[5] This makes it possible to plan preventive or mosquito control strategies. Nevertheless, the efficiency of epidemiological surveillance is uneven and varies between countries. Dengue circulation and incidence are sometimes underestimated, particularly in Africa.[6] Surveillance of travel-acquired dengue could improve dengue

risk estimation in these countries. French soldiers can be considered travelers, since they carry out short missions or can be stationed in dengue endemic areas. Each year, 25,000 French soldiers spend time in an endemic area. Because dengue is a real threat for the French armed forces, this population is under constant epidemiological surveillance. This paper presents selleck chemicals the results of dengue virus circulation and dengue incidence rates for all the areas where French armed forces were stationed in 2010 to 2011, which enabled the dengue risk in each area to be identified. Epidemiological surveillance of dengue in the French armed

forces consists of continuous and systematic collection, analysis, interpretation, and feedback of epidemiological data from all military physicians, wherever R428 solubility dmso they are located. Each patient with dengue symptoms requires blood sample. In French overseas departments and territories, samples are analyzed in local civilian laboratories, otherwise samples are sent to the National Arbovirus Reference Center based at the Institute of Tropical Medicine at the Army Health Service, Marseille, France (tests used are in-house assay, Mac Elisa and direct IgG Elisa).[7] Virus culture and/or reverse transcription polymerase chain reaction (RT-PCR) are carried out if an early sample

is available; otherwise, serology is performed. Complementary Ag NS1 could be performed directly in local laboratories. A specific individual dengue case report form, containing administrative, geographical, clinical, and biological data, is also sent to the Institute of Tropical Medicine at the Army Health Service, Marseille, France. Possible dengue was Bcl-w defined in an epidemic context of dengue as a fever higher than 38.5 °C associated with at least one of the following symptoms: headache, myalgia, retro-orbital pain, rash, hemorrhagic signs. Confirmed dengue was defined as any of the above symptoms with virological evidence (PCR, culture, NS1 antigenemia) or positive serology (IgM or IgG seroconversion). Here we report the results of analysis of the data obtained from specific dengue case report forms from January 1, 2010 to December 31, 2011. Indicators are expressed as annual incidence and annual incidence rate. The denominator for the incidence rate is the average number of soldiers present in each dengue endemic area in 2010 to 2011. Statistical analysis was performed using R software. In 2010 to 2011, 208 possible dengue cases and 122 confirmed dengue cases occurred in the French armed forces.

Injured travelers as well as medical tourists are directly concerned by this strategy. This article has been kindly proofread by Amy Whereat, Medical English Consultant. The authors state they have no conflicts of interest to declare. “
“A 34-year-old Nigerian man presented with nephrotic syndrome. Renal biopsy revealed chronic membranous glomerulopathy with focal segmental sclerosis. Blood Giemsa smear contained rare Plasmodium sp. trophozoites and small subunit

ribosomal RNA polymerase chain reaction amplification confirmed the presence of Plasmodium malariae. This case highlights the importance of obtaining even remote travel histories from ill immigrants and considering occult quartan malaria in patients from endemic locations with nephrotic syndrome. Although quartan Linsitinib mw malaria comprises only a small portion of the global disease burden from malaria, Plasmodium http://www.selleckchem.com/products/Metformin-hydrochloride(Glucophage).html malariae is unique among the plasmodia in which subclinical parasitemia may persist for decades with illness occurring more than 40 years after the last possible exposure.1 Additionally, chronic P malariae infection was linked to nephrotic syndrome in children in the 1960s and subsequently attributed to immune complex basement membrane nephropathy.2,3 We describe a case of P malariae-associated chronic membranous glomerulopathy and nephrotic

syndrome in a US Navy sailor 14 years after his last possible exposure to the risk of malaria. This case highlights the importance of obtaining remote travel histories from Amrubicin immigrants presenting with illness, even decades after emigration from their country of origin. A 34-year-old US-born African American Navy sailor, who moved to Nigeria at the age of 1, migrated back to the United

States at the age of 21 and had not traveled home or to any malaria endemic locations during the ensuing 14 years. While at sea, he presented to his ship’s medical doctor with a 4-month history of bilateral lower extremity pitting edema and swelling of his face and a 5-month history of frothy urine. He was notably hypertensive with hyperlipidemia (total cholesterol 390 mg/dL, low density lipoprotein 305 mg/dL, triglycerides 230 mg/dL) and was placed on hydrochlorothiazide and simvastatin. Upon return to port, the patient was referred to Internal Medicine for suspected nephrotic syndrome. His past medical history was significant for sickle trait, treated latent tuberculosis, and childhood malaria. He denied a family or personal history of kidney disease. Laboratory studies were significant for a spot protein/creatinine ratio of 22.6, consistent with nephrotic syndrome. Additional abnormal laboratory findings included low serum albumin (1.8 g/dL), high serum creatinine (6.2 mg/dL), and a low glomerular filtration rate (14 mL/min).

