Thus, Mys and Mew can be efficiently delivered to dendrites. Integrins are cell-surface receptors of ligands residing in the ECM, including collagen, fibronectin, laminin, tenascin, and vitronectin (Humphries et al., 2006). The binding specificity of the integrin heterodimer is largely determined by the α subunit (Barczyk et al., 2010). As the α1 subunit Mew belongs

to the laminin-binding type α family (Hynes and Zhao, 2000), we tested the role of laminins, which are protein complexes formed by three subunits (Durbeej, 2010). In Drosophila, wing blister (wb), and Laminin A (LanA) encode two α subunits, whereas LanB1 and LanB2 code for the β and γ subunits, respectively. Since null mutations in laminin genes cause lethality

at embryonic or early larval stages, we first sought to use the RNAi strategy to knock down laminins. Expression of a UAS-wb-RNAi construct in the wing selleck compound caused wing blisters, mimicking the wb loss-of-function (LOF) phenotype, whereas the available UAS-LanA-RNAi did not yield obvious wing phenotypes (data not shown). We therefore only tested wb RNAi, which did not generate obvious phenotype when expressed in class IV da neurons (data not shown). Since the basal surface of the larval epidermis contacts no other tissues except at the muscle attachment sites, the epidermis is likely the major source of laminins in the ECM. When we drove the expression of UAS-wb-RNAi in posterior epidermal cells of every segment with hh-Gal4, 21.36% of dendrites were found to be enclosed learn more by the epidermis ( Figures 5B and 5C), compared to just 1.92% in the control ( Figures 5A and 5C). The defective positioning of dendrites is unlikely a result of altered epithelial polarity of epidermal cells, as the localization of several cell polarity markers are normal in cells where wb is knocked down ( Figure S2), suggesting that wb is important

for dendrite attachment to the ECM. We next asked if laminin mutants genetically interact Thalidomide with mys and mew. Transheterozygotes of mys1/wb09437 and mys1/LanA9-32 showed mild but statistically significant increase in dendrite enclosure at the dorsal midline ( Figures 5D, 5E, and 5J) compared to mys1/+. Likewise, mewM6/wb09437 and mewM6/LanA9-32 showed similar enhancement ( Figures 5G, 5H, and 5J) compared to mewM6/+. In addition, a hypomorphic allele of LanB2, LanB2MB04039, showed mild genetic interactions with mys1 and mewM6 ( Figures 5F, 5I, and 5J). The weak genetic interactions between integrin mutants and laminin mutants may indicate that laminins are abundantly expressed in the epidermis even with only one functional copy. Taken together, our data support the idea that laminins are the ECM ligands of neuronal integrins in the dendrite-ECM interaction.

However, the usefulness of the calyx preparation has been limited by the fact that many conventional mouse knock out (KO) models are perinatally lethal. To overcome this limitation and to allow for a direct study of the

presynaptic roles of RIM proteins, we have devised a Cre-lox based conditional KO approach at the calyx of Held synapse, using recently generated RIM1/2 floxed mouse lines (Kaeser et al., 2011). We show that the conditional removal of RIM proteins leads to a strong decrease of Ca2+ currents in the nerve terminal, providing direct evidence that RIMs enrich Ca2+ channels at the presynaptic active zone. RIM1/2 removal also led to a marked reduction in see more the number of readily releasable vesicles, which was paralleled by a similar reduction in the number of docked vesicles.

Moreover, RIM proteins help to speed the rates of transmitter release both intrinsically and by increasing the coupling of readily releasable vesicles with Ca2+ channels. Thus, RIM proteins coordinate essential functions that ensure fast rates of transmitter release Trametinib molecular weight at synapses. We wished to investigate the presynaptic function of RIM proteins at the calyx of Held, a large CNS model synapse at which direct measurement of presynaptic Ca2+ currents can be made (see Introduction). However, constitutive RIM1α/RIM2α double KO mice die at birth (Schoch et al., 2006), which precludes their analysis at the calyx of Held, and deleting individual RIM isoforms might produce only a weak phenotype because of the functional redundancy among the isoforms (Schoch

