The renal subcapsular hematoma which is located in the renal hilum and renal collection area needs to be differentiated from parapelvic cyst and urine containing extravasation cyst caused by renal pelvis injury. The hematoma and urine have different MR signal characteristics, the contrast agent can be found getting into the urine containing cyst from the renal pelvis tear location in retrograde urography and CT enhanced delay scanning, they can be respectively identified. For avoiding the imaging misdiagnosis of the liquid

space-occupying lesion which is located in the renal collecting area, the correct ideal quality imaging examination and all the subtle signs should be paid enough attention. The authors declare that no conflicts of interest regarding the publication of this article. “
“First described in 1740 by Morgani,1 the appearance of ectopic adrenocortical tissue (EACT) in the spermatic cord has occasionally been www.selleckchem.com/products/Fludarabine(Fludara).html reported in children

and adolescents. Sullivan et al2 assessed the incidence of EACT in the groin of children and examined the relationship between the appearance and underlying diagnosis, age, and sex. Of 935 groin explorations, EACT was identified in only 25 children (2.7%). There were no cases in girls, and the occurrence declined with increasing age. Published case reports of EACT in adults are extremely rare.3 and 4 Our 44-year-old patient had the typical signs and symptoms of symptomatic varicocele. Inguinal microsurgical repair AZD2281 in vitro according to Ivanisevic was agreed with him. After inguinal exposure of the spermatic cord, we found a bright yellowish soft nodule (9 × 5 × 4 mm), else clearly different in color and consistency from the surrounding tissue. It was completely resected because a definitive assessment

of the tumor could not be made intraoperatively. Histologic examination revealed EACT (Figure 1 and Figure 2). No further examinations or follow-ups were necessary, because the patient had normal adrenal function and was asymptomatic. Embryologically, adrenal cortex arises from the mesoderm, whereas adrenal medulla develops from ectoderm of the neural crest. During the fourth and fifth week of gestation, primitive cortex originates from mesothelial cells between the mesentery root and the developing gonads, which are proliferating and separating in the mesenchyme of the dorsal abdominal wall. Subsequently, neighboring cells are added to form the definitive cortex, and medulla is formed by invasion of cells from the neural crest. It can be assumed that adrenal residues develop because of mechanical separation and that dislocation can occur as a result of the descent of the sex glands in male embryonic development.5 It is assumed that EACT (also called the Marchand rest or Marchand adrenals) may be common in newborns, but is very rare in adults, because the tissue becomes atrophic during adolescence and adult life.

i.). From the vaccinated pigs, only on day 1 p.i. genome was detected from multiple animals, but

at low amounts (Fig. 1C and D). On day 1 p.i. live virus could be isolated from the control animals from the upper and lower respiratory tract, with the highest titres in the nasal mucosa and trachea. Low amounts of live virus were also detected in the cerebrum and cerebellum. No live virus was isolated from TBLN (Fig. 2A). On day 3 p.i. live virus was only detected from the upper and lower respiratory tract, but no longer from parts of the central nervous system and still not from the TBLN (Fig. 2B). From the vaccinated animals no live Docetaxel mw virus could be isolated from any of the tissue samples at either time point. (Fig. 2A and B) On days 1 and 3 p.i. virus genome could be detected by PCR from all tissue samples from the control pigs, including from the TBLN and central nervous system. In only one of the vaccinated animals, viral genome was detected in nasal mucosa at day 1 p.i. (Fig. 2C and D). BALF from pigs euthanized at day 21 p.i. was negative in the PCR. Already after the first vaccination, at the time of the second vaccination, high

antibody titres against the homologous H1N1v strain were seen, both in the HI-test (Fig. 3A) and in a VNT (Fig. 3B). The second vaccination Talazoparib datasheet resulted in a further rise of these antibody titres to levels >10,000. After inoculation with the challenge virus, the non-vaccinated animals responded with titres up to 2560, peaking at 10 days p.i. and then decreasing again. In the vaccinated animals almost no changes were seen in the levels of the titres after the challenge (Fig. 3A and B). Cross-reactivity, both after vaccination and after inoculation/challenge, was seen in HI-tests and VNT when a swine influenza strain of subtype H1N1 was used in the test, but not when an H1N2 strain of swine origin was used. Results for the HI-tests are those shown in Fig. 4. VNT results are not shown as

they were almost identical to the HI-results. The soluble H1N1v HA trimer was almost completely able to prevent virus replication and excretion after a double vaccination and subsequent homologues challenge. Live virus could not be detected in any of the samples taken from the vaccinated pigs. Viral genome was only detected at day 1 p.i. in nasal and oropharyngeal swabs and at day 1 p.i. in the nasal mucosa from one of the euthanized pigs. The amount of genome detected from the swabs was very low, but genome could be detected in multiple animals. This viral genome may very well represent residual challenge virus. However, some very limited virus replication in the upper respiratory tract in the vaccinated groups can not be excluded, as high levels of virus replication were already observed at day 1 p.i. in the control group. A recombinant purified HA has several advantages compared to whole inactivated vaccines.

