The

authors would like to thank Igor Mijolović for the significant assistance in collection of data regarding the type, conditions, and organization of diving. The authors would also like to thank the two anonymous reviewers for their comments and suggestions which helped to strengthen and improve this manuscript. The authors state that they have no conflicts of interest to declare. “
“We would like to thank Drs Arya and Agarwal for their interest in our report on travel-associated dengue infections in the United States. We agree that, in addition to mosquito avoidance practices, travelers can also be given information Seliciclib mouse on the particularities of Aedes aegypti and Aedes albopictus mosquitoes. We also concur that the NS1 point-of-care test can be used to diagnose dengue early in the course of illness.1 The increasing reports of dengue outbreaks globally indicate a need for greater awareness of dengue among physicians in the United States. Once diagnosed, measures can be recommended to prevent secondary transmission to household contacts in areas where vector mosquitoes are present. The

outbreak of dengue in the Florida Keys in 2009 is a potent reminder of the risk of sporadic outbreaks of autochthonous dengue in non-endemic regions. Although difficult to confirm, check details the source of this outbreak was most likely a traveler. We would also like to thank Drs Chen and Wilson for their letter. With dengue being endemic in many popular travel destinations, Fossariinae the risk of transfusion-associated transmission and nosocomial dengue infections may increase in non-endemic countries. Although nosocomial dengue infections are infrequently reported, universal precautions are necessary when caring for travelers returning with febrile illness. Since the time of writing the initial manuscript,2 dengue has been made a nationally notifiable disease in the United States. Physicians are reminded to report all suspected dengue cases to

the Centers for Disease Control and Prevention’s ArboNET surveillance system via their state and local health departments. Through improved surveillance, any periodic reintroductions of dengue can be more rapidly detected and controlled. Hamish P. Mohammed, PhD, *,† Mary M. Ramos, MD, ‡ Aidsa Rivera, MSc, * Michael Johansson, PhD, * Jorge L. Muñoz-Jordan, PhD, * Wellington Sun, MD, § and Kay M. Tomashek, MD * “
“Cruise ship outbreaks of vaccine-preventable diseases (VPD) such as rubella and varicella have been previously associated with introduction and spread among susceptible crew members originating from countries with endemic transmission of these diseases. During February to April 2006, we investigated a cluster of rash illnesses due to measles, rubella, or varicella on a cruise ship sailing from Florida to the Caribbean.

Ganciclovir is administered at 5 mg/kg bd iv for 21 days [120]. Foscarnet (90 mg/kg bd iv) or cidofovir (5 mg/kg per week http://www.selleckchem.com/products/wnt-c59-c59.html iv) are alternatives in those who are not responsive or who are intolerant to ganciclovir therapy although data in

CMV pneumonia in HIV-seropositive individuals are limited [128]. Valganciclovir 900 mg bd po is an alternative for individuals able to tolerate oral therapy or for whom a switch from intravenous therapy is indicated. Although there is no clinical trial evidence to support the use of CMV prophylaxis, in the exceptional patient with a persistently low CD4 count, detectable CMV viraemia and no HIV treatment options, CMV prophylaxis may be considered. The vast majority of patients with low CD4 T-cell counts will not require CMV prophylaxis. Valganciclovir prophylaxis (900 mg od or bd) can be considered in selected individuals when the CD4 count remains <50 cells/μL, there Dasatinib is persistent detection of CMV DNA or CMV viraemia, coupled with a low risk of prompt immune reconstitution by HAART and there is no evidence of CMV end-organ disease (category IV recommendation), since detection of CMV DNA is a risk factor for death in this setting over and above the risk of low CD4 T-cell count or HIV viraemia [129]. Maintenance

therapy with valganciclovir is not initially required after treatment of CMV pneumonia but may be added if CMV pneumonia relapses or if extra-pulmonary disease is present. Valganciclovir may be considered

