) and patients with adherence below 60% had a 3.26% risk of rebound (RR=1.97; 95% CI 1.40–2.78). When the percentage of drug coverage was analysed as a continuous variable (thus assuming that the true underlying relationship between adherence and the log risk ratio is linear) the risk of viral rebound decreased by 9% (RR=0.91; 95% CI 0.87–0.95; P=0.0001) per 10% higher coverage. After adjusting for potential confounding factors (variables shown in Table 2), low levels of drug coverage continued to be significantly associated with viral rebound: rates of viral rebound were increased by 51% (RR=1.51; 95% CI 1.14–1.99), learn more 70% (RR=1.70; 95% CI 1.24–2.33) and 75% (RR=1.75;

95% CI 1.24–2.47) in patients who had drug coverage of 80–95, 60–80 and <60%, respectively (Fig. 2). When the drug coverage was analysed as a continuous variable, the risk of viral rebound decreased by 7% per 10% higher adherence (RR=0.93; 95% CI 0.88–0.98; P=0.004). Other KPT 330 independent predictors of viral rebound were shorter duration of VL suppression, higher number of previous virological failures, currently being on an unboosted PI regimen compared with an NNRTI-containing regimen, having experienced two or more treatment interruptions (while VL detectable at the time), having started HAART in the calendar period 1997–1999 compared with 2003–2006, and having a time-zero for the DCVL episode in the period 2002–2003 compared with 2006–2007. The results of the analysis stratified by most common current regimen (unboosted PI, boosted PI and NNRTI-based regimen) suggested that the risk of viral rebound at a particular level of adherence differed according to the regimen type received (Fig. 3). For example, at the lowest levels of adherence (≤60%), the risk of rebound was,

respectively, 5.24, 3.50 and 2.19%, for patients receiving unboosted Pyruvate dehydrogenase PI, boosted PI and NNRTI-based regimens, while among subjects who adhered completely these risks were 1.46, 1.89 and 1.47%, respectively. In sensitivity analyses, we considered the proportion of days covered by a prescription for at least one drug, instead of three, as our adherence measure and obtained similar results (data not shown). In addition, we considered the effect of modifying the definition of viral rebound from a threshold of 200 to 50 copies/mL. In this case, the overall risk of rebound was higher (5.36%) but the factors associated with rebound were generally similar. The estimated RR of VL rebound for a 10% higher coverage was 0.95 (95% CI 0.92–0.99), and after adjusting for the risk factors considered in the main analysis, the RR weakened marginally to 0.97 (95% CI 0.93–1.

Arousal was not formally assessed in our study, eg by scores or

Arousal was not formally assessed in our study, e.g. by scores or skin conductance responses. Therefore, we cannot make judgements regarding the level of arousal. However, the fact that there was a matching in the behavioural results of the tasks does aid the interpretation of the motor data in that any differences seen for the two behavioural conditions are a consequence of differences relating to underlying processes in performing them (presumably related to the differences in external and internal attention) rather than potentially a result of different associated difficulties. Whatever

the final explanation, the results are of relevance to a number of different disorders. As noted in the Introduction, focal dystonia often appears to be associated with the repeated performance of movements made under conditions of highly focussed attention, Protein Tyrosine Kinase inhibitor such as occur in professional musicians. Indeed, attention is an important part of learning. However, too great a focus on one area may reduce inhibitory control in other areas and potentially contribute to an overflow of activity. In healthy individuals, this is often seen in the early phases of learning a Dabrafenib new skill, but this is gradually reduced as learning progresses. It may that this natural process is defective in focal dystonia and leads to the persisting and unwanted activity characteristic

of the condition. It is remarkable how widespread is the range of disorders that involve abnormal SICI, e.g. dystonia (Sommer et al., 2002), Tourette’s syndrome (Orth & Rothwell, 2009), and first-episode schizophrenia (Wobrock et al., 2008). The interpretation tends to be that intracortical GABAA circuits per se are impaired. The

current study demonstrates a modulation towards a reduced amount of SICI when healthy participants pay attention to an internal or external locus. Therefore, the reduced inhibition seen in so many disorders might, in some cases, be explained by differences in cognitive states (attention state) rather than being a genuine physiological marker. A practical relevance of the present results seems more striking. High levels of attention are required for learning that interacts with synaptic plasticity processes (Ziemann et al., 2004). Behavioural data are supported by experimental methods that demonstrate the SSR128129E interaction between attention and plasticity-inducing protocols (Stefan et al., 2004) that are facilitated by directing the subject’s attention to their own hand. This might be mediated via the fine tuning of inhibitory and excitatory circuits in the M1. A necessity of all goal-directed movements is the right balance between inhibiting and facilitating components. To reach an overall economical activation it is vital to be able to relax, for example, antagonistic muscles. The playing-related health problems of musicians are often the end-stage of suboptimal learning processes.

