An analysis of teacher's role as motivator to student's learning motivation in English lesson at SMPN 1 Sedati Sidoarjo

Teacher is one of the important components in the process of learning and teaching to form the potential human resource in developed era. One of the teacher's roles is as motivator. Teacher's role as motivator is important to improve student's motivation in learning. Teacher has to stimulate, motivate and reinforce the students to stick out their potency, activity and creativity. When the writer observed the school, he found the school that has a good motivation. The school is SMPN 1 Sedati Sidoarjo. All of the students were enthusiastic to learn English. The grade of the students was good. Their average grade was eight. It was caused by the motivation that had been given by teacher. From that reason, the writer has two problems of the study. These are: (1) How is teacher's role as motivator done by English teacher and (2) how far students are motivated by teacher. And to answer problem of the study, the researcher used qualitative-descriptive method and used four instruments. These are check list observation, interview, questionnaire, and documentation. The teacher of that school was very innovative in teaching the students. He used the application program that he took when he had training in America. It was suitable to be applied in that school because it was supported by complete facilities because laptop and LCD were available in that school and it was suitable with the school's curriculum. Teacher often invite the students to be participated in the English event. It can be proved by the appreciation of students was very more. The relationship between teacher and students was very close. So the students were very enthusiastic to learn English. The students made the teacher as their inspiration and motivation to learn especially in English because the teacher always shared the important to learn English and anything about life

The Experimental Autoimmune Encephalomyelitis Disease Course Is Modulated by Nicotine and Other Cigarette Smoke Components

<div><p>Epidemiological studies have reported that cigarette smoking increases the risk of developing multiple sclerosis (MS) and accelerates its progression. However, the molecular mechanisms underlying these effects remain unsettled. We have investigated here the effects of the nicotine and the non-nicotine components in cigarette smoke on MS using the experimental autoimmune encephalomyelitis (EAE) model, and have explored their underlying mechanism of action. Our results show that nicotine ameliorates the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an EAE/MS therapeutic. In contrast, the remaining components of cigarette smoke, delivered as cigarette smoke condensate (CSC), accelerated and increased adverse clinical symptoms during the early stages of EAE, and we identify a particular cigarette smoke compound, acrolein, as one of the potential mediators. We also show that the mechanisms underlying the opposing effects of nicotine and CSC on EAE are likely due to distinct effects on microglial viability, activation, and function.</p></div

Increased demyelination in CSC-treated mice at day 14.

<p>Frozen sections of spinal cords were isolated from vehicle (saline/DMSO) and CSC-treated mice at day 14 and day 28 of EAE. Eriochrome cyanine <b>(A)</b> or fluoromyelin <b>(B)</b> was used to visualize demyelination. Areas of demyelination are indicated by diminished fluorescence; boxed regions are shown at higher magnification. <b>(C)</b> Demyelinated areas from <b>(B)</b> were measured using ImageJ and calculated based on equation listed in Methods (n = 4, *p<0.05). The levels of demyelination at day 14 in saline- or nicotine-infused spinal cords are also shown for comparison.</p

Non-nicotine components of cigarette smoke and nicotine have opposite effects on microglial state during early stages of EAE.

<p>(<b>A</b>) Resting Iba1+ (M0), pro-inflammatory (M1) and anti-inflammatory (M2) microglia were identified by labeling with anti-iNOS/Iba1 and anti-Arg1/Iba1, respectively. iNOS^+/Iba1⁺ (<b>B</b>) and Arg1^+/Iba1⁺ (<b>C</b>) cells were counted and compared between vehicle (pooled DMSO/saline samples) (n = 4) and CSC (n = 3)/nicotine-treated (n = 3) samples. Percentages of each population after treatment are indicated in (<b>D</b>). Bar = 50 µm (**p<0.01).</p

Therapeutic administration of nicotine attenuates EAE symptoms.