as primary prophylaxis in selected patients with persistent immunosuppression and detectable CMV DNA; or as secondary prophylaxis in those with relapse of CMV pneumonia after appropriate primary therapy (category IV recommendation). HAART has decreased the incidence of all forms of CMV disease and CMV pneumonia is now rare. CMV IRIS occurs more commonly as an ocular complication, although case reports of CMV IRIS in the lung exist [130]. Studies of HIV-seropositive individuals have not Urease consistently demonstrated a greater incidence of IAV; they have, however, suggested a greater risk of more severe disease [131,132], but this likely reflects an association with concomitant medical comorbidities [133]. In suspected cases diagnosis is confirmed by detection of viral antigen or viral culture from nasopharyngeal aspirate (NPA) or nasal swab specimen [131]. HIV-seropositive individuals should receive the neuraminidase inhibitor oseltamivir (assuming the majority of circulating strains in a given flu season show susceptibility) (category IV recommendation). HIV-seropositive individuals should be treated when IAV is documented, and fever >38.0 °C has been present for less than 48 h, although for individuals with significant immunosuppression (CD4 T-cell count <200 cells/μL) treatment may be administered if afebrile or if symptoms have been present for more than 48 h.

Given the results of a previous study showing that TA systems are ubiquitous in VRE (Moritz & Hergenrother, 2007), and the current survey showing that TA systems are also highly prevalent and transcribed in MRSA and PA, it appears that these problematic bacterial pathogens would indeed be susceptible to TA-based antibacterial strategies. Specifically, activation of MazEFSa should be considered for MRSA, and activation of RelEPa or HigBAPa appear to be attractive strategies against PA. This work was supported

Romidepsin in vitro by National Institutes of Health Grant 2R01-GM068385. J.J.W and E.M.H. were partially supported by a National Institutes of Health Cell and Molecular Biology Training grant T32 GM007283. E.M.D. was partially supported by the Center for Nano-CEMMS (NSF DMI-0328162) at the University of Illinois. We thank the bacterial laboratories at Carle Foundation Hospital (Urbana, IL),

Memorial Medical Center (Springfield, IL), and Delnor Community Hospital (Geneva, IL) for the MRSA isolates. We also thank Cubist Pharmaceuticals Inc. (Lexington, MA) and Carle Foundation Hospital (Urbana, IL) for the PA isolates. J.J.W. and E.M.H. contributed equally to this work. Fig. S1. Alignment of mazEFSa sequences. Fig. S2. Alignment of parDEPa sequences. Fig. S3. Alignment of relBEPa sequences. Fig. S4. Alignment of higBAPa sequences. Fig. S5. Alignment of mazEFSa upstream (a) and downstream (b) flanking sequences. Fig. S6. Alignment of parDEPa upstream (a) and downstream (b) flanking sequences. Fig. S7. Alignment of relBEPa selleck kinase inhibitor upstream (a) and downstream (b) flanking sequences. Fig. S8. Alignment of higBAPa upstream (a) and downstream (b) flanking sequences. Table S1. Presence of TA Systems in MRSA and Pseudomonas aeruginosa. Table S2. Flanking regions of TA Systems in MRSA Atorvastatin and Pseudomonas aeruginosa. Please note: Wiley-Blackwell is not responsible

for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Phytophthora ramorum,Phytophthora alni, and Phytophthora kernoviae present significant threats to biosecurity. As zoosporic oomycetes, these plant pathogens may spread through natural waterways and irrigation systems. However, survival of these pathogens in aquatic systems in response to water quality is not well understood. In this study, we investigated their zoospore survival at pH 3–11 in a 10% Hoagland’s solution over a 14-day period. The results showed that all three pathogens were most stable at pH 7, although the populations declined overnight irrespective of pH. Extended survival of these species depended on the tolerance of pH of their germinants. Germinants of P. alni ssp. alni and P.

sanguinis have been detected in clinical specimens of atheromatous plaque (Chiu, 1999; Nakano et al., 2006; Koren et al., 2011). Moreover, foam cell formation was accelerated by heat-inactivated S. sanguinis

as well as viable bacteria (Fig. 1). Activation of macrophages by bacterial components such as LPS has been reported to be sufficient to induce foam cell formation (Funk et al., 1993; Kakayoglu & Byrne, 1998). Based on recent understanding of atherosclerosis as an inflammatory disease (Erridge, 2008), our results suggest that both live and dead S. sanguinis may be potential atherogenic LGK-974 manufacturer stimuli, as each were shown to be promoters of inflammatory foam cell formation. Although the periodontal pathogen P. gingivalis is known to induce