The use of highly active antiretroviral therapy (HAART) has increased the life expectancy of HIV-infected patients. With prolonged survival and improved control of infectious susceptibility, vascular complications have emerged as a significant source of morbidity and mortality in HIV-infected patients [1]. These vascular complications, affecting >10% of those with HIV infections, include myocardial and pericardial tumours, cardiomyopathy, selleck products peripheral vasculitides, ischaemic heart disease and pulmonary hypertension

[1]. Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary arterial pressures and pulmonary vascular resistance (PVR) leading to right ventricular failure and premature death [2]. The pathological abnormalities in the small pulmonary arteries are characterized by intimal, medial and adventitial proliferation and hypertrophy, endothelial dysfunction and the development of plexogenic lesions [2]. PAH can exist in idiopathic and familial forms but can also be associated with other causes including connective tissue disorders, drugs, portal hypertension,

pulmonary veno-occlusive disease, congenital right to left shunts and HIV infection [2]. Although HIV-related PAH is clinically and histologically similar to idiopathic pulmonary arterial hypertension (IPAH), the pathobiological mechanism leading to the development of PAH in patients with HIV infection remains unclear [3], as it does in IPAH. HIV-related PAH is a rare entity. The prevalence HSP targets was estimated to be approximately 0.5% in HIV-infected patients in a study by Opravil et al. [4] in 1997, before the HAART era. This rate is 25-fold higher than the prevalence of PAH in the general population [5]. According to a more recent study by Sitbon et al. [6] in 2008, the prevalence has remained at 0.5% even in the modern era of HIV therapy, suggesting that HAART has not made a dramatic impact on the prevention of HIV-related PAH. Most of the literature

on HIV-related PAH is based on case reports and small cohort studies. Since the last analytical summary of these case reports in 2000 by Mehta et al. [7] and the last systematic review by Pellicelli et al. [8], there have selleck screening library been an additional 60 cases reported in the literature and several additional cohort studies. Furthermore, the majority of these new cases have been reported in the modern age of HAART therapy. The purpose of our study was to synthesize the published data on HIV-related PAH by performing a systematic review of the current literature. We decided a priori to examine the published evidence on HIV-related PAH. Searches were conducted on MEDLINE (inclusive as of March 2009); EMBASE (inclusive as of March 2009), the Cochrane collaboration and the Cochrane Register of controlled trials for relevant trials.

The channels forward scatter (FSC), side scatter and fluorescent channels FL1 Doxorubicin mw (530/30 BP) and FL2 (661/16 BP) were used for detection.

Threshold was set for SSC and compensation was not used. The carrier liquid used was 0.22 μm filtered MilliQ water. Samples were measured for 30 s at low flow speed (12 ± 3 μL min−1) with event counts below 3000 s−1. In our hands, the plasmid-free P. putida KT2440 wild-type strain is a rather weak biofilm former in minimal medium citrate-fed flow cell experiments, whereas earlier reports indicated stronger biofilm formation (Tolker-Nielsen et al., 2000), especially with different carbon sources or under coculture conditions (Hansen et al., 2007). After 2 days, small microcolonies Etoposide molecular weight were found, but after 7 days, these had either died or detached, and hardly any adherent biomass was found (Fig. 1 and Table 1). Carriage of the TOL plasmid considerably enhanced biofilm formation: all TOL biofilms consisted of multiple cell layers after 2 days, with single microcolonies measuring up to 50 μm in height and 25 μm in diameter. After 7 days, some microcolonies measured up to 100 μm in height, suggesting that detachment had not affected KT2240 (TOL) biofilms (Fig. 1 and Table 1). All differences in biovolume and average thickness between plasmidless and TOL-carrying strains were significant (P<0.0001). In addition, P. putida forms poor air–liquid interface biofilms

