Students with dyslexia: research projects at Northumbria University

Northumbria University has about 700 registered disabled students, the majority of whom (around 58 per cent) are registered as having dyslexia and account for approximately two per cent of the total student population. Therefore dyslexic students represent the largest single group of disabled students and are those with whom most staff are likely to come into contact. The research authors were keen to ascertain whether there was a difference in academic performance between dyslexic and non-dyslexic students in respect of degree classification and assignment marks and to investigate whether dyslexic students generally felt supported in their academic studies. Research involved both qualitative and quantitative strands and the areas explored include pre expectations; general support throughout study; methods, flexibility and clarity of learning tasks, in particular assessment and levels of performance throughout and at the end of their study. This research is ongoing, however, findings have proved invaluable as a basis in the construction of good practice guidelines in dealing with the pedagogic needs of this diverse student grou

Precocious Gauge Symmetry Breaking in SU(6)×SU(2)RSU(6) \times SU(2)_R Model

In the $SU(6) \times SU(2)_R$ string-inspired model, we evolve the couplings and the masses down from the string scale $M_S$ using the renormalization group equations and minimize the effective potential. This model has the flavor symmetry including the binary dihedral group $\tilde{D}_4$. We show that the scalar mass squared of the gauge non-singlet matter field possibly goes negative slightly below the string scale. As a consequence, the precocious radiative breaking of the gauge symmetry down to the standard model gauge group can occur. In the present model, the large Yukawa coupling which plays an important role in the symmetry breaking is identical with the colored Higgs coupling related to the longevity of the proton.Comment: 15 pages, 2 figure

アルツハイマー型認知症患者における前頭葉機能と介護負担の関係

AIM: Understanding of the relationship between caregiver burden and the degree of behavioural deficits in patients with Alzheimer's disease (AD) is relatively limited. Therefore, it is worthwhile to examine the correlations between the various relevant factors to improve the efficacy of care for patients with AD. The aim of this study was to investigate the specific contributions of frontal lobe dysfunction in AD patients to caregiver burden, while controlling for other predictor variables. METHODS: Participants included 30 pairs of caregivers and patients with AD. The Zarit Burden Interview and Frontal Assessment Battery were used to measure the caregiver burden and patients' frontal lobe function, respectively. To investigate the effects of frontal lobe dysfunction on caregiver burden, hierarchical regression equations with steps incorporating additional predictor variables were fitted. We also performed a correlation analysis between the individual subdomains of the Zarit Burden Interview and the predictor variables. RESULTS: Our study suggests that the degree of frontal lobe dysfunction in AD patients predicts their caregiver burden, when other factors of daily functional limitations and neuropsychiatric symptoms are controlled. Daily functional limitations and neuropsychiatric symptoms affected caregivers' psychosocial burden, whereas frontal lobe dysfunction affected caregivers' burden due to the increase in the dependency of the patients. CONCLUSION: Our findings indicate that to ameliorate the disabilities of patients and reduce caregiver burden, there is a need for interventions that focus on psychosocial burdens, as shown in previous studies, as well as on excessive dependency due to frontal lobe dysfunction.博士（医学）・甲第661号・平成29年3月15日© 2017 Japanese Psychogeriatric SocietyThis is the pre-peer reviewed version of the following article: http://dx.doi.org/10.1111/psyg.12231, which has been published in final form at http://dx.doi.org/10.1111/psyg.12231. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving

Cadmium Induces the Expression of Grp78, an Endoplasmic Reticulum Molecular Chaperone, in LLC-PK1 Renal Epithelial Cells

To reveal the effects of cadmium exposure on the endoplasmic reticulum (ER) stress response, we examined the expression and function of 78-kDa glucose-regulated protein (Grp78), an ER-resident molecular chaperone, in LLC-PK1 cells. In cells treated with 10 μM cadmium chloride, Grp78 protein levels increased after 6 hr and remained elevated at 24 hr. When cells were incubated with 1–20 μM CdCl(2) for 6 hr, Grp78 increased in a dose-dependent manner. In addition, Grp78 mRNA levels were elevated in response to CdCl(2) exposure. After exposure to 10 μM CdCl(2), the levels of activating transcription factor 4 (ATF4) were increased at 2 hr, with a further enhancement after that; this accumulation followed the transient but marked phosphorylation of the α subunit of eukaryotic translation initiation factor 2 (eIF2α) on serine 51. Although ATF4 mRNA levels increased mildly by CdCl(2) exposure, treatment with actinomycin D did not suppress CdCl(2)-induced accumulation of ATF4 protein, suggesting the involvement of posttranscriptional and, in part, transcriptional mechanisms. Compared with other heavy-metal compounds such as manganese chloride, zinc chloride, mercuric chloride, and lead chloride, CdCl(2) could increase the levels of Grp78, ATF4, and the phosphorylated form of eIF2α more markedly without definite cellular damage. The silencing of Grp78 expression using short-interference RNA enhanced CdCl(2)-induced cellular damage. These results show that cadmium induces the expression of Grp78 probably via phosphorylation of eIF2α and resultant translation of ATF4, and this ER stress response plays a role in protection against cadmium cytotoxicity in this renal epithelial cell

Age-dependent motor dysfunction due to neuron-specific disruption of stress-activated protein kinase MKK7.

c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and controls various physiological processes including apoptosis. A specific upstream activator of JNKs is the mitogen-activated protein kinase kinase 7 (MKK7). It has been reported that MKK7-JNK signaling plays an important regulatory role in neural development, however, post-developmental functions in the nervous system have not been elucidated. In this study, we generated neuron-specific Mkk7 knockout mice (MKK7 cKO), which impaired constitutive activation of JNK in the nervous system. MKK7 cKO mice displayed impaired circadian behavioral rhythms and decreased locomotor activity. MKK7 cKO mice at 8 months showed motor dysfunctions such as weakness of hind-limb and gait abnormality in an age-dependent manner. Axonal degeneration in the spinal cord and muscle atrophy were also observed, along with accumulation of the axonal transport proteins JNK-interacting protein 1 and amyloid beta precursor protein in the brains and spinal cords of MKK7 cKO mice. Thus, the MKK7-JNK signaling pathway plays important roles in regulating circadian rhythms and neuronal maintenance in the adult nervous system