foam cell formation (Giacona et al., 2004; Qi et al., 2003), our literature search indicated that the involvement of oral streptococci in foam cell formation has not been reported. Thus, the molecular mechanism by which S. sanguinis induces foam cell formation requires Target Selective Inhibitor Library order further investigation. Our subsequent experiment revealed that infection with viable S. sanguinis at higher doses (MOI > 100) induced cell death of differentiated THP-1 macrophages (Fig. 2). Induction of cell death of macrophages may contribute to atherosclerosis, because several investigations have suggested that dead macrophages are involved in the development of atherosclerosis plaque (Tabas, 2010). Therefore, S. sanguinis is potentially able to stimulate eltoprazine the progression of atherosclerosis by inducing cell death of macrophages, as well as by stimulating foam cell formation. Recent investigations have reported that several pathogenic streptococci and staphylococci induce cell

death of macrophages (Fettucciari et al., 2000; Craven et al., 2009; Harder et al., 2009). Those studies suggested that bacterial pore-inducing toxins such as streptolysin O, β-hemolysin and α-hemolysin trigger the cell death of infected macrophages. As S. sanguinis has no pore-forming toxins, our finding that S. sanguinis-induced cell death of macrophages was unexpected. Therefore, we examined the possible involvement of the cell death pathway in phagocytic cells. The initial recognition of microorganisms is mediated by pattern recognition receptors such as toll-like receptors, which recognize bacterial components (Ishii et al., 2008). Another class of pattern recognition receptors, intracellular nucleotide-binding oligomerization receptors (NLRs), have been identified (Ishii et al., 2008). A group of NLRs participates in the formation of protein complexes called inflammasomes, which mediate the induction of caspase-1 activation in response to microbial stimulation (Yu & Finlay, 2008; Schroder & Tschopp, 2010). In the present study, we found that S. sanguinis infection induced the secretion of IL-1β and ATP (Fig. 4), which are known to be implicated in activation of inflammasomes (Petrilli et al., 2007).

J Cancer Res Clin Oncol 2012; 138: 425–430. 127 González-Molleda L, Wang Y, Yuan Y. Potent antiviral activity of topoisomerase I and selleckchem II inhibitors against Kaposi’s sarcoma-associated herpesvirus. Antimicrob Agents Chemother 2012; 56: 893–902.

128 Davies BR, Logie A, McKay JS et al. AZD6244 (ARRY-142886), a potent inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 kinases: mechanism of action in vivo, pharmacokinetic/pharmacodynamic relationship, and potential for combination in preclinical models. Mol Cancer Ther 2007; 6: 2209–2219. People living with HIV have an increased risk of developing non-Hodgkin lymphoma (NHL) [1–4]. The two commonest subtypes are diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma/leukaemia GSK-3 inhibitor (BL), which are considered AIDS-defining illnesses (ADI). NHL is the second most common tumour in individuals with HIV and although studies show a decline in incidence since the introduction of HAART [5–8], AIDS-related lymphomas (ARLs)

have increased as a percentage of first ADI [9,10]. The development of ARL has been shown to be related to older age, low CD4 cell count and no prior treatment with HAART [11]. Patients tend to present with advanced clinical stage, B symptoms and extranodal involvement, including bone marrow. Before the introduction of HAART, the outlook for patients with ARL was poor, with the median survival for patients treated with chemotherapy being around 2–13 months. Median survival in the post-HAART era is beginning to approach that observed in the HIV-negative population and depends critically on histological subtype and stage of disease

[12–20]. The diagnosis of ARL should be based on a tissue biopsy rather than a cytological sample. In addition to the routine investigations advised as part of HIV clinical care, all patients require staging with clinical evaluation, blood tests, computerized tomography (CT) scanning and bone Idelalisib chemical structure marrow aspiration and trephine (Table 4.1). 18fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET) scanning at diagnosis improves the staging accuracy and the Imaging Subcommittee of the International Harmonisation Project in Lymphoma has produced guidelines strongly recommending a baseline pretreatment 18F-FDG PET scan [21]. Cerebrospinal fluid (CSF) examination is recommended if there are clinical signs of central nervous system (CNS) disease, or paranasal sinus, breast, epidural or testicular involvement. Cytological assessment by cytospin and flow cytometry is recommended [22]. Indications for intrathecal prophylaxis will be outlined in BCSH guidelines and should be administered at time of first CSF examination in these patients.