(Ude et al., 2006). Here, again, the TOL-carrying strain formed slimy, coherent pellicles at the air–liquid interface of liquid cultures, even with shaking at moderate speed, whereas the plasmid-free strain did not form coherent pellicles

(Supporting Information, Fig S1). After prolonged incubation, the liquid cultures of the TOL strain became increasingly viscous [KT2440: 1.6 centistoke (cSt) (cSt=mm2 s−1) vs. KT2440 (TOL) 6.6 cSt], suggesting that extracellular polymeric substances (EPS) were produced. We dismiss the possibility that enhanced biofilm and pellicle formation is due to a growth enhancement associated with Dynein TOL plasmid carriage per se. First, plasmid carriage, under nonselective conditions – as used here – typically results in growth impairment, rather than in enhancement, and we have – specifically for these two strains –documented a slight reduction in intrinsic growth kinetics due to plasmid carriage (Seoane et al., 2010). Second, detailed monitoring of total cell densities in both static (Table 2) and shaken (data not shown) cultures indicates very similar profiles and final cell densities of approximately 108 after 1 day and 109 from day 3 onward. Only with genetic modification (e.g. by loss of a genomic EAL domain-encoding gene, or expression of a heterologous GGDEF domain-encoding gene) does P. putida form persistent biofilms or perceivable pellicles (Gjermansen et al., 2006; Ude et al., 2006).

, 2008). Experiments performed with viable bacteria yielded the equivalent of 5 × 108S. aureus Cowan I from a suspension with an optical density (OD600 nm) of 1.0. Staphylococci were adjusted to an estimated concentration of 2 × 108 CFU mL−1 cell culture medium and kept at +4 °C until use.

Three FACS experiments were performed as previously described, on different days in duplicates, Epacadostat and up to 5000 invasion events were counted, unless described elsewhere. Staphylococcus aureus Cowan I and S. carnosus TM 300 were measured in the same experiment as a positive control and a negative control, respectively. The arbitrary value of FITC-stained bacteria, used as a surrogate for invasion of cells, was normalized to the positive control S. aureus Cowan I to display the relative invasiveness of the tested strains to the strongly invasive S. aureus Cowan I. Purified fibrinogen (plasminogen, von Willebrand-factor and fibronectin depleted; Enzyme Research Laboratories, Ceritinib nmr South Bend, IL) was coated to a 96-well microtiter as previously described (Szabados et al., 2011). For the fibronectin binding, a precoated microtiter plate was used (BD Biocoat™ Cellware Human Fibronectin; BD, Bedford, MA). The binding experiments were performed as previously described (Szabados et al., 2011). An OD550 nm

value of 0–0.06 was interpreted as negative, 0.07–0.15 as intermediately positive (+), 0.15–0.3 as positive (++), and > 0.3 as strongly positive (+++). Staphylococcus aureus Cowan I was used as positive control for fibrinogen and fibronectin binding. A sample without bacteria 2-hydroxyphytanoyl-CoA lyase and the S. carnosus TM 300 were used as negative controls. Bacteria (1 × 108) were washed with PBS and suspended in an estimated 1 μg mL−1 FITC and incubated for 30 min. Bacteria were washed three times with ice-cold PBS. Sulfo-NHS-LC-biotin (Pierce Biotechnology, Rockford, IL) was solved at a final concentration of 0.3 mg mL−1

in PBS as previously described (Agerer et al., 2004). Samples were washed three times with PBS, mounted with embedding medium ProLong® Gold (Invitrogen) in glass slides and sealed with nail polish. The glass slides were examined using confocal microscope Leica DM IRE2 (Leica, Solms, Germany). A suspension of human urinary bladder carcinoma cells 5637 from the FACS assay was used. The lysis step was omitted and cells were centrifuged gently (1000 g) for 60 s and transferred into 500 μL D-PBS (PAA) and fixed with 500 μL glutaraldehyde 2.5% as previously described. Only three of eight strains (Stlu 12, Stlu 50, and Stlu 108) showed binding to solid-phase fibrinogen (Fig. 1a)- as seen in previous results (Szabados et al., 2011). Four of eight strains (Stlu 30, Stlu 33, Stlu 36 and Stlu 108) showed binding to solid-phase fibronectin (Fig. 1b). One strain (Stlu 108) showed binding to immobilized fibrinogen and also to immobilized fibronectin.