For live attenuated strains containing other disabling

mutations, sustaining colonisation by inclusion of capsule may be a strategy to enhance the immunogenicity of the non-capsular antigens present in the strain and induce protection against invasive disease. The authors are grateful to the staff at the UCL Biological Services Unit for assistance with animal maintenance. This work was undertaken at UCLH/UCL who received a proportion of funding from the Department of Health’s NIHR Biomedical Research Selleck Ibrutinib Centre’s funding scheme. JMC was supported by a Clinical Research Training Fellowship from the Medical Research Council (G0700829). “
“The authors regret that there was an error in their paper. The primers reported for cloning the DR2 domain of H. somni IbpA were not Ivacaftor correct. The error was present in the original data. The correct forward and reverse primers used for IbpA DR2 (p. 4507) are as follows: 5′-AGCTCCATGGGAAAATCATCTCCGCAAGAG-3′; 5′-AGCTGGATCCTGATTTTTTTGCCAACTCTTTTAAA-3′. These primers were published in a later paper

by Geertsema RS, Zekarias B, La Franco Scheuch L, Worby C, Russo R, Gershwin LJ, Herdman DS, Lo K, Corbeil LB. IbpA DR2 subunit immunization protects calves against Histophilus somni pneumonia. Vaccine 2011;29:4805–12. “
“The authors wish to update the corresponding author’s contact email to: [email protected]. “
“TB remains one of the world’s most serious infectious diseases and is responsible for more than 2 million deaths each year [1]. The only available vaccine, Mycobacterium bovis Bacille Calmette Guérin (BCG), confers some protection against disseminated TB in childhood but is largely ineffective at protecting against adult pulmonary disease [2]. Thus, a more effective TB vaccine is urgently needed. New vaccines for TB are assessed on measures

including safety, the ability to confer see more protection against Mycobacterium tuberculosis (MTB) challenge in preclinical animal models, and the ability to induce an antigen specific IFN-γ immune response. Although there is no immune correlate of protection for TB, impairment of IFN-γ and IL-12 signalling in humans is associated with susceptibility to mycobacterial disease and the measurement of antigen specific IFN-γ remains the primary immune outcome in Phase I testing of new TB vaccine candidates [3]. We have previously reported that recombinant Modified Vaccinia virus Ankara (MVA) expressing antigen 85A from MTB (MVA85A) is well-tolerated and enhances the frequency of antigen-specific IFN-γ producing T cells in adults, children and infants previously vaccinated with BCG [4], [5], [6], [7], [8], [9] and [10]. We have also shown that antigen specific T cells induced by MVA85A are highly polyfunctional, and can express IFN-γ, TNF-α, IL-2, MIP1-β and IL-17 [11] and [12]. However, to date we have not performed any dose-finding studies in UK adults.

In addition, the more stringent Center for Biologics Evaluation and Research (CBER) criteria [lower limits of 95% CI for SPR ≥70% and SCR ≥40%] [26] were met for all study vaccines at Day 21. Six months after the first vaccine dose and prior to the booster dose, the CHMP criteria were still met for all study vaccines, with the highest HI antibody SPRs and GMTs in subjects who received two primary doses of the AS03B-adjuvanted 1.9 μg HA H1N1/2009 vaccine. At this time point,

the CBER criteria were not met for the single dose regimen of the 1.9 μg HA AS03B-adjuvanted HA H1N1/2009 vaccine but were met for all other formulations. The HI antibody SPRs observed following one dose of the AS03-adjuvanted H1N1/2009 vaccines in the current study (98.5–100.0%) are consistent with previously observed SPRs (96.7–100.0%) for similar vaccines in children between selleck chemicals llc 6 months and 17 years old [21], [22] and [27]. The observations in the current study are consistent with published literature that one dose of non-adjuvanted H1N1/2009 vaccines can elicit putatively protective levels of HI antibodies in adolescents 10 to 17 years old, 21 days after vaccination [22], [28], [29], [30], [31] and [32], although two doses may be required in younger children [29], [30], [31], [32] and [33].

