Miskonsepsi Atas Konsep Asam-Basa, Kesetimbangan Kimia, Dan Redoks Dalam Berbagai Buku-Ajar Kimia SMA/MA

Analisis isi buku-buku Kimia SMA/MA telah dilakukan untuk mengungkap miskonsepsi atas bebe-rapa konsep, yakni asam-basa, kesetimbangan kimia, dan redoks. Sampel penelitian dengan teknik purposesive sampling yang dilakukan terhadap berbagai buku yang beredar di pasaran di DIY diperoleh 9 macam buku. Metode analisis dilakukan berdasarkan kisi-kisi kebenaran konsep yang terdapat dalam tiga konsep, asam-basa, kesetimbangan kimia, dan redoks. Hasilnya menunjukkan adanya miskonsepsi yang berlaku secara umum pada semua sampel perihal pemahaman terhadap formula larutan basa amonia dalam air yang dipahami sebagai NH4OH dengan tanpa adanya penjelasan lanjut terkait dengan formula NH3(aq), rumusan pH dalam hubungannya dengan konstanta kesetimbangan asam lemah poliprotik, dan penyetaraan reaksi redoks dalam suasana basa dengan melibatkan ion penunjuk asam H+ yang kemudian dinetralkan dengan ion OH-. Secara khusus ditemui adanya miskonsepsi asam-basa model Bronsted-Lowry pada reaksi amonia dengan asam klorida membentuk amonium klorida dalam pelarut benzena, dan ketergantungan nilai konstanta kesetimbangan pada koefisien persamaan reaksi kesetimbangan yang boleh dilipatgandakan secara sembarangan. Ditinjau dari isi buku-buku tersebut ada kecenderungan yang nampak bahwa para penulis buku dipengaruhi oleh referensi buku-teks Kimia Umum (General Chemistry) tanpa pendalaman buku-teks yang lebih advanced

Effect of interleukin (IL)-15 on CD69 expression of CD56⁺CD3^- NK cells from SLE patients and healthy controls.

<p>A. Gating of CD56^birght and CD56^dim CD3^- NK cells by flow cytometry. B representative profile of Representative histograms of SLE patients (SLE) and controls (Normal); C. Comparison between SLE patients as a whole and normal controls (Normal) using scattergram (transverse lines indicate means); D. Comparison between SLE patients with active disease and inactive disease; E. Comparison of CD69 expression on CD56^dim NK subsets in SLE patients with different severity as well as normal controls; F. Comparison of CD69 expression on CD56^bright NK subsets in SLE patients with different severity as well as normal controls. PBMC were stimulated with or without IL-15 (10ng/ml) for 18hrs For D,E,F, data was expressed as mean percent expression (%) ± S.E.M. (Normal, n = 25; SLE, total n = 84, SLE with active disease, n = 44, SLE with inactive disease, n = 40) * p<0.05, ** p<0.01, The Wilcoxon signed rank test was applied for analysis of the difference of responses before and after IL-15 treatment. SLE patient and healthy control data were compared between groups using the Mann–Whitney U-test. (calculated by SPSS 17.0 software).</p

Characteristics of controls and patients with SLE.

<p>Characteristics of controls and patients with SLE.</p

Effect of interleukin (IL)-15 on CD94 expression of CD56⁺CD3^- NK cells from SLE patients and healthy controls.

<p>A. Representative histograms of SLE patients (SLE) and controls (Normal) B.Comparison between SLE patients as a whole and normal controls (Normal) using scattergrams (transverse lines indicate means) C. Comparison between SLE patients with active disease and inactive disease; D. Comparison of CD94 expression on CD56^dim NK subsets in SLE patients with different severity as well as normal controls; E. Comparison of CD94 expression on CD56^bright NK subsets in SLE patients with different severity as well as normal controls. PBMC were stimulated with or without IL-15 (10ng/ml) for 18hrs. For C,D,E, data was expressed as mean percent expression (%) ± S.E.M. (Normal, n = 25; SLE, total n = 80, SLE with active disease, n = 40, SLE with inactive disease, n = 40) * p<0.05, ** p<0.01, The Wilcoxon signed rank test was applied for analysis of the difference of responses before and after IL-15 treatment. SLE patient and healthy control data were compared between groups using the Mann–Whitney U-test. (calculated by SPSS 17.0 software).</p