Changing physician behaviour in low-prevalence countries to deliver comprehensive targeted testing to high-risk groups is a challenge and, even with the introduction of national guidelines, HIV testing rates have been slow to increase [6-8]. For these reasons, national guidelines advocate universal testing in healthcare settings serving populations with a higher HIV prevalence (2 per 1000 in the UK [9]; 1 per 100 in the USA [10]). Successful initiatives in antenatal and genitourinary medicine services, and US emergency departments [9,

11], have shown that point-of-care HIV testing (HIV POCT) reduces specific barriers for testing. These barriers include the need for

follow-up visits, venepuncture and the anxiety associated with waiting for a result [12, 13]. Thus, HIV POCT may be a critical tool for implementing universal testing selleck in many settings. New studies piloting HIV testing in hospital, primary care and community services suggest that HIV testing is feasible and acceptable in these settings [14]. A high HIV prevalence has previously been demonstrated in the Hospital for Tropical Diseases out-patient clinic [15, 16]. The aim was to establish nurse-delivered universal HIV POCT in an acute medical setting in an inner London hospital – the Hospital for Tropical Diseases selleckchem open-access emergency clinic. The Hospital for Tropical Diseases open-access emergency clinic offers a specialist service for acutely unwell patients who have a history of foreign travel in the last 6 months. Patients over 18 years of age may self-refer or attend with a referral from a primary care physician. We conducted a prospective study of all patients attending this clinic from the introduction of an Access database on 26 August 2008 until click here 31 December 2010. During this study period, we introduced a universal offer of an HIV test. A fast-track referral service to

the local genitourinary medicine clinic was established with designated health advisor appointments for patients who received a reactive result. Patient leaflets were generated to support the service, and included information on the potential for a false negative (as a result of a recent infection) and false reactive tests. Prior to universal testing, targeted HIV testing was offered to patients (phase 0), as part of clinical diagnosis and management, by the junior doctor who assessed the patient after triage by the tropical clinical nurse specialist. Doctors were aware of, and had received training that covered, the 2008 UK guidelines on testing patients from high-risk groups and with indicator diseases [British HIV Association (BHIVA) / British Association of Sexual Health and HIV (BASHH) / British Infection Society (BIS) 2008] [9].

Numbered sera of BD showed no reactivity to B. henselae proteins (Figs 1, 3 and 4). Table 2 shows the Se and Sp of clinical biomarkers based on the immunoreactivity of the B. henselae proteome against serum samples from CSD and IE patients. For these biomarker proteins, combining both IE and CSD, the sensitivity ranged AZD8055 price from 21% to 100%. The sensitivity for IE serum samples was higher than that of CSD serum samples, ranging from 43% to 100%, with the lowest and the highest reactivity percentage observed for Pnp and GroEL, respectively. Although ATPD, GroEL and FusA each showed a sensitivity of 100% for CSD serum samples, these proteins were also detected using the control group serum samples as shown in

Fig. 2. The proteins that showed 100% specificity for both diseases were GroES, HbpD, Pap31, PdhD2, SodB, Ppi and two proteins of a nonapplicable locus: BH11510 (OMP) and BH12180 (ABC see more transporter, periplasmic oligopeptide-binding protein). Based on these results, BH11510, BH12180, GroES, Pap31, PdhD2 and SodB were selected as biomarkers for IE, while BH02000 was selected as a biomarker for CSD. The aim of this study was to identify the serodiagnostic markers of CSD and endocarditis due to B. henselae and expand the number of biomarkers selected previously by others (McCool et al., 2008; Eberhardt et al., 2009). Indirectly, our study allowed cross-validation of some

protein targets for clinical application. The systemic infection leading to the massive infiltration of bacteria may be explained by the higher IFA titer serum samples obtained from patients suffering from IE compared with samples from CSD patients. The titers for the IE samples ranged from 1 : 400 to 1 : 6400 as reported previously (Fournier et al., 2002; Jacomo et al., 2002). The main problem with IFA is that cross-reactive antibodies between Bartonella species, especially B. henselae and B. quintana, prevent the identification of the bacteria at the species level (La Scola & Raoult 1996) (Table 1). Only serologically

sophisticated methods such AMP deaminase as Western blots with cross-adsorption studies may help to eventually identify the causative agent at the species level (Houpikian & Raoult, 2003). Several diagnostic assays based on whole-cell detection have been used in clinics (Giladi et al., 2001; Herremans et al., 2007, 2009; Vermeulen et al., 2007). According to ELISA assays for B. henselae infection, recombinant proteins rGroES, rRplL, rBepA and rGroEL yielded high sensitivity >70%, but low specificity ≤59% (Table 3). Only the B. henselae r17-kDa protein has high sensitivity and specificity (Loa et al., 2006; McCool et al., 2008; Hoey et al., 2009) (Table 3). The application of an immunoproteomic strategy to identify the antigenic proteins associated with diseases has been used recently for B. quintana (Boonjakuakul et al., 2007) and B.