Previous studies have reported that two doses of AS03B-adjuvanted 1.9 μg HA or 3.75 μg HA H1N1/2009 vaccines induced persistence of HI antibody responses (SPR: >98.0%; SCR: >89.0%) in children through 6 months after vaccination [22] and [23]. In one www.selleckchem.com/products/BAY-73-4506.html of these studies [22], enrolling healthy children

from 6 months to 9 years of age, the parallel study arm with non-adjuvanted 15 μg HA H1N1/2009 vaccine (but not 7.5 μg HA) also elicited long-term persistence of HI antibody response (SPR: 91.5%; SCR: 74.5%), although the HI antibody GMTs (122.7) were lower than that observed for the AS03-adjuvanted vaccines (267.9–296.2). Nassim et al. reported from a dose-ranging study that only the MF59-adjuvanted vaccines with 3.75–15 μg HA antigen doses, but not the non-adjuvanted vaccines with 7.5–30 μg HA antigen doses, met the regulatory criteria through one year after vaccination Idoxuridine [34]. This is the first study to assess the concept of priming for immunological memory with AS03-adjuvanted H1N1/2009 vaccines in children 10–17 years old. A rapid increase in HI antibody titers after the booster dose administered at month 6 was observed for all study vaccines, suggesting effective priming irrespective of the one- or two-dose priming regimens. The HI antibody SPRs 7 days after the booster dose were comparable across the treatment groups (97.2–100.0%), although the HI antibody GMTs were higher for the AS03-adjuvanted vaccines (416.7–589.4) compared with those for the non-adjuvanted vaccine (273.4).

From 2000 through 2006, meningococcal serogroup was identified for isolates from 127 (45%) of 281 confirmed cases (Fig. 1); 105 (83%) were serogroup B, 20 (16%) were serogroup C and 2 Selleckchem 3MA (1%) were other serogroups (A [n = 1] and W135 [n = 1]). From 2007 through 2011, serogroup was determined for 335 (77%) of 437 meningococcal cases, and serogroup C replaced B as the most prevalent serogroup identified among confirmed

cases of meningococcal disease ( Fig. 1). Based on cases with known serogroup, cumulative incidence of serogroup C meningococcal disease in the city of Salvador was 0.1 cases per 100,000 population per year from 2000 through 2006 (Fig. 2) with 1 death (case-fatality, 5%). In 2007, 13 cases (0.45 cases/100,000 population) of serogroup C meningococcal disease were

identified with 2 deaths (case-fatality, 15%); in 2008, 53 cases (1.8 cases/100,000 population) were identified with 4 deaths (8%) and in 2009, 69 cases (2.3 cases/100,000 population) with 10 deaths (14.5%). From click here 2007 to 2009, children younger than five years old accounted for 34 (25%) of 135 cases (incidence, 4.8 cases/100,000 children <5 per year; Fig. 3) and 4 (25%) of 16 deaths. Among 10–24 year olds, there were 43 (32%) cases (5.2 cases/100,000 population/year) and 3 deaths. MenC vaccine was introduced into the routine infant immunization schedule in the city of Salvador in February 2010,

with a catch-up vaccination campaign for all children younger than 5 years. In the first month, 87,111 doses of MenC were administered to children <5 years, reaching an estimated 44% coverage of the target population with at least one dose. By December 2010, an estimated 92% of children younger than 5 years had received at least one dose of MenC vaccine (Table 1). In the first six months of 2010, cases of meningococcal disease continued to increase, with 93% of 63 cases among persons 10–24 years of age. The state health department purchased an additional MenC vaccine and conducted mass vaccination in three phases of persons 10–24 years of age. The first phase, targeting 10–14 year olds, Adenosine began May 30; 160,554 (93%) of 172,624 MenC doses administered in this age group were applied in the first weekend of the campaign, reaching 75% of the target population. The second phase, targeting those 15–19 years began June 12; 145,249 (96%) of 151,884 MenC doses administered in this age group were applied in the first weekend. The third phase, targeting 20–24 year olds, was delayed until August 14; only 68,362 (67%) of 102,565 MenC doses administered in this age group were applied in the first weekend. At the end of the third phase, coverage with at least one dose of MenC had reached 80% among 10–14 year olds, 67% among 15–19 year olds, and 40% among 20–24 year olds (Table 1).