et al., 2006 and Kaeser et al., 2008). We therefore aimed to remove RIM1/2 conditionally at the calyx of Held, using recently produced floxed mouse lines in which the expression of all RIM1 and RIM2 isoforms, including RIM1β and RIM2β, can be abolished by expression of Cre-recombinase (Kaeser et al., 2011). For this purpose, we searched for a Cre-driver mouse line that expresses Cre-recombinase specifically in the lower auditory brainstem where calyces of Held are located. We found that in Krox20+/Cre mice (Voiculescu et al., 2000), Cre-activity as revealed of by a tandem-dimer red fluorescence protein (tdRFP) reporter mouse line (Luche et al., 2007) was present in the lower auditory brainstem as well as in the trigeminal nucleus and some adjacent areas, but importantly, most other areas of the brainstem and CNS were devoid of Cre activity (Figure S1A, available online). In the ventral cochlear nucleus, which harbors globular bushy cells that generate calyces of Held (see Cant and Benson, 2003, and references therein), a large number of tdRFP-positive neurons were found (Figure S1B and Figure 1A).

Therefore, we tested whether hSK3Δ-expressing mice are less anxious than GFP controls, which could explain the lack of impact of the light on the GSK2656157 mw latency of reward retrieval. We detected no significant differences between groups in either an open field or elevated plus-maze task (Figure S6). Failure to attend to an unexpected sensory

stimulus in hSK3Δ-expressing mice is consistent with a deficit in sensory gating. To confirm this hypothesis, we tested mice in an acoustic prepulse inhibition (PPI) paradigm, a standard reflexive measure of sensory gating used in both humans and rodents that is sensitive to alterations in dopamine (Swerdlow et al., 1994 and Ralph-Williams et al., 2002). We observed significantly

reduced PPI in hSK3ΔGFP-expressing mice compared to GFP controls (Figure 6E). Consistent with a disruption of the dopamine system, this effect was reversed by acute treatment with the antipsychotic dopamine D2 receptor antagonist haloperidol (Figure 6F). No differences were detected in baseline startle responses between groups (Figure S6). To establish whether disruption of sensory gating caused by expression of hSK3Δ is related to changes in dopamine neuron activity, we used a genetic mouse line in which activation of dopamine neurons can be induced rapidly and reversibly (Güler et al., 2012). In this model, TRPV1, a calcium-permeable cation channel, is expressed exclusively in dopamine Bafilomycin A1 mw neurons (TRPV1-DA mice; Figure 6G), and moderate doses of the TRPV1 agonist capsaicin, a component of chili peppers, increase dopamine burst firing (Güler et al., 2012). The effects of capsaicin are transient, lasting only 15–20 min (Güler et al., 2012); therefore, we assessed PPI in TRPV1-DA mice with an abbreviated protocol using only one prepulse volume (75 dB). Injection of capsaicin immediately prior

to testing reduced PPI compared to vehicle injections in the same animals (Figure 6H). As in hSK3ΔGFP-expressing mice, this reduction was blocked by haloperidol PDK4 (Figure 6H). Disruption of sensory-motor gating in hSK3Δ-expressing mice is consistent with an alteration in corticostriatal dopamine signaling (Swerdlow et al., 1994). In addition to impairing PPI, enhanced dopamine release can also potentiate behavioral responses to psychomimetic drugs, such as MK-801 (Gainetdinov et al., 2001), in part through a glutamate- and dopamine-dependent corticomeso feedback loop (Moghaddam et al., 1997). To establish whether altered dopamine activity and potentiated dopamine release associated with hSK3Δ expression alters sensitivity to a psychomimetic drug, we monitored locomotor responses in hSK3ΔGFP- or GFP-expressing mice before and after administration of low doses of MK-801. Systemic administration of MK-801 significantly enhanced locomotion in hSK3ΔGFP mice relative to GFP controls. This effect was blocked by pretreatment with haloperidol (Figures 7A and 7B).

However, very long-term expression of any membrane (or other exogenous) protein with even more moderate-strength promoters can cause toxicity,

and we have found that expression strength and time of expression interact in giving rise to this phenomenon. When employed, fusion proteins could appear to mimic such an effect, but some fluorescent proteins such as mCherry to which opsins www.selleckchem.com/products/fg-4592.html are commonly fused themselves can clump and accumulate, while not necessarily impairing opsin function or cell health (e.g., Adamantidis et al., 2007). Regardless, it is important to track membrane resistance and resting potential; modest trends of effects on these membrane properties are occasionally seen with high level opsin expression. Especially when such an effect is observed, it is important to carry out no-light controls