“
“The aim of this study was to characterize the status of vitamin D in patients with active and recently diagnosed Behcet’s disease (BD) and the relationship between vitamin D levels and BD activity. In this cross sectional study 48 patients with BD and 47 age- and sex-matched healthy controls were included. BD was diagnosed by the International Criteria for BD. Behcet’s patients were Dabrafenib solubility dmso new cases who were not on any treatment. BD activity was measured by

the Iranian Behcet’s Disease Dynamic Activity Measure (IBDDAM) and Behcet’s Disease Current Activity Form (BDCAF). 25(OH)D measured by enzyme-linked immunosorbent assay method as an indicator of vitamin D status. The mean 25-hydroxyvitamin D (25(OH)D level in the BD group was lower than the control group. Insufficiency and deficiency of 25(OH)D in the BD group was more common than the control group. No correlation was observed between the total IBDDAM,

ophthalmic IBDDAM, and BDCAF with 25(OH)D levels. No correlation was found between the major symptoms of BD and 25(OH)D value. Our study suggests that deficiency of 25(OH)D may be a trigger factor for BD. “
“To describe the clinical features and course of a cohort of patients with juvenile dermatomyositis (JDM) at a tertiary referral pediatric centre in Australia and examine changes in diagnostic and therapeutic approach over time. Retrospective review of patients diagnosed with JDM at the Royal Children’s Hospital, Melbourne, between 1989 and 2010. Fifty-seven Belnacasan patients were identified. The female : male ratio was 2 : 1 and median age at diagnosis was 7.1 years (2.2–15.3). At diagnosis, 95% had weakness, all had typical rash and 68% had nailfold capillary changes. Calcinosis was not present in any patients at diagnosis and

occurred in 18% over time. Creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and aldolase levels were abnormal in 65%, 92%, 88%, 58% and 100%, respectively. Magnetic resonance imaging (MRI) was abnormal Amisulpride in 97% of patients, electomyograph (EMG) in 83% and muscle biopsy in all four patients in whom it was performed. MRI was used in 86% (24/28) of patients diagnosed after 2000. Muscle biopsy was used in four and EMG in no patients over the same period. Treatment used throughout the disease course included oral steroids (93%), high-dose pulse intravenous steroids (82%), methotrexate (63%), intravenous immunoglobulin (32%) and cyclosporin (18%). The disease was monophasic in 46.7% (21/45), polyphasic in 17.7% (8/45) and chronic in 35.5% (16/45). Australian patients with JDM have similar characteristics to previously described cohorts. In practice, MRI has replaced the invasive diagnostic tests included in the Bohan and Peter criteria for the diagnosis of JDM. The early use of disease-modifying anti-rheumatic drugs has become the most common treatment approach.

Pain anticipation has previously been shown to involve activity in sensorimotor regions but also in the insula, anterior cingulate cortex and PCC

(Porro et al., 2002, 2003; Wager et al., 2004; Koyama et al., 2005; Brown et al., 2008; Atlas et al., 2010; Drabant et al., 2011; Worthen et al., 2011; Seifert et al., 2012). Secondly, we used dynamic visual stimuli instead of static pictures, which possibly enhanced the threatening aspect of the needle (Ehrsson et al., 2007). Activity within the PCC has been repeatedly associated with selleck chemicals processing of threat-related stimuli (for a recent meta-analysis see Hayes & Northoff, 2012). Finally, the focus of our analysis was on the interval before the needle or the Q-tip hit the hand. These differences selleck kinase inhibitor in experimental protocols may have accounted for the different effects of visual stimulation on ABA in the present compared with some previous studies (Perry et al., 2010; Whitmarsh & Jensen, 2011). The effect of viewing a needle prick on anticipatory ABA was robustly localised to the PCC. The PCC has frequently been related to the default mode network and to different cognitive processes such as memory, attention, and change detection (for reviews