The extracts obtained were concentrated in rotary evaporator under vacuum. Out of the four extracts obtained the ethanolic and the aqueous extract were used for further studies. For preliminary phytochemical screening the ethanolic and aqueous extracts were screened by using battery of chemical test viz., determining the presence of Alkaloid by Dragendorff’s, Mayer’s test, Shinoda test

for flavonoid, Foam test for saponins, Salkowski www.selleckchem.com/products/forskolin.html test for steroid, Ferric Chloride test for tannins and phenolics, Biuret test for proteins.10 and 11 The ABTS radical scavenging activity was assessed according to the method of Re and co-worker.12 ABTS was dissolved in distilled water to a concentration of 7 mmol/L. ABTS radical cation (ABTS+) was produced by reacting ABTS stock solution with 2.45 mmol/L of potassium persulfate13 and the mixture was allowed to stand in the dark at room temperature for 12–16 h before use. The percent scavenging activity of the plant extract was determined by carrying out the percent inhibition which was calculated by the following formula and results were compared with ascorbic acid as standard. %Inhibition=Absorbancecontrol−AbsorbancetestAbsorbancecontrol×100 The concentration equivalent to ascorbic acid was calculated by plotting the values of the test extracts on standard curve of ascorbic acid.14 The ability of the D. esculentum to scavenge hydrogen

peroxide was determined according to the method of Ruch et al. 15 Plant

extract (2 ml) prepared by distilled water at various concentration was mixed with 0.3 ml of 4 mm H2O2 CHIR-99021 nmr solution prepared in phosphate buffer (0.1 M pH 7.4) and incubated for 10 min. The absorbance of the solution was taken at 230 nm against blank solution containing the plant extract without H2O2. Total phenolic content of the fern was determined by the Folin–Ciocalteu method. The ethanolic and aqueous extracts Phosphoprotein phosphatase of DE at a concentration of 1 mg/ml were analysed for phenolic content. The assay was performed in triplicates. In brief, 1 mg/ml of the extracts were prepared and diluted to 45 ml with distilled water. 1 ml of FC reagent was then added and the content mixed properly. After 3 min, 3 ml of 20% sodium carbonate was added and the mixture was incubated for 2 h with occasional shaking. The absorbance of the blue colour that developed was read at 760 nm. The concentration of total phenols was expressed as Gallic acid equivalents in mg/g of dry extract.16 The total flavonoid content was determined by following the Aluminium chloride colorimetric methods described by Lobo et al.17 Where, 1 ml of plant extract (1 mg/ml) was added to 2 ml of water and after 5 min 3 ml of 5% sodium nitrite and 0.3 ml of 10% aluminium chloride were added. Then 6 min later, 2 ml of 1 M sodium hydroxide was added to the solution and the volume was made upto 10 ml with distilled water. The red coloured complex formed was measured at 510 nm.

The authors express their thanks to Bart Hoogstraten, Katalin Farkas, Mano Loeb, Ton Ultee, and Ronald Molenbeek for expert technical assistance. Furthermore the authors thank Ruurd van der Zee, Mayken Grosfeld† and Alida Noordzij for generating synthetic peptides. This study was supported by a grant from the Technology

Foundation (STW) of the Dutch Research Council (NWO), grant number STW-UDG5589. “
“The induction of responses that protect at mucosal portals of virus entry poses a particular problem for vaccine design and development. Nowhere is this more critically highlighted than in the search for an HIV vaccine where prevention of infection at, and/or rapid clearance from, the mucosal surface may be essential Selleck OSI906 for vaccine efficacy. Ideally an effective vaccine would induce virus neutralising activity in the fluids present at susceptible mucosal surfaces such as the lower female genital tract. Despite over 20 years of intensive research, this is proving to be a complex problem with many roadblocks

to progress. In part this is due to the particular biology of HIV including (1) the structure of the virus glycoprotein spikes that are largely resistant to the induction and action of neutralising antibodies through conformational masking [1] and [2], glycan shielding [3] and [4] and sequence hypervariability [5]; (2) the rapid dissemination of virus from mucosal sites of infection [6], [7] and [8] and (3) selleck chemicals llc the potential for HIV to evade antibody through intimate cell-to-cell spread (reviewed in Martin and Sattentau [9]). However, significant progress is being made. Examples of broadly reactive virus-neutralising antibodies and their cognate epitopes are increasingly being described [10], [11] and [12] and significantly, protective efficacy has been reported in macaques against vaginal, oral and rectal challenge with HIV-simian immunodeficiency (SIV) Env-chimeric viruses (SHIVs) following intravenous infusion of neutralising monoclonal antibodies [13], [14],