<p><b>(A)</b> 14-day pumps filled with 200 mg/ml nicotine were placed in the backs of EAE mice at day 14 (***<0.001). Peak score <b>(B)</b> as well as cumulative score <b>(C)</b> from day 14 to day 28 were recorded and compared between the vehicle (n = 8) and nicotine-treated (n = 3) groups. <b>(D)</b> Weekly weights were plotted as a percentage of day 0 weights. (***p<0.001; *p<0.05)</p

Simulation Studies on Robust Contacts in V₂CT₂/MoSi₂N₄ (TO, F, OH) van der Waals Heterojunction Nanostructures: Implications for Optoelectronic Devices

Research on metal electrode–semiconductor contacts has primarily focused on adjusting the Schottky barrier height (SBH), with little attention paid to the stability of electronic properties upon contact. Herein, we comprehensively investigate the sensitivity of contact properties to the external electric field (ΔE), out-plane strain (Δd), and in-plane biaxial strain (Δδ) taking the V2C(T2)/MoSi2N4 (TO, OH, F) van der Waals heterojunction (vdWH) as an example. Our findings suggest that surface functionalization (-T termination) is a powerful tool for controlling contact characteristics. Importantly, when ΔE0.3 V/nm, Δd = −0.1 Å, and Δδ < 0%, the intrinsic contact properties of V2C/MoSi2N4 may be changed. However, V2CT2/MoSi2N4 can maintain the intrinsic contact properties over a wider range of ΔE, Δd, and Δδ. Furthermore, we design a p–i–n optoelectronic transistor (V2CO2/MoSi2N4/V2CO2H2), which has excellent tunneling probability (100%), photocurrent density (11.336 A/m2), responsivity (0.322 AW–1), and external quantum efficiency (71.061%). Our work not only serves as a reference for eliminating the error of information transmission and the degradation of device performance caused by contact property sensitivity to electric field and strain but also provides theoretical guidance for the experimental design of high-performance MoSi2N4-based optoelectronic devices

Effects of nicotine and non-nicotine components of cigarette smoke on EAE severity.

<p>EAE was induced by injection of MOG_35–55 in CFA and pertussis toxin. <b>(A)</b> CSC was infused at 10 or 20 mg/ml into EAE mice starting at day 0 of EAE for 28 days, with DMSO as vehicle. <b>(B)</b> 20 mg/ml CSC was infused into the mice from 14 days prior to EAE induction through day 28, with 50% DMSO as vehicle. <b>(C)</b> Nicotine (200 mg/ml) was infused into EAE mice starting at Day 0 of EAE for 28 days, with saline as vehicle. Peak score <b>(D)</b> and cumulative score <b>(E)</b> were compared between CSC (n = 3)/nicotine (n = 6) and control mice (n = 8). (*** p<0.001; **p<0.01; *p<0.05).</p

Decreased demyelination in nicotine-treated mice during EAE.

<p><b>(A)</b> Frozen sections of spinal cords were isolated from vehicle (saline) and nicotine-treated mice at different time points during EAE. Eriochrome cyanine (EC) was used to visualize demyelination. Intact white matter (WM) is indicated by the blue staining and demyelination is revealed by diminished color. Areas of demyelination are indicated by asterisks; boxed regions are shown at higher magnification. <b>(B)</b> Demyelinated areas were measured using ImageJ and calculated based on equation listed in Methods. (n = 3–4, *p<0.05).</p

Effects of nicotine and non-nicotine components of cigarette smoke on microglia/macrophage activation during EAE.

<p><b>(A)</b> Iba1 staining (green) was used to detect microglia in vehicle (saline), CSC-treated and nicotine-treated samples collected at D0, D14 and D28 during EAE. DAPI is indicated by blue fluorescence. Higher magnifications show morphologies of microglia in white matter (the box in D0 vehicle indicates the location of the high magnification images). <b>(B)</b> Iba1 staining (green) was used to detect microglia in vehicle (saline/DMSO) and CSC-treated samples collected at D14 and D28 during EAE. Quantification of Iba1 signals at days 0 and 14 of EAE after vehicle and nicotine (n = 3–4), or day14 CSC treatment (n = 4). Bar = 20 µm. *p<0.05.</p

Weight changes of CSC- or nicotine-treated EAE animals.

<p>Weight changes were recorded and compared between vehicle (DMSO, n = 3 at all time points) and CSC- <b>(A)</b> or nicotine-treated <b>(B)</b> mice. In <b>(B)</b>, * denote significance compared to mice treated with vehicle (saline) alone (n = 3 at all time points). #: significance compared to mice treated with nicotine alone (n = 3 at all time points). Weights were plotted as a ratio over day 0 weights. (*** p<0.001; **p<0.01; ##p<0.01). On day 28 there were n = 9 mice in the EAE+vehicle group and n = 6 in the EAE+nicotine group. On day 21 there were n = 12 mice in the EAE+vehicle group and n = 11 in the EAE+nicotine group. On days 0, 7 and 14 there were n = 17 mice in the EAE+vehicle group and n = 14 in the EAE+nicotine group.</p