scholarly journals Apical dendrite degeneration, a novel cellular pathology for Betz cells in ALS

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Barış Genç ◽  
Javier H. Jara ◽  
Amiko K. B. Lagrimas ◽  
Peter Pytel ◽  
Raymond P. Roos ◽  
...  
Keyword(s):  
Apical Dendrite ◽  
Cellular Pathology ◽  
Betz Cells

Drug Induced Changes in Cell Organelles

1968 ◽  
Vol 26 ◽  
pp. 110-111
Author(s):  
Sarah A. Luse
Keyword(s):  
Clinical Medicine ◽  
Cell Organelles ◽  
Riboflavin Deficiency ◽  
Drug Induced ◽  
New Era ◽  
Health And Disease ◽  
In The Beginning ◽  
Cellular Pathology ◽  
Induced Changes ◽  
The Impact

In the mid-nineteenth century Virchow revolutionized pathology by introduction of the concept of “cellular pathology”. Today, a century later, this term has increasing significance in health and disease. We now are in the beginning of a new era in pathology, one which might well be termed “organelle pathology” or “subcellular pathology”. The impact of lysosomal diseases on clinical medicine exemplifies this role of pathology of organelles in elucidation of disease today.Another aspect of cell organelles of prime importance is their pathologic alteration by drugs, toxins, hormones and malnutrition. The sensitivity of cell organelles to minute alterations in their environment offers an accurate evaluation of the site of action of drugs in the study of both function and toxicity. Examples of mitochondrial lesions include the effect of DDD on the adrenal cortex, riboflavin deficiency on liver cells, elevated blood ammonia on the neuron and some 8-aminoquinolines on myocardium.

Molecular and cellular pathology of hepatocellular carcinoma

1998 ◽  
Vol 13 (11-s4) ◽  
pp. S299-S303
Author(s):  
IRENE NG
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cellular Pathology

scholarly journals The Parkinson’s Disease-Associated Protein DJ-1 Protects Dictyostelium Cells from AMPK-Dependent Outcomes of Oxidative Stress

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1874
Author(s):  
Suwei Chen ◽  
Sarah J. Annesley ◽  
Rasha A. F. Jasim ◽  
Paul R. Fisher
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Respiration ◽  
Cysteine Residue ◽  
Reduced Form ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Pathology

Mitochondrial dysfunction has been implicated in the pathology of Parkinson’s disease (PD). In Dictyostelium discoideum, strains with mitochondrial dysfunction present consistent, AMPK-dependent phenotypes. This provides an opportunity to investigate if the loss of function of specific PD-associated genes produces cellular pathology by causing mitochondrial dysfunction with AMPK-mediated consequences. DJ-1 is a PD-associated, cytosolic protein with a conserved oxidizable cysteine residue that is important for the protein’s ability to protect cells from the pathological consequences of oxidative stress. Dictyostelium DJ-1 (encoded by the gene deeJ) is located in the cytosol from where it indirectly inhibits mitochondrial respiration and also exerts a positive, nonmitochondrial role in endocytosis (particularly phagocytosis). Its loss in unstressed cells impairs endocytosis and causes correspondingly slower growth, while also stimulating mitochondrial respiration. We report here that oxidative stress in Dictyostelium cells inhibits mitochondrial respiration and impairs phagocytosis in an AMPK-dependent manner. This adds to the separate impairment of phagocytosis caused by DJ-1 knockdown. Oxidative stress also combines with DJ-1 loss in an AMPK-dependent manner to impair or exacerbate defects in phototaxis, morphogenesis and growth. It thereby phenocopies mitochondrial dysfunction. These results support a model in which the oxidized but not the reduced form of DJ-1 inhibits AMPK in the cytosol, thereby protecting cells from the adverse consequences of oxidative stress, mitochondrial dysfunction and the resulting AMPK hyperactivity.

scholarly journals Alterations of the Giant Pyramidal Neurons (Betz Cells) in Brain Cortex of Rat Offspring Born from Gestational Diabetic Dams: A Morphometric Study

2015 ◽  
Vol 33 (3) ◽  
pp. 1120-1125 ◽  
Author(s):  
Soraya Ghafari ◽  
Elnaz Golalipour ◽  
Mohammad Jafar Golalipour
Keyword(s):  
Brain Cortex ◽  
Pyramidal Neurons ◽  
Morphometric Study ◽  
Rat Offspring ◽  
Betz Cells

The molecular and cellular pathology of inflammatory muscle diseases

2001 ◽  
Vol 1 (3) ◽  
pp. 300-306 ◽  
Author(s):  
M Dalakas
Keyword(s):  
Muscle Diseases ◽  
Cellular Pathology

SP10.2.12 Information Sustainability: The revitalisation and upcycling of 373,342 historic surgical pathology records into the contemporary electronic patient record in one UK NHS Hospital Trust

2021 ◽  
Vol 108 (Supplement_7) ◽  
Author(s):  
Fatima Rahman ◽  
Alan Hales ◽  
David Cable ◽  
Keith Burrill ◽  
Adrian Bateman ◽  
...  
Keyword(s):  
Electronic Patient Record ◽  
Clinical Decision Making ◽  
Clinical Decision ◽  
Patient Record ◽  
Clinical Use ◽  
Data Resource ◽  
Cancer Data ◽  
Transition Points ◽  
Pathology Reports ◽  
Cellular Pathology

Abstract Aims Surgical and Cellular pathology (‘e-pathology’) record sets are a valuable data resource with which to populate the Electronic Patient Record (EPR). Accessible reports, even decades old, can be of great value in contemporary clinical decision making and as a resource for longitudinal clinical research. They commonly identify the operation, the location and the pathology, even if not to modern reporting standards. Methods Since 2010, we have built and implemented a timeline structured EPR for the ‘whole-of-life’ visualisation of the electronic documents (e-Docs) of 2.5M+ patients on our Master Index. Prior to this project, our earliest e-Docs dated to 1995. We tracked down 373,342 inert e-pathology reports from our legacy Ferranti (1990-1997) and Masterlab (1997-2004) systems. These were uploaded into our active file servers, following appropriate data quality and patient identity reconciliation checks. Results We have progressively restored 373,342 previously inaccessible e-pathology records to clinical use and to immediacy of access, and in the process extending our “addressable EPR” back to 1990 for living and deceased patients. This process has also allowed us to populate and validate an EPR-integral breast cancer data system of 20,000 cases with e-pathology records dating back to 1990. Conclusions The sustainable revitalisation of old e-pathology reports into a timeline structured EPR creates preserves and upcycles the investment in pathology reporting which is otherwise progressively lost to clinical use. E-pathology records provide reliable, life-long evidence of critical transition points in individual lives and disease progression for clinical and research use, when they can be instantly accessed.

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