in opsin-expressing tissue or animals. Indeed, in theory not only intrinsic neuronal properties (such as input resistance, membrane capacitance, and excitability) could be altered by toxicity linked Crenolanib price to long-term or very high-level membrane protein overexpression, but even functional output and effective synaptic connectivity could be altered. A no-light control condition in which the tissue is virally transduced, but no light is delivered, can address these effects and is especially valuable when the light delivery paradigm does not involve switching on-and-off and therefore within-animal controls are less feasible (Tsai et al., 2009). For invertebrates such as C. elegans and D. melanogaster, where retinal is not present but may be easily supplied in food or substrate, another type of control is possible, the retinal-negative condition ( Zhang et al., 2007). Light used to activate opsins may also produce nonspecific effects. Light leaking

from the delivery apparatus, or scattered through brain tissue may reach light-sensing organs such as the retina, directly affecting neural activity, or leading to changes in an animal’s behavior. Light absorbed by the tissue could also result in photodamage or local temperature increases. It is therefore critical that parallel no-opsin control experiments using identical illumination conditions are included in optogenetic experiments (e.g., Adamantidis et al., 2007, Tsai et al., 2009 and Lee et al., 2010). The issue of tissue heating by light deserves special consideration, since even temperature changes too small to cause detectable tissue damage can lead to significant physiological (Moser et al., 1993) and behavioral (Long and Fee, 2008) effects. Consider pulsed laser light delivered to a deep brain region by a thin optical fiber. Light is emitted in a conical pattern, then scattered and absorbed as it passes through optically inhomogeneous brain tissue. Heat will be generated wherever light is absorbed, in proportion to the light intensity at each point, giving rise to a heat source that is distributed throughout the tissue.

Intracarotid infusions of graded concentrations of NaCl (0.3, 0.9, and 2.1 Osm/l) induced a significant and dose-dependent increase in RSNA (p < 0.0001, n = 7; Figures 8C and 8D). This osmotically driven sympathoexcitatory response was significantly attenuated (∼50%) by a previous bilateral microinjection of the V1a antagonist within the PVN (2 nmol in 100 nl; p < 0.001 versus control; Figures 8C and 8D). As shown in Figure 8E, the intracarotid osmotic stimulation evoked a significant increase in VP release within the SON (p < 0.001, one-way ANOVA repeated measures; n = 7). These results indicate that osmotically driven

dendritic VP release participates in the recruitment of presympathetic neurons during a homeostatic challenge requiring an orchestrated neurosecretory and sympathetic response. The two modalities by which the PVN commands the KU-55933 mw learn more generation of complex homeostatic responses are represented in distinct neuronal populations, including neurosecretory neurons projecting to the median eminence or the posterior pituitary, and presympathetic neurons innervating the spinal cord and/or brainstem nuclei, including the RVLM (Swanson and Sawchenko, 1980). Given its diverse, though well-characterized anatomical and functional

organization, the PVN stands as an ideal brain region to study interpopulation signaling modalities in the brain. Despite its highly integrative function, it is well documented that neurosecretory and presympathetic PVN neuronal populations are anatomically compartmentalized, displaying a minimal or complete lack of hardwired see more interconnections (Hatton et al., 1985, Swanson and Kuypers, 1980 and Swanson et al., 1980). This has led to the notion that polymodal homeostatic control by the PVN involves parallel processing of neuroendocrine and autonomic information. In this study, we challenged this prevailing idea by testing the hypothesis that dendritic release of peptides serves as an interpopulation signal mediating crosstalk between neurosecretory and presympathetic PVN

neuronal populations. Along with nigrostriatal dopaminergic neurons (Cheramy et al., 1981), hypothalamic MNNs are one of the best-characterized prototypes of dendritic neurotransmitter release (Ludwig and Leng, 2006). Dendritic release of VP and OT from MNNs acts as powerful feedback signals by which MNNs autoregulate their own activity, to optimize systemic hormone release in response to physiologically relevant challenges (Kombian et al., 1997 and Ludwig and Leng, 1997). Results from the present study demonstrate that in addition to its autocrine actions, VP acts as a diffusible signal to bridge information across neurosecretory and presympathetic neuronal populations. This crosstalk involves Ca2+-dependent dendritic release of VP, diffusion in the ECS, and activation of V1a VP receptors coupled to a CAN channel in presympathetic neurons.