Activating and inhibitory receptors on natural killer cells in patients with systemic lupus erythematosis-regulation with interleukin-15

<div><p>Natural killer (NK) cells may play an important role in the pathogenesis of SLE. Interleukin(IL)-15, an NK-enhancing cytokine, is over-expressed in SLE patients. In the present study, we examined the effect of IL-15 on NK cytotoxicity of SLE patients, and the expression of various activating and inhibitory NK receptors on NK cells from SLE patients in relation to disease activity. We also sought to determine how IL-15 would affect the NK receptor expression on NK cells from SLE patients. PBMCs were collected from 88 SLE patients with inactive disease activity (SLEDAI score<6) and active disease activity (SLEDAI score≥6), 26 age-matched healthy adults were used as controls. PBMC were incubated in the presence or absence of IL-15 (10ng/ml) for eighteen hours. CD3^-CD56⁺ lymphoctes were gated using flow cytometry and further divided into CD56^dim and CD56^bright subsets according to the MFI of CD56. We observed that 1. Serum IL-15 was elevated in SLE patients, and higher in active disease than in inactive disease; 2. NK cytotoxicity of SLE patients was deficient compared to controls and showed an impaired response to IL-15 compared to controls; 3.CD69, CD94, NKG2A, NKp30, and CD158b on NK cells from SLE patients were higher than controls, and could be further enhanced by IL-15; 4. NKp46 expression from SLE patients was higher than controls, but down-regulated by IL-15; 5.Deficient NKG2D and NKAT-2 expression were found on NK cells from SLE patients, which were enhanced by IL-15; 6. A unique NKp46^- subset and CD158b⁺ subsets were observed in NK cells from SLE patients but not controls. 7. Unlike controls, CD158k on NK cells from SLE patients failed to respond to IL-15. Taken together, we demonstrated the aberrant NCR and iNKR expression on NK cells and their distinct response to IL-15 in SLE patients. As IL-15 predominantly aggravates the aberrant NKR expression found in SLE, IL-15 antagonist may have therapeutic benefits in SLE patients.</p></div

Baseline characteristics of chronic hepatitis C patients with genotype 1 and 2.

<p>Continuous variables were expressed as mean ± standard deviation; BMI: body mass index; HbA1c: glycohemoglobin; ALB: albumin; AST: aspartate transaminase; ALT: alanine transaminase; GGT: gamma-glutamyl transpeptidase; ALP: alkaline phosphatase; RVR: rapid virologic response; cEVR: complete early virologic response; SVR: sustained virologic response.</p

Effect of interleukin (IL)-15 on NKp46 expression of CD56⁺CD3^- NK cells from SLE patients and healthy control.

<p>A. Representative histograms of SLE patients (SLE) and controls(Normal); B. Comparison between SLE patients as a whole and controls (Normal) using scattergrams (transverse lines indicate means); C. Comparison between SLE patients with active disease and inactive disease; D. Comparison of NKp46 expression on CD56^dim NK subsets in SLE patients with different severity as well as normal controls; E. Comparison of NKp46 expression on CD56^bright NK subsets in SLE patients with different severity as well as normal controls. PBMC were stimulated with or without IL-15 (10ng/ml) for 18hrs For C,D,E, data was expressed as mean percent expression (%) ± S.E.M. (Normal, n = 19; SLE, total n = 47, SLE with active disease, n = 23, SLE with inactive disease, n = 24) * p<0.05, ** p<0.01, The Wilcoxon signed rank test was applied for analysis of the difference of responses before and after IL-15 treatment. SLE patient and healthy control data were compared between groups using the Mann–Whitney U-test. (calculated by SPSS 17.0 software).</p

Comparison of serum levels of IL-15 determined by ELISA in samples from healthy controls (<i>n</i> = 18) and inactive (<i>n</i> = 41) and active (<i>n</i> = 27) SLE patients using scattergram (transverse lines indicate means).

<p>* p<0.05/**p<0.01, by Mann–Whitney U-test. (calculated by SPSS 17.0 software).</p