The primary endpoints of the present substudy were changes from b

The primary endpoints of the present substudy were changes from baseline in plasma levels of interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte

chemotactic protein-1 (MCP-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble CD40 ligand (sCD40L), soluble P-selectin (sP-selectin) and tissue plasminogen activator (t-PA) in selleck chemicals llc the two arms at months 12, 24 and 36. Secondary endpoints were correlations of these biomarkers with viral load and plasma lipids. At baseline and at months 12, 24 and 36, venous blood samples were obtained after an overnight fast and frozen at −70°C until analysis. IL-6, IL-8, MCP-1, sVCAM-1, sCD40L, sP-selectin and t-PA levels were measured in cell supernatants by a multiplex cytometric bead-based assay (Human Cardiovascular MAPK Inhibitor Library 7plex FlowCytomix Multiplex; Bender Medsystems GmbH, Vienna, Austria), using an EPICS-XL-MCL

flow cytometer (Beckman Coulter, IZASA, Barcelona, Spain), following the manufacturer’s protocol. In brief, 25 μL of the 7 mixed beads and biotin-conjugate mixture was mixed with 25 μL of the standards or samples provided and incubated in the dark for 2 h at room temperature. Samples were then washed, 25 μL of streptavidin-phycoerythrin (PE) solution was added, and incubation was carried out for a further 1 h. After the second incubation, samples were washed and resuspended in 300 μL of assay buffer. The EPICS-XL-MCL flow cytometer was calibrated with set-up beads and 300 events were acquired for each factor and each sample, respectively. Individual analyte concentrations were indicated by their fluorescence intensities (FL-2) and

computed with the respective standard reference curve and FlowCytomixPro 2.2 software. Standard curves were determined for each biomarker from a range of 27 pg/mL to 40 000 ng/mL. According to the manufacturer, the detection limits of the assay are 0.9 pg/mL for IL-6, 7.9 pg/mL for IL-8, 53.0 ng/mL for sP-selectin, 8.0 pg/mL for t-PA, 11.0 pg/mL for MCP-1, 0.4 ng/mL for sVCAM-1, and 50.0 pg/mL for sCD40L. Total-c, HDL-c and triglycerides were measured using standard methods. LDL-c was calculated using the Friedewald equation. Peripheral blood CD4 T-cell count was determined by flow cytometry and plasma viral load by real-time polymerase chain reaction (PCR) (Abbott RealTime HIV-1; Parvulin Abbott Laboratories, Abbott Park, IL). Quantitative variables are expressed as the median and interquartile range (IQR). Before the statistical analysis, the normality of distributions and homogeneity of variances were tested. sP-selectin and sCD40L were log10-transformed because of high distribution variability. The two-sample t-test or Mann–Whitney U-test was used to compare continuous variables between arms. Qualitative variables were compared using the χ2 or Fisher exact test. Baseline and follow-up values in each arm were compared with the paired t-test or Wilcoxon signed rank test.

For each experimental session a new word list was presented The

For each experimental session a new word list was presented. The list was composed of complexity-matched words (see Supporting Information). During the mental activity, subjects were instructed to imagine the movements from a first person perspective and to employ kinesthetic cues (e.g. the feeling of the pen in their hand). The anodal tDCS was administered for 13 min during the whole course of the MP. Continuous direct currents were transferred by saline-soaked surface sponge electrodes (surface 20 cm2) and delivered by a clinical microcurrent stimulator (Soterix, USA) with a maximum output of 2 mA. Five different electrode montages

were tested to find the optimal position for DC stimulation in increasing the neuroplastic effects of mental imagery on motor

