Central Limit Theorems For Multicolor Urns With Dominated Colors

An urn contains balls of d >= 2 colors. At each time n >= 1, a ball is drawn and then replaced together with a random number of balls of the same color. Let An =diag (An,1, . . . ,An,d) be the n-th reinforce matrix. Assuming EAn,j = EAn,1 for all n and j, a few CLT’s are available for such urns. In real problems, however, it is more reasonable to assume EAn,j = EAn,1 whenever n >= 1 and 1 limsup EAn,j whenever j > d0, for some integer 1 = 1) is independent but need not be identically distributed. Some statistical applications are given as well.Central limit theorem, Clinical trials, Random probability measure, Stable convergence, Urn model.

Central limit theorems for multicolor urns with dominated colors

An urn contains balls of d≥2 colors. At each time n≥1, a ball is drawn and then replaced together with a random number of balls of the same color. Let A n = diag (An,1,…,An,d) be the n-th reinforce matrix. Assuming that EAn,j=EAn,1 for all n and j, a few central limit theorems (CLTs) are available for such urns. In real problems, however, it is more reasonable to assume that EA n,j = EA n,1 whenever  n ≥ 1  and  1 ≤ j ≤ d0 , liminfn EAn,1 > limsupn EAn,j whenever  j > d0 for some integer 1≤d0≤d. Under this condition, the usual weak limit theorems may fail, but it is still possible to prove the CLTs for some slightly different random quantities. These random quantities are obtained by neglecting dominated colors, i.e., colors from d0+1 to d, and they allow the same inference on the urn structure. The sequence (An : n ≥ 1) is independent but need not be identically distributed. Some statistical applications are given as well

ANALISIS KARAKTERISTIK KECELAKAAN LALU LINTAS PADA TITIK BLACKSPOT di RUAS JALAN AHMAD YANI KILOMETER 21, JALAN WAHID HASYIM II dan JALAN CIPTO MANGUNKUSUMO SAMARINDA

Tingginya angka kecelakaan di Kota Samarinda dan salah satu kecelakaan tertinggi di Samarinda yaitupada Jalan Ahmad Yani KM. 21, Jalan Wahid Hasyim II dan Jalan Cipto Mangun Kusumo. Untukmengatasi permasalahan kecelakaan lalu lintas pada tiga jalan tersebut, maka dilakukan penelitianmengenai analisis karakteristik faktor kecelakaan lalu lintas pada jalan tersebut. Berdasarkan Hasil Surveypenyebab kecelakaan yang terjadi di Jalan Ahmad Yani Km 21 yakni karena adanya faktor manusia (67%),Jalan Wahid Hasyim II (83%), Jalan Cipto Mangunkusumo (100%). Dari hasil analisis angka kecelakaanmenggunakan metode EAN, BKA dan UCL bahwa pada Jalan Ahmad Yani Km 21 pada titik 1(EAN=24>BKA=24,4 UCL=22,4) pada titik 5 (EAN=40>BKA=24,4, UCL=24,62). Pada Jalan WahidHasyim II pada titik 4 (EAN=21>BKA=19,26, UCL=18,39) pada titik 11 (EAN=44>BKA=19,26,UCL=22,93). Pada Jalan Cipto Mangunkusumo pada titik 2 (EAN=24>BKA=22,88 UCL=20,76) pada titik13 (EAN=32>BKA=22,88, UCL=22,07)

The Effects of Prophylactic Cyclosporin A on Experimental Allergic Neuritis (EAN) in the Lewis Rat: Induction of Relapsing EAN Using Low Dose Cyclosporin A