[15], [16] and [17]. A further significant roadblock to progress, addressed in the study reported here, is how to induce and maintain anti-HIV antibody responses at mucosal surfaces. Not only is there a lack of licensed mucosal adjuvants but there is also the danger of creating additional targets for HIV-infection through Megestrol Acetate the activation and/or recruitment of local T cells, a potential problem highlighted in the STEP IIb clinical trial using recombinant adenovirus 5 (Ad5) vectors [18]. Furthermore, mucosal effector B-cell responses are relatively short-lived. Thus, for pathogens such as HIV, that gain direct access to the immune system, it may be necessary to provide repeated or sustained stimulation of local specific immunity in the absence of generalised inflammation to maintain a protective antibody response. We are addressing this issue in animal models and in women using vaginal immunisation with stable recombinant HIV-1CN54 clade C trimeric gp140 produced in CHO cells.

The antagonist binding pocket identified from literature for alpha-1A-adrenergic receptor is shown in the figure below (Fig. 2). Outcome of molecular docking of five established (lead) molecules showing appreciable interactions in terms of re-rank scores are provided in Table 1.

Perusal of tables concludes that among five chosen lead compounds (Phenoxybenzamine, Phentolamine, Prazosin, Ergoloid Mesylate, and Labetalol), Prazosin binds strongly and efficiently to alpha-1A-adrenergicas an antagonist (Fig. 3). Surprisingly, when all similar compounds from library were analyzed based on re-rank score, two new chemical compounds (Table 2) were identified which are structurally similar

to Ergoloid Mesylate (pubchem CID 10289950) and Prazosin this website (pubchem CID 16191408). Hydrogen bond and electrostatic interactions are shown in diagrams separately (Fig. 3, Fig. 4 and Fig. 5). Best candidate obtained in present studies is a compound similar to Ergoloid Cyclopamine Mesylate (pubchem CID 10289950). Chemically this compound is N-(4,6-dimethoxy-2-[3-(piperidin-1-yl)propyl]aminopyrimidin-5-yl)-5-[(1,1,3,3,6-pentamethyl-1,3-dihydro-2-benzofuran-5-yl)methyl]furan-2-carboxamide with Molecular docking score −183.386 and re-rank score −113.571 ( Table 2). The next molecule with accepted antagonist effect is a compound similar to Prazosin with pubchem CID 16191408, which is chemically 3-[5-(2H-1,3-benzodioxol-5-yl)-1,3,4-oxadiazol-2-yl]-N-ethyl-N-[2-(1H-pyrazol-1-yl)ethyl]propanamide

with Molecular docking score −150.702 and re-rank score is −112.604 ( Table 2). Both the molecules mentioned above are newer and have never been tested for their alpha-1A-adrenergic receptor antagonist effects. Identification of the pharmacophores was achieved from the study of presence of amino acids around docked molecules with the best scores, as illustrated in Table 3. A comparative perusal of Table 3 proves that amino acids which play crucial role are Val 107, Val 157, Asp 106, Ile 157, Ser 158, Ala 189, and Ser 192, with most important and repetitive Phe 288 and Phe 289. Based on the chemical nature of amino acids, it was significantly concluded that the antagonist binding site Carnitine dehydrogenase of alpha-1A-adrenergic receptor is extensively and completely hydrophobic in nature. The above analysis is obtained from structure based pharmacophoric studies. Table 3 is a strong support of our statement and confirmation of hydrophobic nature of antagonist binding site. The conclusive framework achieved from structure based and ligand based studies confirms the hydrophobic nature of antagonist binding site of alpha-1A-adrenergic receptor. Structure based analysis confirms repetitive presence of amino acids Val 107, Val 157, Asp 106, Ile 157, Ser 158, Ala 189,Ser 192, Phe 288 and Phe 289 around antagonists.