performance. The excitatory tDCS was applied over the: (i) right JQ1 mouse M1, (ii) right premotor area (PMA), (iii) right SMA, (iv) right cerebellar hemisphere, and (v) left dorsolateral prefrontal cortex. For M1 tDCS, the anode electrode was positioned above C3 (international 10-20 system) (Nitsche et al., 2003b). For stimulation of the premotor cortex, it was moved 2 cm forward and 2 cm to the midline relative to the M1 position (Nitsche et al., 2003b). The SMA tDCS was performed with the anode electrode placed 2 cm anterior to the vertex (position Cz), in the sagittal midline (Cunnington et al., 1996). For DC stimulation of the dorsolateral prefrontal cortex, the anode electrode was positioned 5 cm forward relative to C3 (Nitsche et al., 2003b). In all cases, the reference electrode was placed above the contralateral orbit. For cerebellar tDCS, electrodes were placed with Dabrafenib one (anode electrode) over the right cerebellar hemisphere, 3 cm lateral to the inion (Ugawa et al., 1995), and the other over the deltoid muscle (Ferrucci et al., 2008). These methods of electrode montage have been used in previous studies and been shown to be effective in the modulation of cerebral activity. The order of stimulation condition was counterbalanced across subjects. The anodal tDCS was administered with a current strength of 2 mA. In

the sham session, tDCS was applied over the M1 for 30 s, Chlormezanone a method shown to achieve a good level of blinding (Gandiga et al., 2006). In each experimental session, motor performance was assessed by the handwriting test. This test measured legibility and writing time, important elements in handwriting performance (Bonney, 1992). Handwriting is a complex perceptual–motor skill that includes fine motor control (hand manipulation, bilateral integration, and motor planning) (Feder & Majnemer, 2007). For the test, the subjects were instructed to copy a six-word set with the non-dominant hand on a blank sheet of paper positioned on a table to the left of the subject. The word list was presented approximately three inches away from the paper. The handwriting task was performed with spontaneous production, free from the influence of the writing instructions.

Although the great majority of parents were knowledgeable about t

Although the great majority of parents were knowledgeable about the malaria risk in their home countries, malaria chemoprophylaxis was insufficiently used by children

traveling to the families’ countries of origin.7 Hickey and colleagues complement this picture by elegantly showing, with specialized mapping software, how children diagnosed with malaria in Washington, DC reside mainly in neighborhoods of the city and surrounding suburban districts that are predominantly home to recent immigrants from sub-Saharan Africa. Likewise, the analysis of national data in their study highlights that US selleckchem regions, where immigrants from sub-Saharan Africa have preferentially settled, carry a disproportionate burden of pediatric malaria cases.8 So the bull’s SAHA HDAC nmr eye has been identified once again and travel medicine practitioners need to be proactive. The first step, obviously, is to engage such children and their families in pretravel health advice. This target group is, however, difficult to reach. Strategies ranging from innovative educational initiatives, utilizing community-based avenues via eg, schools, sports clubs, and religious institutions to local language media programs via eg, radio, television, and internet to actively highlight malaria prevention are imperative. Additionally,

easy access to effective pretravel advice within primary care offices is essential as this target group is unlikely to consult a specialized pretravel clinic.1–3 The efficacy of such community programs is unclear, and needs to be formally assessed. Furthermore, it is important to note that the development of such programs will have to compete for public Etofibrate health funds with the urgent need to tackle other major costly public health challenges (eg,

asthma and obesity) that notoriously affect children in large urban inner cities and therefore acutely overlap with areas where immigrant populations prefer to settle.9 Malaria is a preventable infectious disease. The use of personal protection measures such as mosquito nets, insecticides, and repellents is effective and can be recommended even for very young children and this approach should be explained in detail to parents if they present for pretravel advice. Failure to take appropriate antimalarial chemoprophylaxis is probably the central risk factor for contracting malaria in pediatric travelers to high risk malaria endemic areas. Use of and adherence to chemoprophylaxis regimens is poor.3 Licensing and recommendations on the use of antimalarials in children differ internationally. For example, mefloquine is not licensed in Australia for children younger than 14 years and in Japan, no malaria chemoprophylaxis is licensed for use in children.