The presence of sialorrhea and the development of diaphragmatic paresis delayed extubation and necessitated a tracheostomy. She remained in the intensive care unit for 3 weeks. During the following month,

her general condition improved but a left arm paresis was noted. A dysphagia requiring a nasogastric feeding tube was also observed. She was discharged to a rehabilitation center after 5 weeks of hospitalization. The nasogastric feeding tube was maintained for an additional month. A cerebral MRI 2 months after her hospital discharge remained normal. At an outpatient follow-up visit 5 months post-discharge, the dysphagia had www.selleckchem.com/products/Adrucil(Fluorouracil).html resolved but the left upper arm 2/4 paresis was stable. Fatigue and emotional lability were noted. The patient eventually emigrated from Canada and was lost to follow-up. JE is rarely diagnosed in North American health

care facilities.1 However, it should be suspected in non-vaccinated patients returning from rural Asia and presenting with acute encephalitis within the incubation period of 5 to 15 days. The diagnosis could be challenging. In our patient, acute and convalescent phase HI titers indicate the presence of JEV antibodies but could not Quizartinib mouse establish a definite diagnosis. The PRNT is more specific, and considered the gold standard for confirmation. Our patient had a fourfold PRNT rise between her acute and convalescent sera titers. Serologic cross-reactivity among flaviviruses, including West Nile virus (WNV) which is present in much of North America, and Dengue virus which is Methane monooxygenase endemic throughout Thailand,

is well established.2,3 It likely explains the positive IgM results for WNV and Dengue virus, and the low positive HI titers for St. Louis encephalitis observed in our patient. The PRNT is labor intensive, and not widely available. In this case, its use was essential to confirm a diagnosis. Although the presence of antibody in CSF is an additional confirmatory result, not all patients have detectable amounts of IgM or IgG in CSF when infected with JE or other neuroinvasive flaviviruses. In our case, CSF JEV serologies remained negative. The timing of CSF collection and potentially lower viral antibody level in CSF compared to serum may contribute to negative results. JEV infection is mainly transmitted by Culex mosquitoes. It is the most common cause of viral encephalitis in Asia.4 It is prevalent in the rural zones and the rice fields of northern Thailand, notably in Chiang Mai province, with higher rates during the rainy season (summer and fall).5 It particularly affects young children who live in these regions, presumably leading to some degree of immunity in adulthood. In a review of JE cases reported between 1973 and 2008 among travelers from non-endemic countries, only 55 cases were recorded, giving an estimated incidence rate of <1 case per 1 million travelers to JE-endemic countries.

, 2004b). Unexpectedly, data on fibronectin-binding adhesins and invasins of S. lugdunensis are scarce. Binding to fibronectin has previously been

investigated in a small collection of strains, but all of eleven isolates showed only weak binding to fibronectin compared with that of strain Cowan I of S. aureus (Paulsson et al., 1993). S. lugdunensis has been described as being part of several niches of the human skin flora (Bieber & Kahlmeter, 2010). The clinical presentation of S. lugdunensis-caused infections is similar to infections caused by S. aureus. Staphylococcus lugdunensis can cause potentially fatal endocarditis, osteomyelitis, and skin and soft tissue infections (Vandenesch et al., 1993; Pareja et al., 1998; Patel et al., 2000; Hellbacher et al., 2006; Frank et al., 2008). Staphylococcus lugdunensis is thought to be rarely http://www.selleckchem.com/products/Bafetinib.html isolated; nevertheless, the low prevalence of S. lugdunensis in skin infection has recently been questioned (Bocher et al., 2009). We therefore sought to analyze the invasion of epithelial and endothelial cells (human urinary bladder carcinoma cell line 5637 and the endothelial cell line EA.hy 926) using a previously described fluorescence-activated cell-sorting (FACS)-based invasion assay. We correlated these results

with the binding of clinical isolates of S. lugdunensis to fibronectin. The bacteria used were S. aureus Cowan I, Staphylococcus carnosus TM 300 and eight clinical isolates of S. lugdunensis: Stlu 12, Stlu 30, Stlu 33, Stlu 35, Stlu 36, Stlu 39, Stlu 50, and Stlu 108 and the isogenic knockout mutant Selleckchem 17-AAG Stlu 108Δfbl::ermB (Table 1).