Experimental allergic neuritis (EAN) was induced in Lewis rats by inoculation with bovine intradural root myelin plus adjuvants. Animals treated with high dose (30 mg/kg) cyclosporin A (CsA) 3 times per week did not develop clinical EAN during the period of CsA treatment, but had an episode of EAN after cessation of CsA treatment. Animals treated with low dose (4 mg/kg) CsA 3 times per week developed EAN during the period of treatment, and after cessation of CsA treatment all of these animals developed relapsing EAN with disease continuing for up to four episodes. In contrast, 30-40% of untreated animals had a mild second episode of EAN but no further attacks. Histological studies performed in treated and untreated animals at the time of clinical episodes revealed inflammation and demyelination in the spinal roots and dorsal root ganglia. When animals were challenged with a second inoculation at age 7 months, one of 15 untreated control animals but none of the CsA treated animals developed an episode of EAN

Role of apolipoprotein E isoforms and cytokines in immune responses and inflammation of the mouse peripheral nervous system

Experimental autoimmune neuritis (EAN) as an animal model for Guillain-Barré syndrome (GBS) in humans is an immune-mediated disorder affecting the peripheral nervous system (PNS). Apolipoprotein E (apoE) is a glycosylated protein characterized by its wide tissue distribution and multiple biological functions. ApoE can suppress proinflammatory signalings, and vice versa, indicating an intricate apoE-mediated feedback regulation of inflammatory and immune responses. Immune cells together with cytokines produced by various cells contribute to the inflammatory process of EAN by acting as mediators or effectors. In Paper I, the effects of apoE isoforms on the functions of immune cells were investigated. Clinical signs of EAN were most severe in wild type (WT) C57BL/6 mice and apoE4 transgenic (Tg) mice, followed by apoE2 Tg mice and apoE3 Tg mice (WT ≈ E4 > E2 > E3). Proliferation tests of purified T cells from naive mice stimulated with phytohemagglutinin or interleukin (IL)- 12 showed isoform-specific differences (WT ≈ E4 > E3 ≈ E2). Macrophages from both naïve and EAN mice produced nitric oxide (NO) upon inflammatory stimulation in an isoformdependent manner (WT ≈ E4 > E2 > E3). During the recovery stage of disease, the highest expression of CD178 (FasL) on Schwann cells (SCs) was found in apoE3 Tg mice. In Paper II, the effects of different isoforms of apoE on SCs in response to inflammatory stimulation (lipopolysaccharide plus interferon (IFN)-γ) were studied. Upon stimulation, a change in the morphology of cultured SCs was observed. Pronounced production of IL-6 and IL-10 within SCs, and increased levels of IL-6 and NO in culture supernatants were found in an isoform-dependent manner (apoE3 > apoE2 ≈ apoE4). Further results indicated that both nuclear factor kappa B (NFκB) and Akt signaling pathways were involved in the process by the same isoformdependent pattern. In Paper III, the role of IFN-γ, a signature T helper (Th)1 cytokine, in the pathogenesis of EAN was investigated. The clinical signs of EAN in IFN-γ knockout (KO) mice were evidently aggravated. At the peak of EAN, the proportion of IL-17A expressing cells in cauda equina (CE) infiltrating cells, and the serum levels of IL-17A were elevated in IFN-γ KO mice. The proportions of MHC II, macrosialin, and IL-12/IL-23p40 expressing cells, relative to total CE infiltrating cells were correspondingly higher in IFN-γ KO than WT mice with EAN. In Paper IV, the role of tumor necrosis factor alpha (TNF-α), another Th1 cytokine, in the pathogenesis of EAN was studied. TNF-α deficiency significantly attenuated EAN. Furthermore, TNF-α deficiency induced an antiinflammatory phenotype of macrophages (M2) characterized by reduced production of IL-12 and NO, and enhanced production of IL-10. Moreover, TNF receptor (TNFR)1 monoclonal antibodies markedly suppressed the severity of EAN when they were administered from the beginning of EAN induction. In summary, our data support an isoform-dependent effect of apoE on EAN. This might be due to the isoform-specific effects of apoE on functions of T cells, macrophages and SCs, which contribute to the distinct clinical courses of EAN. SCs from apoE2 and apoE4 Tg mice bear some dysfunction in producing cytokines (IL-6 and IL-10) and NO as compared with their apoE3 counterparts, probably resulting from their insufficiency to suppress the activation of NFκB and Akt pathways. IFN-γ deficiency exacerbates EAN via upregulating Th17 cells despite a mitigated systemic Th1 immune response. TNF-α exacerbates EAN via TNFR1 by inducing the proinflammatory phenotype of macrophage (classically activated macrophage, M1)