We also expected to find a greater impact of CDSSs on prescribing

We also expected to find a greater impact of CDSSs on prescribing outcomes than clinical outcomes and examined whether multi-faceted Cisplatin in vivo interventions would have a greater impact than CDSS alone. We included English-language studies, published between 1990 and March 2009, reporting RCTs and strong quasi-experiments (non-randomised studies with comparison groups or interrupted

time-series designs with or without comparison groups). The studies had to: target pharmacists; compare the performance of the CDSSs to routine care and/or paper-based decision support; provide information that could be applied to a specific patient (e.g. provide advice to prescribe a particular drug, to monitor a drug or adjust the dose or to perform laboratory tests related to safe prescribing); generate information or advice to the pharmacist in an electronic format (however, subsequent delivery of information to physicians or patients could be in electronic or paper formats); and report data on at least one outcome relating to prescribing, clinical or patient outcomes (see Table 1). Studies were excluded if: interventions were based around hypothetical scenarios rather than actual clinical

practice, studies did not undertake statistical analyses or studies reported only cost outcomes. We searched Medline (1990–March see more 2009), PreMedline (18 March 2009), Embase (1990–March 2009), CINAHL (1990–March 2009) and PsycINFO (1990–March 2009). We combined keywords and subject headings to identify computer-based

decision support (e.g. decision support systems clinical, decision making computer assisted), medicines use (e.g. prescription Vasopressin Receptor drug, drug utilization) and pharmacy or pharmacists. We also searched INSPEC (March 2009) and the Cochrane Database of Systematic Reviews (March 2009) including reviews and protocols published under the Effective Practice and Organisation of Care Group (EPOC). Finally, we hand-searched the reference lists of retrieved articles and reviews. Table 2 details the full search strategy. Two reviewers (JR, EW) evaluated independently the study titles and abstracts identified in the search. Full-text articles were retrieved if either reviewer considered a citation potentially relevant. Studies deemed eligible for review underwent data extraction by two reviewers (JR, EW). Disagreements were resolved by discussion to reach consensus. We extracted the following information from eligible studies: objectives, clinical setting (ambulatory or institutional care) and details of the decision-support intervention (e.g. system-initiated or user-initiated, multi-faceted or CDSS alone, clinical target). We classified studies as having a safety or a QUM focus. Given the lack of uniformity in relation to terminology about prompts, alerts and reminders we extracted details as they were reported in the articles.

, 1995; Kanoh et al, 1999) We noticed that the efficiency of ge

, 1995; Kanoh et al., 1999). We noticed that the efficiency of genomic DNA extraction during incompatible combination was reduced, suggesting that random genomic DNA degradation might have occurred. This phenomenon seems to be reflected in EPZ-6438 the reduction of the electron density of nuclei and nucleolus. Mitochondrion was the most stable cell component in the incompatible reaction. In mammals, Ras-mediated caspase-independent cell death was a typical feature of stable mitochondria (Chi et al., 1999). These phenomena were different from

typical features of known PCD. The alteration of the vacuole is inherent in fungal and plant species. The vacuole contains numerous hydrolytic enzymes, i.e. lipase, nuclease, and protease, and is therefore considered to be a ‘lytic compartment’ (Klionsky et al., 1990; Wink, 1993; Weber et al., 2001). Once the vacuole is collapsed, these degrading enzymes would sequentially break down the cell components. Although this process seems to be passive, the alteration of vacuole may be highly programmed, which suggests that a novel type of PCD may exist in fungi. A similar type of PCD was observed with mycelial incompatibility in ascomycetes fungus Rosellinia necatrix (Inoue et al., 2010). Another important finding was that PCD started with

one of the two approaching hyphae. A possible explanation is that the strength of recognition of the incompatibility factor AG-014699 concentration or the efficiency of the signaling cascade responsible for the incompatibility reaction differs among the combinations of isolates. Understanding the mechanism of PCD will help to develop a strategy PRKACG to transmit virocontrol agent to the arbitrary isolates. Further studies are needed to identify the genes involved in PCD of the heterogenic incompatibility system. We thank Drs Naoyuki Matsumoto