, changes occur rapidly. The biochemicals measured in ginkgo leaf extracts, in HDAC inhibitor the present study, are on the higher side as compared to the earlier reports from other countries.13 and 14 The 5 locations in the present study, falling between 1742 and 2260 m altitude representing temperate climatic conditions,

are likely to be associated with the higher contents of phytochemicals and antioxidants. Findings on production of polyphenols and antioxidants, in respect to environmental stress, have been linked to the defense mechanism.15 Total phenolic content in ginkgo leaf extracts varied significantly with respect to season and organic solvent, being maximum in autumn (Fig. 2A). Phenolic content was exceptionally higher in rainy and spring season in EA and n-B. Total flavonoid content

was higher in spring in 3 solvents, AW, WE and n-B, during rainy season in ME and during autumn in EA (Fig. 2A). FG-4592 Antioxidant activity performed by three assays showed significant variation with respect to the seasons, maximum being in ABTS and DPPH in autumn (Fig. 2B). In case of FRAP, higher activity was recorded during spring followed by autumn (Fig. 2B). Importance of seasonal variation in accumulation of total phenolic and flavonoid contents and antioxidants has been recognized. Although a clear and regular trend due to seasonal variation was not observed in the present study, the total phenolic content was relatively higher in autumn. Kobus et al13 reported higher level of polyphenols in October as compared to August. Besides, higher accumulation of phenolic and flavonoids during winter is likely to be attributed to the stress conditions such as temperature and plant growth stage. In general, the secondary metabolites remain at low level in ginkgo during spring and summer which are the initial stages for the growth of shoots and leaves. Afterward, towards autumn and winter, as the growth and metabolism become slower, the phytochemicals tend to accumulate in higher

amounts. The optimization experiments conducted for preference of solvent revealed that AW was the best solvent for extracting phenolic content in all the three seasons; followed by ME > WE > n-B > EA. Similarly, total PAK6 flavonoid content was recorded highest in AW during rainy and autumn followed by ME during spring (Fig. 3A). Different solvent systems also influenced the extraction of antioxidant activity in different seasons. Antioxidant activity measured by ABTS assay was highest in ME in rainy and autumn and in WE in spring. In DPPH assay, the activity was recorded highest in WE in all the seasons. Also, the reducing power assay showed higher antioxidant activity in AW during all the seasons (Fig. 3B). Factorial analysis exhibited that the solvents and seasons individually and their interaction significantly (p < 0.001) influenced the accumulation of phytochemicals and antioxidant activity ( Table 1).

Neurorehabil Neural Repair 27: 79–86. [Prepared by Marco YC Pang, CAP Editor.] Question: Does adding repetitive transcranial magnetic

stimulation (rTMS) to treadmill training modulate cortical excitability and improve walking in people with Parkinson’s disease (PD)? Design: Randomised controlled trial with blinded outcome assessment. Setting: A medical centre in Taiwan. Participants: Individuals with Parkinson’s disease (Hoehn and Yahr Stage 2–3), and ability to walk independently were key inclusion criteria. Absence of selleck products motor evoked potential in response to rTMS, history of seizure, and use of cardiac pacemaker were key exclusion criteria. Randomisation of 22 participants allocated 11 to each of the experimental and control groups. Interventions: Both groups underwent 12 treatment sessions over 4 weeks. In each session, the experimental group received rTMS (5 Hz) applied over the leg area of the motor cortex in the hemisphere contralateral to the more affected leg for 6 minutes, immediately followed by 30 minutes of treadmill training. The control group received sham rTMS in addition to the 12 sessions of treadmill training. Outcome measures: The primary outcomes were indicators of corticomotor excitability – motor threshold, silent period, short-latency and long-latency intracortical inhibition – measured

in both cerebral hemispheres. The secondary outcomes were comfortable and fast walking speeds, and the timed-up-andgo test. The outcomes were measured at baseline and after the 4-week intervention period. Results: 20 participants completed the study. At the end of the 4-week MS-275 intervention

period, the increase in motor threshold of 3.5% and silent period of 14.0% of the contralateral hemisphere relative to the more affected leg was significantly more in the experimental group than the control group. Significantly more reduction of no short-latency intracortical inhibition in the same hemisphere was also found in the experimental group relative to the control group 10.9%. The experimental group also had significantly more improvement than the control group in fast walking speed (by 10.1 cm/s) and in the timedup- and-go test (by 2.0 s). No significant differences between the groups were reported in other outcomes. Conclusion: Repetitive transcranial magnetic stimulation can enhance the effects on corticomotor inhibition and improvement of walking function induced by treadmill training in patients with Parkinson’s disease. The application of non-invasive brain stimulation in rehabilitation has received considerable attention recently. Repetitive transcranial magnetic stimulation (rTMS) has been shown to enhance upper and lower extremity functions and/or modulate cortical excitability (Gonzalez-Garcia 2011, Khedr et al 2003, Lefaucheur et al 2004, Lomarev et al 2006).