We assessed the significance of differences between conditions with a nonparametric randomization test. We first will explain the procedure for the example of Figure 2K, testing the significance of the difference in coherence between attention conditions. First, the coherence spectra were calculated across all epochs per condition. If more epochs were available for one condition, a random subset was chosen to equate epoch numbers and corresponding biases. The difference between the two coherence spectra is the observed coherence

difference spectrum. Second, 1,000 randomizations were performed. In each randomization, the following steps were performed: (1) the epochs from both conditions were randomly redistributed into two sets of equal size; (2) the two randomized coherence spectra were determined; (3) the corresponding randomized coherence difference spectrum was determined; and (4) BVD-523 price only the maximum and the minimum of this difference spectrum was retained and entered into two randomization distributions, for maximal and minimal differences. For each frequency of the observed coherence difference spectrum, the difference was compared to learn more the two randomization distributions. If the difference was smaller than the 2.5th percentile of the minimal randomization distribution or larger than the 97.5th percentile

of the maximal randomization distribution, it was considered significant at a p < 0.05 level. This corresponds to a two-sided test with multiple comparison correction across

frequencies. The multiple comparison correction results from the fact that for each randomization, only the maximal and Oxalosuccinic acid minimal differences across all frequencies entered into the randomization distributions (Nichols and Holmes, 2002; Maris et al., 2007). Frequencies with significant coherence differences are marked with a gray bar in all figures. This procedure, as explained for the example coherence spectrum, was applied similarly for the average across the entire sample of coherence spectra. The only difference was that, for each randomization, the random condition assignment was done per coherence spectrum contributing to the average, rather than per epoch. The same approach as used for coherence spectra was also applied to GC influence spectra. Similar randomization procedures were also used for the average across the 60–80 Hz band and for gamma peak frequencies or amplitudes: the observed difference was compared to the randomization distribution of differences. A correction for multiple comparisons was not necessary in this case. Statistical testing for the cross-frequency interaction is described below. The main requirement for V1-V4 site pairs to be included in the analysis was that the V4 site had to be driven roughly equally by the two stimuli, while the V1 site had to be driven primarily by one of the two stimuli.

In this experiment, 4 ticks at Day 2 and 6 ticks at Day 16 were recovered from one control dog. It is below the 20% of attachment rate proposed by Marchiondo et al. (2013). Nevertheless the geometric mean count values ranged from 13.9 to 23.7 which were above the 20% attachment

rate. The geometric mean counts were used to calculate the percent efficacy, which is therefore valid based on the guidelines ( Marchiondo et al., 2013). A single oral treatment with the chewable formulation of afoxolaner achieved 100% curative efficacy for treating preexistent infestation of H. longicornis. It also controlled re-infestation by eliminating >90% of the ticks within the first 48 h after infestation for 4 weeks after treatment. The Day 30 efficacy

of afoxolaner seems lower than what has been observed for other tick species Palbociclib concentration ( Kunkle et al., 2014 and Mitchell et al., 2014). This may be related to a lower attachment rate in the control dogs, but also the variability of each experiment. There are some reports on the efficacy of current veterinary topical products against H. longicornis, e.g. imidacloprid/permethrin, fipronil/(S)-methoprene ( Hagimori et al., 2005). However, unlike these topical combinations, ticks are exposed to afoxolaner while feeding on the host’s blood. Afoxolaner is absorbed rapidly by the intestinal mucosa, and its plasma concentration peaks within 2–4 h after administration ( Letendre et al., 2014), which ultimately results in rapid uptake of the active ingredient by the ticks and a tick efficacy assessed at 48 h is similar to that of imidacloprid/permethrin or fipronil/(S)-methoprene Anti-diabetic Compound Library in vivo combinations ( Hagimori et al., 2005). The systemic distribution offers advantages compared to topical formulations. There is no period after treatment-administration during which the application site should be avoided by the owners and wetting of the haircoat or any other topical treatment does not interfere with the product efficacy. Another product for

oral administration containing spinosad includes a registered claim for H. longicornis tick curative treatment in Japan (Comfortis 1); however, this product is not registered for use against ticks elsewhere ( Beugnet and Franc, 2012 and Snyder et al., 2009). Snyder et al. (2009) reported a limited, short-lasting however efficacy of 50 mg/kg spinosad against new tick infestations on dogs with 67.8% efficacy at Day 9, 49.1% at Day 14, dropping to 5% at Day 30, against Rhipicephalus sanguineus by counting ticks 48 h after infestations. In this study, afoxolaner provided both curative and prophylactic efficacy for up to 30 days against H. longicornis. Nexgard® chewable formulation containing afoxolaner represents the first oral ectoparasiticide treatment providing a month-long efficacy against H. longicornis, the main Japanese tick species infesting dogs. The work reported herein was funded by Merial Limited, GA, USA. All authors are current employees of Merial.