All S. lugdunensis isolates used in this study were confirmed by two reference methods: S. lugdunensis specific tanA and fbl PCRs and by MALDI-TOF MS, as described previously (Noguchi et al., 2009; Szabados et al., 2010; Szabados et al., 2011). Human urinary bladder carcinoma cell line 5637 (DSMZ, Braunschweig, Germany) and endothelial cell line EA.hy 926 (DMSZ) were used throughout this study. Bacteria were grown until the mid-logarithmic phase, as described previously (Szabados et al., 2008). The mutagenesis construct for the homologous recombination cloned into pBT2, and named pMB2503, has previously been described (Marlinghaus Clomifene et al., 2011). The homologous recombination of the fbl gene in strain Stlu 108 was also performed as previously described (Marlinghaus et al., 2011). The Δ fbl knockout mutant was confirmed by sequencing (data not shown). Human urinary bladder carcinoma cell line 5637 was cultured in RPMI 1640 with phenol red (PAA, Pasching, Austria). The endothelial cell line EA.hy 926 was cultured in HAT medium (Invitrogen) with addition of HAT medium supplement (hypoxanthine, aminopterin, and thymidine). Both media were also supplemented with 10% heat-inactivated fetal calf serum (PAA) and 1 g L−1 pyruvate (Invitrogen) and 1.5 g L−1 glucose (Invitrogen).

Hajj, the pilgrimage to Mecca, Kingdom of Saudi Arabia (KSA), is one of the obligatory rituals of worship in Islam. Muslims with good health and sufficient financial status are required to visit Mecca at least once in their lifetime. Hajj is the largest, most diverse mass gathering of people in the world and attracts more than 2.5 million Muslims from more than 160 countries each year. Mecca is also the setting for a less critical ritual called Umrah, which can be done at any time during the year.1 Vorinostat research buy In the Netherlands, the Saudi

Arabia Embassy issues about 5,000 to 6,000 visas for Hajj every year (personal communication, April 17, 2010). Hajj lasts for 5 days, and it takes place from the 8th to the 12th day of the last month of the

Islamic calendar. As the Islamic calendar is lunar, the precise Gregorian calendar dates of the Hajj season vary each year.2 This continuous seasonal movement has implications for the spread of disease and other health risks.3 Transmission of infectious disease during mass gatherings has a global effect when visitors return to their country of origin. Individuals going on Hajj contributed to a global cholera outbreak in the 19th century.1 Several outbreaks of meningococcal serogroup A disease occurred during the 1987 Hajj season. For the following Hajj of 1988, the Saudi Arabian government required selleck compulsory next divalent AC vaccination to

issue a Hajj visa. During the Hajj seasons 2000–2002, there was a shift in the epidemic pattern of the meningococcal disease with a predominance of Neisseria meningitidis serogroup W135. In the year 2002, the Ministry of Health decided to demand the tetravalent ACYW135 polysaccharide vaccine. These interventions have quelled meningococcal disease since 2002.4 The travelers’ advice and vaccination clinic (TAVC) of the Public Health Service (PHS) Amsterdam, administers vaccinations including meningitis ACYW135 vaccine and provides about 25,000 travelers annually with individual recommendations for all their travels. Each year a large number of Muslims, in preparation for Hajj, visit the TAVC for the required tetravalent ACYW135 vaccine whereby they also receive standard recommendations. Although most travelers who visit the TAVC follow our advice, many Hajj pilgrims only take meningitis vaccination, and not the other recommended vaccinations. The aim of this study is to investigate the acceptance of non-required, but advised, vaccinations by the Mecca travelers who visit the PHS before departure for a mandatory vaccine. Further, we investigated predictors for this acceptance.

It is possible that dose escalation can improve tolerance by reducing the rates of side effects such as gastrointestinal disturbance, fatigue, myalgias and arthralgias, but no studies have compared a dose escalation protocol to initial full Erastin dose thiopurine. Once target dose has been reached, performance of complete blood count and liver enzymes every 3 months is considered mandatory in view of the risk of late myelosuppression

and hepatotoxicity.[68] There are two ways of using thiopurine metabolites in clinical practice – reactively or proactively. The former is the standard approach where patients who exhibit an inadequate response to thiopurines after at least 3 months’ therapy on an adequate weight-based dose of thiopurines or have an