and Hitoshi Nakamura for valuable suggestions. This research was supported by the program for Promotion of Basic and Applied Researches for Innovations in Bio-oriented Industry. “
“Neocarzinostatin (NCS) is an enediyne antibiotic produced by Streptomyces carzinostaticus. The NCS chromophore consists of an enediyne core, a sugar moiety, and a naphthoic acid (NA) moiety. The latter plays a key role in binding the NCS chromophore to its apoprotein to protect and stabilize the bioactive NCS chromophore. In this study, we expressed three genes: ncsB (naphthoic acid synthase), ncsB3 (P450 hydroxylase), and ncsB1 (O-methyltransferase), in Streptomyces lividans TK24. The three genes were sufficient to produce 2-hydroxy-7-methoxy-5-methyl-1-naphthoic acid. Production was analyzed and confirmed by LC–MS and nuclear magnetic resonance. Here, we report the functional characterization of ncsB3 and thereby elucidate the complete biosynthetic pathway of NA moiety of the NCS chromophore. A variety of organisms, including Streptomyces carzinostaticus, naturally produce enediyne compounds.

[40] Tall-man lettering has been reported to reduce medication na

[40] Tall-man lettering has been reported to reduce medication name confusion Metformin in a number of different groups of people, of different ages and professions, in laboratory-based tasks.[45] However, an evaluation

conducted for the UK National Health Service cautions a pragmatic approach to the widespread implementation of tall-man lettering and suggests that the prevalence of other more likely errors indicate the need for broad research rather than just this limited potential solution to one aspect of the problem.[47] Some suggested solutions focus on the characteristics of the locations where people obtain and take medicines. Strategies for use at the health centre level include: adding

special warning labels to identify medications with the potential to be confused; adding a verification step (by a second staff member) to the process of medication selection; publishing information bulletins warning of potential look-alike, sound-alike drug names; and proactively identifying potential look-alike products through the involvement of inventory control technicians.[31] No evaluation to determine whether this intensive programme reduces errors was reported. Another strategy for managing look-alike, sound-alike drugs suggests using the JCAHO STAT inhibitor list of problematic drug names to: identify drugs that are used by a home-care or hospice organisation; review patient medication profiles; and conduct home

medication management reviews.[35] Other suggested risk reduction strategies have included: healthcare workers being kept aware of medications that look or sound alike; the installation of pop-up alerts and bar coding on computer systems; putting distinctive labels and warning stickers on storage bins; and storing confusable medications in non-adjacent locations.[18] Bar coding of medicines is sometimes considered Olopatadine a promising approach to reducing the level of dispensing errors.[22] However, this is dependent on the correct medicine being ordered and so does not eliminate problems of confusion in actual prescription. It also relies on pharmaceutical companies following a consistent bar-coding convention. Educating patients on the risks of look-alike, sound-alike medications has also been suggested as an important line of defence against this type of medication error.[17,35] A systems approach to risk reduction suggests that solutions should be implemented at all levels; medication production, dispensing, preparation and administration stages. This includes manufacturers and regulatory authorities being vigilant when new medications are named.[7] Such an approach must be complemented with a consumer focus, including consumer education, access to pharmacist counselling, and ensuring that consumers know and feel empowered to ask questions.

Sixteen percent took acetazolamide preventively (median dose 250

Sixteen percent took acetazolamide preventively (median dose 250 mg/d or 3 mg/kg/d, range 1–7 mg/kg/d) for a median of 4 days (range

1–21 d). Those who took acetazolamide preventively spent the same number of nights between 1,500 and 2,500 m, but their mean-maximum overnight altitude was slightly higher than of those who did not take it preventively: 4,178 m versus 3,917 m (p = 0.000). Five hundred and thirty-one (74%) travelers find more had physical complaints on the first days at or above 2,500 m: headache (47%), shortness of breath (44%), fatigue (23%), nausea/vomiting (14%), sleeping disorders (14%), and dizziness (4%). Other complaints included diarrhea, epistaxis, palpitations, and edema of the fingers. One person was “talking Z-VAD-FMK ic50 nonsense” for 20 minutes without any other complaint. Seven individuals had tingling sensations, six of whom took acetazolamide as prevention or treatment. One hundred and eighty-four responders (25%) had complaints that met the definition of AMS. Most (76%) of these complaints disappeared within 3 days. Some travelers with AMS adapted their travel schedule, while about half of them climbed higher despite symptoms (Table