80, p < 0.001; right t(53) = 7.51, p < 0.001). In addition, coordinate-based analysis of hippocampal volume and RM appeared to capture a memory benefit associated with a longer PF-06463922 pHPC and shorter aHPC ( Figure 2C), especially in the left hemisphere (peak left pHPC t(52) = 3.87, p < 0.001; left aHPC t(52) = −2.42, p < 0.05; right pHPC t(52) = 2.27, p < 0.05; right aHPC t(52) = −1.84, p = 0.071). However, pHPC volume ratios were predictive of RM even after separating variance associated with pHPC length ratios (left t(52) = 2.01, p < 0.05; right t(52) = 3.48, p < 0.001), whereas the opposite pattern did not hold (left

t(52) = 1.02, p > 0.3; right t(52) = −0.49, p > 0.6). That is, hippocampal SB431542 ic50 volumetric information contributed the same information provided by apex position, plus additional information. Just as concurrent increases in pHPC volume and decreases in aHPC volume have been observed following massive accumulation of spatial memories by London taxi drivers (Maguire et al., 2000), a negative relationship was observed between left pHPC and aHPC volumes in our combined analysis

(t(52) = −3.36, p < 0.005) confirming that a tradeoff effect was present (although this effect did not reach significance in the right hemisphere, t(52) = −1.22, p > 0.2). That pHPC and aHPC also made opposite, but overlapping, predictions about RM further suggests a tradeoff effect. Along these lines, although variance in pHPC was predicted

by HPC (left t(52) = 4.12, p < 0.001; right t(52) = 5.63, p < 0.001), it was the non-HPC portion of pHPC variance that predicted RM in both hemispheres. pHPC was in fact a slightly better predictor in the left hemisphere after controlling HPC (t(51) = 4.48, p < 0.001; without control t(52) = 4.02, p < 0.001) and in the right hemisphere after controlling HPC (t(51) = 3.91, p < 0.001; without control t(52) = 3.38, p < 0.005). This pattern may explain why HPC has failed to predict RM in past studies involving healthy adults, even though pHPC volume over ratio was a reliable predictor in all of the studies we analyzed. In part because there is both little direct communication between pHPC and aHPC (Moser and Moser, 1998 and Fanselow and Dong, 2010) and in part because different large-scale connectivity (i.e., neural context; McIntosh, 2000) has been associated with each region (Moser and Moser, 1998, Kahn et al., 2008, Fanselow and Dong, 2010 and Poppenk et al., 2010b), the notion of functional specialization along the long hippocampal axis has gained favor (Moser and Moser, 1998 and Fanselow and Dong, 2010). Drawing upon this idea, we tested the hypothesis that pHPC neural context differs from that of aHPC and is supportive of RM. We began by searching for patterns in the ambient functional networks associated with left pHPC, left aHPC, right pHPC, and right aHPC in our resting-state fMRI data.

elegans, we were able to induce long-lasting paralysis (>1 hr) with

480 nm light. Animals recovered movement when re-tested 24 hr later. We name this technique Inhibition of Synapses with CALI (InSynC). We believe InSynC is a powerful optogenetic technique for inhibiting neurotransmitter release with light and interrogating neurocircuitry in a spatially precise manner. To design a CALI-based synapse inhibition system, we chose candidate fusion proteins based on two criteria: (1) the protein is essential for vesicular synaptic release in synapses of the central nervous system; and (2) the engineered Panobinostat concentration protein can achieve inhibition in a dominant-negative manner, without the need to eliminate endogenous protein expression. The SNARE protein synaptobrevin 2/VAMP2 is the core protein in the vesicular SNARE complex, with a cytosolic N-terminal α-helix capable of binding to the α helices of SNAP-25 and syntaxin during vesicle fusion. The C-terminal of VAMP2 consists of a transmembrane