Исследование соответствия размеров элементов штрих-кодового знака и структуры кода EAN-13 на картонных упаковках

У статті наведено результати експериментальних досліджень відповідності розмірів елементів штрих-кодового знаку та структури штрих-кодових знаків EAN-13 надрукованих на картонних пакованнях.The article presents the results of the experimental studies of conformity of the dimensions of elements of a barcode and structure of barcodes EAN-13, printed on cardboard packaging.В статье приведены результаты экспериментальных исследований соответствия размеров элементов штрих-кодовых знаков EAN-13 напечатанных на картонных упаковках

Increased phosphorylation of c-Jun NH (2)-terminal protein kinase in the sciatic nerves of Lewis rats with experimental autoimmune neuritis

The phosphorylation of c-Jun NH (2)-terminal protein kinase (JNK), one of the mitogen-activated protein kinases, was analyzed in the sciatic nerves of Lewis rats with experimental autoimmune neuritis (EAN). Western blot analysis showed that the expression levels of both phosphorylated JNK1 (p-JNK1, approximately 46 kDa) and phosphorylated JNK2 (p-JNK2, approximately 54 kDa) in the sciatic nerves of rats with EAN increased significantly (p < 0.05) at day 14 post-immunization (PI) and remained at this level at days 24 and 30 PI, with a slight decrease. In EAN-affected sciatic nerves, there was intense immunostaining for p-JNK in the infiltrating inflammatory cells (especially ED1-positive macrophages) and Schwann cells on days 14-24 PI, compared with those of controls. Some macrophages with increased p-JNK immunoreactivity was shown to be apoptotic, while some Schwann cells remained survived in this rat EAN model, suggesting that JNK is differentially involved in the EAN-affected sciatic nerves. These findings suggest that JNK phosphorylation is closely associated with the clearance of inflammatory cells as well as the activation of Schwann cells in the EAN affected sciatic nerves

Attenuated EAN in TNF-α Deficient Mice Is Associated with an Altered Balance of M1/M2 Macrophages

The role of tumor necrosis factor (TNF)-α and its receptors in neuroautoimmune and neuroinflammatory diseases has been controversial. On the basis of our previous studies, we hereby aimed to further clarify TNF-α’s mechanism of action and to explore the potential role of TNF-α receptor (TNFR)1 as a therapeutic target in experimental autoimmune neuritis (EAN). EAN was induced by immunization with P0 peptide 180–199 in TNF-α knockout (KO) mice and anti-TNFR1 antibodies were used to treat EAN. Particularly, the effects of TNF-α deficiency and TNFR1 blockade on macrophage functions were investigated. The onset of EAN in TNF-α KO mice was markedly later than that in wild type (WT) mice. From day 14 post immunization, the clinical signs of TNF-α KO mice were significantly milder than those of their WT counterparts. Further, we showed that the clinical severity of WT mice treated with anti-TNFR1 antibodies was less severe than that of the control WT mice receiving PBS. Nevertheless, no difference with regard to the clinical signs of EAN or inflammatory infiltration in cauda equina was seen between TNF-α KO and WT mice with EAN after blockade of TNFR1. Although TNF-α deficiency did not alter the proliferation of lymphocytes in response to either antigenic or mitogenic stimuli, it down-regulated the production of interleukin (IL)-12 and nitric oxide (NO), and enhanced the production of IL-10 in macrophages. Increased ratio of regulatory T cells (Tregs) and reduced production of interferon (IFN)-γ in cauda equina infiltrating cells, and elevated levels of IgG2b antibodies against P0 peptide 180–199 in sera were found in TNF-α KO mice with EAN. In conclusion, TNF-α deficiency attenuates EAN via altering the M1/M2 balance of macrophages