2). Of the latter a quarter experienced worsening of symptoms. Of those who did not climb higher with symptoms, 64% were free from symptoms within 2 days, compared with 48% for those who continued to climb, but the difference was not significant (p = 0.655). The majority took medication, mostly analgesics, followed by acetazolamide and coca-leaves or -tablets. Thirty-four percent took acetazolamide for treatment at a median dose of 375 mg/d or 5 mg/kg/d (range 1–11 mg/kg/d) and a median duration of 3 days (range 1–15 d). Several travelers remarked that they did not know when to start taking acetazolamide exactly and that traveling companions had received different advice on its use. Four travelers received oxygen; all reported dyspnoea but only one met the AMS criteria. Those who did not take any medication often argued Mannose-binding protein-associated serine protease that their symptoms

were not severe enough to start acetazolamide. Those who took coca preparations often remarked that the guides had recommended coca or “soroche-pills” over acetazolamide. The majority climbed higher after the AMS symptoms disappeared; 26% of them reported that the AMS symptoms recurred. In univariate analysis, previous AMS (p = 0.014), gender (p = 0.030), age (p = 0.037), maximum overnight altitude (p = 0.015), average altitude increase in meter per day above 2,500 (p = 0.046), and number of nights between 1,500 and 2,500 m at the beginning of the journey (p = 0.000) were associated with the development of AMS (Table 3). There was no association between AMS and destination (p = 0.

To truly distinguish whether a streptomycin-resistant mutant is i

To truly distinguish whether a streptomycin-resistant mutant is introduced by transformation

via electroporation or generated by spontaneous mutation, we created two silent mutations flanking the missense mutation of codon 43 of rpsL-SR1 (Fig. 1). PCR amplicon was generated from this mutation, named rpsL-WM, and used to transform V. parvula PK1910. Obeticholic Acid chemical structure In five independent experiments, we obtained similar results: when equal amounts of DNA was used, rpsL-WM transformation always gave two to three times more streptomycin-resistant colonies than rpsL-WT transformation. The result of one transformation was shown in Fig. 2a. The rpsL gene from all these streptomycin-resistant colonies was then sequenced. Of the 19 colonies from rpsL-WM transformation, 11 contained the rpsL-WM sequence (Fig. 2b), three had the rpsL-SR1 sequence, and five had the rpsL-SR2 sequence. In contrast, of the nine colonies from the rpsL-WT transformation, five had the rpsL-SR1 sequence, four had the rpsL-SR2, and no colony had the rpsL-WM sequence. This result unequivocally demonstrates that V. parvula PK1910 is transformable. Veillonellae bacteria have so far remained as one of the most prevalent yet least studied microorganisms

in the human oral microbiome, largely due to our inability to genetically transform them. In this study, we set forth to test the transformability of Dinaciclib V. parvula strain PK1910, inspired by the finding of multiple competence-related genes on its genome. To this end, we have generated a ‘watermarked’rpsL gene conferring streptomycin resistance and shown that V. parvula PK1910 is transformable by electroporation. To our knowledge, this is the first report of genetic transformation in veillonellae. Electroporation has been successfully

used for DNA transformation in a large number of bacteria, such as Lactococcus lactis, Clostridium perfringens, Propionibacterium acnes, and Fusobacterium nucleatum, with varying optimal conditions for each bacterium (McIntyre & Harlander, 1989; Jiraskova et al., 2005; Kinder Haake et al., 2006; Cheong et al., 2008). In our efforts to optimize the procedure for transformation, we identified several parameters important to V. parvula transformation. First, the culturing media and Phosphatidylinositol diacylglycerol-lyase cell growth stage are important. Veillonella parvula could be reproducibly transformed only when cells were grown in ASSPL medium and harvested at the early exponential phase. Another parameter important to transformation is MgCl2 in the electroporation buffer. The incorporation of 1 mM MgCl2 in the electroporation buffer is required for the success of transformation. The pulse length and voltage of electroporation are also important. Success was repeatedly achieved with field strength of 20 kV cm−1, capacitance of 25 μF, and resistance setting of 200 Ω. Because our goal in this study was to examine the possibility of using electroporation to introduce DNA into V.