scholarly journals Progressive cerebellar atrophy in a patient with complex II and III deficiency and a novel deleterious variant in SDHA: A Counseling Conundrum

2021 ◽  
Author(s):  
Beattie R. H. Sturrock ◽  
Ellen F. Macnamara ◽  
Peter McGuire ◽  
Shannon Kruk ◽  
Ivan Yang ◽  
...  
Keyword(s):  
Cerebellar Atrophy ◽  
Complex Ii ◽  
Deleterious Variant

Macroorganisation and flexibility of thylakoid membranes

2019 ◽  
Vol 476 (20) ◽  
pp. 2981-3018 ◽  
Author(s):  
Petar H. Lambrev ◽  
Parveen Akhtar
Keyword(s):  
Light Harvesting ◽  
Current Knowledge ◽  
Three Dimensional ◽  
Photosynthetic Apparatus ◽  
Dynamic Responses ◽  
State Transitions ◽  
Photochemical Quenching ◽  
Light Harvesting Complex ◽  
Complex Ii ◽  
Light Harvesting Complex Ii

Abstract The light reactions of photosynthesis are hosted and regulated by the chloroplast thylakoid membrane (TM) — the central structural component of the photosynthetic apparatus of plants and algae. The two-dimensional and three-dimensional arrangement of the lipid–protein assemblies, aka macroorganisation, and its dynamic responses to the fluctuating physiological environment, aka flexibility, are the subject of this review. An emphasis is given on the information obtainable by spectroscopic approaches, especially circular dichroism (CD). We briefly summarise the current knowledge of the composition and three-dimensional architecture of the granal TMs in plants and the supramolecular organisation of Photosystem II and light-harvesting complex II therein. We next acquaint the non-specialist reader with the fundamentals of CD spectroscopy, recent advances such as anisotropic CD, and applications for studying the structure and macroorganisation of photosynthetic complexes and membranes. Special attention is given to the structural and functional flexibility of light-harvesting complex II in vitro as revealed by CD and fluorescence spectroscopy. We give an account of the dynamic changes in membrane macroorganisation associated with the light-adaptation of the photosynthetic apparatus and the regulation of the excitation energy flow by state transitions and non-photochemical quenching.

Brain atrophy in Parkinson's disease - Cerebral and cerebellar atrophy.

1985 ◽  
Vol 22 (4) ◽  
pp. 354-359
Author(s):  
Mitsuhiro Kitani ◽  
Shoutai Kobayashi ◽  
Shuhei Yamaguchi ◽  
Tokugoro Tsunematsu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Brain Atrophy ◽  
Cerebellar Atrophy

scholarly journals Assembly and Activity of Respiratory Complex II in Nanolipoprotein Particles

2013 ◽  
Vol 104 (2) ◽  
pp. 594a
Author(s):  
Christine Schwall ◽  
Nathan Alder
Keyword(s):  
Complex Ii ◽  
Respiratory Complex

scholarly journals ZBP1 promotes LPS-induced cell death and IL-1β release via RHIM-mediated interactions with RIPK1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hayley I. Muendlein ◽  
Wilson M. Connolly ◽  
Zoie Magri ◽  
Irina Smirnova ◽  
Vladimir Ilyukha ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Complex Formation ◽  
Complex I ◽  
Yersinia Pseudotuberculosis ◽  
Caspase 8 ◽  
Inflammasome Activation ◽  
Inflammatory Signaling ◽  
Complex Ii ◽  
Dependent Model

AbstractInflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, here we show that a TRIF-dependent complex containing FADD, RIPK1 and caspase-8 (that we have termed the TRIFosome) mediates cell death in response to Yersinia pseudotuberculosis and LPS. Furthermore, we show that constitutive binding between ZBP1 and RIPK1 is essential for the initiation of TRIFosome interactions, caspase-8-mediated cell death and inflammasome activation, thus positioning ZBP1 as an effector of cell death in the context of bacterial blockade of pro-inflammatory signaling. Additionally, our findings offer an alternative to the TNFR1-dependent model of complex II assembly, by demonstrating pro-death complex formation reliant on TRIF signaling.

scholarly journals Neurological Evaluation of Patients with Newly Diagnosed Coeliac Disease Presenting to Gastroenterologists: A 7-Year Follow-Up Study

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1846
Author(s):  
Marios Hadjivassiliou ◽  
Iain D. Croall ◽  
Richard A. Grünewald ◽  
Nick Trott ◽  
David S. Sanders ◽  
...  
Keyword(s):  
Coeliac Disease ◽  
Brain Imaging ◽  
Cerebellar Atrophy ◽  
Neurological Dysfunction ◽  
Close Monitoring ◽  
Newly Diagnosed ◽  
Positive Serology ◽  
Original Cohort ◽  
Follow Up Study

We have previously shown that 67% of patients with newly diagnosed coeliac disease (CD) presenting to gastroenterologists have evidence of neurological dysfunction. This manifested with headache and loss of co-ordination. Furthermore 60% of these patients had abnormal brain imaging. In this follow-up study, we re-examined and re-scanned 30 patients from the original cohort of 100, seven years later. There was significant reduction in the prevalence of headaches (47% to 20%) but an increase in the prevalence of incoordination (27% to 47%). Although those patients with coordination problems at baseline reported improvement on the gluten free diet (GFD), there were 7 patients reporting incoordination not present at baseline. All 7 patients had positive serology for one or more gluten-sensitivity related antibodies at follow-up. In total, 50% of the whole follow-up cohort were positive for one or more gluten-related antibodies. A comparison between the baseline and follow-up brain imaging showed a greater rate of cerebellar grey matter atrophy in the antibody positive group compared to the antibody negative group. Patients with CD who do not adhere to a strict GFD and are serological positive are at risk of developing ataxia, and have a significantly higher rate of cerebellar atrophy when compared to patients with negative serology. This highlights the importance of regular review and close monitoring.

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