see Vogt, 2005; Pearson et al., 2011). The PCC is also involved in visual aversive conditioning (Maddock & Buonocore, 1997), pain anticipation (Porro et al., 2003; Brown et al., 2008; Seifert et al., 2012), and the initial detection of threat (Mobbs et al., 2009, 2010). Furthermore, Acesulfame Potassium larger PCC activity has been observed during the anticipation of aversive

compared with neutral pictures (Grupe et al., 2013). Based on its anatomical connections, comprising amongst others the anterior cingulate cortex and cingulate motor regions (Vogt et al., 2006), the PCC has been supposed to play a role in orienting the body to motivationally salient stimuli (McCoy & Platt, 2005; Vogt, 2005). Salient sensory stimuli, especially threatening stimuli, presented near the body have been shown to evoke defensive responses (for reviews see Graziano & Cooke, 2006; Legrain et al., 2011). Thus, in the present study, the effects on ABA and PDR may reflect the preparation of adequate defensive behavior when viewing a needle approaching the body. In agreement with our previous study (Höfle et al., 2012), we observed a positive correlation between the effects in the PDR and perceived unpleasantness across participants. Interestingly, we found a difference in timing between the effect in the PCC and PDR. The effect in the PCC started at about −0.7 s, whereas it started at about −0.2 s in the PDR. This observation might be due to the more sluggish response of the PDR, which takes several hundred milliseconds to differentiate between stimulus content. For instance, in our previous study, we found that the pupil starts differentiating between painful and nonpainful electrical stimulation at about 0.4 s after electrical stimulus onset (Höfle et al., 2012).

41)]. All

participants from this cohort also completed the cTBS paradigm. All participants gave informed consent to the study, which was reviewed and approved by the institutional review boards at each participating institution. Participants were recruited through local community advertisement and local Asperger’s Associations and clinics. All AS participants in both cohorts had an IQ > 80 based on the Weschler Abbreviated Scale of Intelligence (WASI) and a formal clinical diagnosis from an independent clinician prior to participation in the study. All met DSM-IV-TR criteria for Asperger’s Syndrome and met criteria for ASD on the Autism Diagnostic Observation Schedule, Module 4 (ADOS) (mean ± SD Social and Communication score, 10.2 ± 4.6). Additionally, the Autism Diagnostic

Interview Revised was completed Trametinib in vivo on 11 participants whose parents were available for interview. For these individuals the mean Social score was 18.2 ± 5.1, Communication score was 20.0 ± 2.6 GSK 3 inhibitor and Repetitive Behavior score was 6.0 ± 2.3. Cognitive and clinical evaluation was identical for the two cohorts, with Spanish-translated versions of the ADOS and WASI used for the participants in cohort two. Participants in the neurotypical group were healthy controls with no neurological or psychiatric disorders. This group was matched with respect to chronological age, gender and full-scale IQ with the AS group. All participants were given a comprehensive neurological exam by a board-certified neurologist to confirm normal gross motor and fine motor functioning. Lastly, all participants were screened following published recommendations (Rossi et al., 2009) to ensure that they did not have any condition that would put them at greater risk of an adverse event related to TMS (e.g. a personal or family history of epilepsy). Study procedures were identical

in the two study locations. The experimenters Fossariinae who collected the data at each location were trained by Dr Pascual-Leone and used the same equipment and procedures described herein. cTBS and iTBS were applied as described in Huang et al., 2005. The cTBS paradigm consisted of three pulses of 50 Hz stimulation repeated at 200-ms intervals for 40 s (for a total of 600 pulses) at an intensity of 80% of active motor threshold (AMT). In the iTBS paradigm participants received a 2-s train of TBS repeated every 10 s for a total of 190 s (600 pulses), also at an intensity of 80% of AMT (Fig. 1). Corticospinal excitability was assessed prior to and following cTBS or iTBS by measuring peak-to-peak amplitude of MEPs induced in the contralateral first dorsal interosseus (FDI) muscle in response to single-pulse TMS at a rate of approximately 0.1 Hz (a random jitter of ± 1 s was introduced to avoid any train effects). Three batches of 10 MEPs were recorded prior to cTBS or iTBS and used as a baseline. Following cTBS or iTBS, batches of 10 MEPs were measured at periodic intervals for a total of 120 min to track changes in MEP amplitude over time.