adverse event are tested. For patients who are in steroid-free remission and have no side effects, there would appear to be little LEE011 research buy advantage in measuring metabolites. As 6TGN levels take at least 2 weeks to achieve steady state after a dose change in adults[69] and up to 55 days in children,[70] metabolites should be monitored every month during optimization after a dose change until a therapeutic level is achieved. The second approach would include early measurement of thiopurine metabolites to hasten the optimization Grape seed extract of drug dosage. This would identify shunters, non-compliers, and fast and slow metabolizers early, and permit appropriate action taken rather to wait for inefficacy or adverse events to occur. This approach has been applied only to fast metabolizers to date,[61] but requires evaluation. The other major reason for failure of thiopurine therapy is the occurrence of adverse events leading to the drug’s cessation. Most episodes of myelosuppression and hepatotoxicity relate to elevated 6TGN and 6MMP levels,

respectively. In these situations, thiopurine metabolites should be measured and a reduced dose with or without the addition of allopurinol is indicated. However, a newer development is the management of idiosyncratic reactions to thiopurines, such as nausea, vomiting, myalgias, arthralgias, fatigue, fevers and a flu-like illness, which can affect up to 33% of patients.[69] In IBD in particular, where the therapeutic options are more limited, cessation of the drug and exclusion of thiopurines from that patient is undesirable. On the basis that the adverse events are due to the primary drug used and not its metabolites, up to 50% of patients who develop an idiosyncratic reaction on AZA (possibly the imidazole group[71]) can be safely switched to 6MP without recurrence of the adverse event.

12; unpaired t-test; Fig. 5A and B). Next, we asked whether the developmental changes and effects of TTX treatment on average velocities and short-pause rates were cargo specific. Membrane organelles positive for amyloid precursor protein (APP) are also known to be transported by kinesin-1, which mediates anterograde transport of axonal mitochondria (Kamal et al., 2000; Hirokawa et al., 2010). Therefore,

we compared the behavior of mCherry-OMP-positive mitochondria with that of APP-mCherry-positive membrane organelles. Cultured hippocampal neurons expressing APP-mCherry and EGFP-VAMP2 were imaged at intervals of 1 s for 10 min [2 weeks (12–13 DIV), n = 53 Antero, n = 32 Retro from seven cells; 3 weeks (19–20 DIV), n = 76 Antero, n = 48 Retro from eight cells; 3 weeks

(19–20 DIV) with TTX treatment, n = 78 Antero, n = 49 Retro from eight cells]. OSI-906 purchase A short pause of APP-containing vesicles was defined as an event with inter-frame velocities < 0.25 μm/s and duration of more than 1 s, together with the occurrence of restart during observation periods. An average velocity was calculated using the same method as we used for mitochondria. Consistent with the previous work, APP-containing vesicles moved faster in the anterograde NU7441 mw direction than in the retrograde direction (Fig. 5C) (Kaether et al., 2000). The transport of APP-containing vesicles showed properties that were different from those of mitochondrial transport. Both the average velocities and short-pause rates of APP-containing vesicles were similar at 2 and 3 weeks after plating (average velocity: Antero, t127 = 1.14, P = 0.26; Retro, t78 = 1.34, P = 0.19; short-pause rate: Antero, t127 = 0.79, P = 0.43; Retro, t78 = 0.46, P = 0.65; unpaired t-test; Fig. 5C and D). In addition, TTX did not affect the transport of APP-containing vesicles (average velocity: Antero, t152 = 0.66, P = 0.51;

Retro, t95 = 0.09, P = 0.92; short-pause rate: Methane monooxygenase Antero, t152 = 0.28, P = 0.78; Retro, t95 = 0.34, P = 0.73; unpaired t-test; Fig. 5C and D). These results indicate that the regulation of organelle transport by neuronal maturation and activity is cargo specific. High-frequency time-lapse imaging revealed developmental regulation of mitochondrial transport in the axon (Fig. 5). In the presence of TTX, the short-pause rates of mobile mitochondria were reduced, suggesting the involvement of axonal excitability and associated events in the regulation of mitochondrial short pause. Many mitochondrial short pauses occurred near presynaptic sites [number of synaptic short pauses/number of all short pauses = 67 ± 6% (Antero) and 44 ± 5% (Retro); Fig. 6A]. However, even if mitochondrial short pause occurred randomly, short pauses near presynaptic sites could be observed by chance, due to the high density of presynaptic sites. To critically evaluate whether short pauses of mitochondria preferentially occur near presynaptic sites, experimental data were compared with values generated by a stochastic simulation.