domain that is anchored to the vesicular membrane. Both N and C termini of VAMP2 have previously been fused to fluorescent proteins without disrupting function (Deák et al., 2006). The second protein candidate that we chose was synaptophysin (SYP1), which is closely associated with the VAMP2 protein (Arthur and Stowell, 2007), although its role in vesicular release is still unclear. SYP1 has 4 proposed transmembrane domain helices transversing the vesicular membrane, with both N and C termini facing the cytosol. ABT-737 mouse The C terminus of SYP1 has been previously tagged with fluorescent proteins without

affecting its function (Dreosti et al., 2009). We genetically fused miniSOG to the N terminus and C terminus of VAMP2 and SYP1, respectively (Figure 1A). To visualize expressing cells, mCherry was placed after the coding sequence of miniSOG-VAMP2 and SYP1-miniSOG, connected by a cotranslationally self-cleaving Thosea asigna virus 2A-like sequence (T2A) ( Osborn et al., 2005). The expression of the tagged synaptic proteins and the cytosolic red fluorescent protein were tightly linked genetically, even though the proteins were not fused Levetiracetam to each other. To assay the effects of miniSOG fused to VAMP2 and SYP1 on synaptic release, cultured hippocampal neurons were plated on microislands to induce autaptic synapse formation. The self-stimulated excitatory postsynaptic potential (EPSP) was typically observed as a prolonged depolarization after an action potential in current-clamp recording in response to a depolarizing current injection pulse (Wyart et al., 2005; Figure 1D). In voltage-clamp recording, a depolarizing voltage step can evoke a self-stimulated excitatory postsynaptic current (EPSC; Figure 1B). After establishing a stable baseline with repetitive stimulation, the recorded cell was illuminated for 2.5 min with 9.8 mW/mm2 of 480 nm light.

, 2011). New decontamination methods are needed to contact and kill microorganisms without any negative effects. The application of ultrasound in fruit and vegetable washing is one of

the alternative methods and is recommended for the food industry (Sapers, 2001, Seymour et al., 2002, Huang et al., 2006, Knorr et al., 2004, Alegria et al., 2009, Cao et al., 2010, Zhou et al., 2009, Elizaquivel et al., 2011, Rivera et al., 2011, Sagong et al., 2011, São José and Vanetti, 2012, Alexandre et al., 2012 and Alexandre et al., 2013). The limited research, carried out until today, regarding ultrasound applications in the washing step of fruits and vegetables is summarized in Table 1. Despite there being no knowledge of the commercial application click here of ultrasound in the wash-water decontamination processes, nowadays most studies are concentrated on studying the physical cleaning and decontamination effect of ultrasound on fruit

and Cabozantinib solubility dmso vegetable surfaces. Moreover, researchers were trying to evaluate the effectiveness of ultrasound in washing procedures. As seen in Table 1, most of the research was carried out and published in the years between 2002 and 2012 and are directly related to the decontamination treatments of fruits and vegetables. In studies using ultrasound for decontamination purposes, mostly lettuce, spinach, shredded carrot, truffles, cherry tomatoes, and strawberries were used as food materials. The high power ultrasound with low frequencies and treatment times between 20–45 kHz and 1–10 min were Thiamine-diphosphate kinase generally used in the applications. In different applications in combination with the parameters such as power, frequency, temperature, and time, the microbial reduction with ultrasound varies between 0.5 and 1.98 log CFU/g (Huang et al., 2006, Zhou et al., 2009, Alegria et al., 2009, Cao et al., 2010, Sagong et al., 2011, Chen and Zhu, 2011, Rivera

et al., 2011, Elizaquivel et al., 2012, São José and Vanetti, 2012, Alexandre et al., 2012 and Alexandre et al., 2013). Seymour et al. (2002), studied the effect of tap water, chlorinated water (25 ppm free chlorine), ultrasound in water (10 W/L, 32–40 kHz, 10 min), and ultrasound in chlorinated water in four different treatments and tried to determine the decontamination efficiency of these treatments on ampicillin resistant strains of Salmonella typhimurium, E. coli and Listeria monocytogenes in iceberg lettuce, cucumber, carrot, pepper, white cabbage, onion, parsley, strawberry, mint, and other herbs. Table 1, shows the results of S. typhimurium and iceberg lettuce regarding the researchers’ conclusion. Literature reports that all experiments were also repeated for E.