scholarly journals Intracellular compartment-specific proteasome dysfunction in postmortem cortex in schizophrenia subjects

2019 ◽  
Vol 25 (4) ◽  
pp. 776-790 ◽  
Author(s):  
Madeline R. Scott ◽  
James H. Meador-Woodruff
1959 ◽  
Vol 14 (6) ◽  
pp. 1026-1028 ◽  
Author(s):  
D. S. Kronfeld ◽  
E. G. Tombropoulos ◽  
Max Kleiber

The size, turnover time and transfer rate of the glucose pool were estimated with glucose–C14 in normal and ketotic cows. The size and turnover time of the pool were both about 1/5 greater in the ketotic than in the normal cows, so that the transfer rate remained similar, being about 1 gm/min. The hypoglycemia which is characteristic of the disease appeared to be associated with an expansion of the glucose space, which in the normal cows approximated the extracellular volume, into the intracellular compartment of the ketotic cows. These results do not favor theories of bovine ketosis which presume a shortage of body glucose. Submitted on June 25, 1959


2011 ◽  
Vol 16 (1) ◽  
pp. 129-141 ◽  
Author(s):  
Alena Dabrazhynetskaya ◽  
Jinxia Ma ◽  
Andre Ortlieb Guerreiro-Cacais ◽  
Zita Arany ◽  
Eva Rudd ◽  
...  

1998 ◽  
Vol 72 (1) ◽  
pp. 527-534 ◽  
Author(s):  
G. H. Hansen ◽  
B. Delmas ◽  
L. Besnardeau ◽  
L. K. Vogel ◽  
H. Laude ◽  
...  

ABSTRACT Aminopeptidase N is a species-specific receptor for transmissible gastroenteritis virus (TGEV), which infects piglets, and for the 229E virus, which infects humans. It is not known whether these coronaviruses are endocytosed before fusion with a membrane of the target cell, causing a productive infection, or whether they fuse directly with the plasma membrane. We have studied the interaction between TGEV and a cell line (MDCK) stably expressing recombinant pig aminopeptidase N (pAPN). By electron microscopy and flow cytometry, TGEV was found to be associated with the plasma membrane after adsorption to the pAPN-MDCK cells. TGEV was also observed in endocytic pits and apical vesicles after 3 to 10 min of incubation at 38°C. The number of pits and apical vesicles was increased by the TGEV incubation, indicating an increase in endocytosis. After 10 min of incubation, a distinct TGEV-pAPN-containing population of large intracellular vesicles, morphologically compatible with endosomes, was found. A higher density of pAPN receptors was observed in the pits beneath the virus particles than in the surrounding plasma membrane, indicating that TGEV recruits pAPN receptors before endocytosis. Ammonium chloride and bafilomycin A1 markedly inhibited the TGEV infection as judged from virus production and protein biosynthesis analyses but did so only when added early in the course of the infection, i.e., about 1 h after the start of endocytosis. Together our results point to an acid intracellular compartment as the site of fusion for TGEV.


1962 ◽  
Vol 203 (4) ◽  
pp. 609-614 ◽  
Author(s):  
A. Van Harreveld ◽  
M. P. Biber

A loss of electrical conductivity after circulatory arrest was observed in the submaxillary salivary gland, liver, kidney, and skeletal muscle. A drop in conductivity of 85–90% of the original value developed in about 0.5 hr in the liver. In the kidney the loss was less severe. Salivary glands lost about 70–80% of their conductivity in 1.5 hr. The losses in muscle conductivity developed late and were not greater than 50%. The drop in conductivity observed in the various organs after circulatory arrest can be accounted for by losses of extracellular electrolytes from the tissues, which could be demonstrated in preparations stained for chloride. In this context the electrolytes in the blood plasma have to be included in the extracellular compartment. The extracellular electrolytes are lost either because they are transported into the intracellular compartment or because they leave the tissue with blood that flows out of the organ after circulatory arrest.


Author(s):  
Alain Doucet ◽  
Gilles Crambert

The equilibrium between the concentration of K+ in the extracellular space (low) and the intracellular compartment (high) is crucial for maintaining the electrical properties of excitable and non-excitable cells, because it determines the membrane resting potential. The high intracellular concentration of K+ (120–140 mmol/L) also contributes to the intracellular osmolarity, a determinant of cell volume. It is therefore crucial to finely tune both extracellular and intracellular K+ concentrations. There is a coordinated regulation between processes/mechanisms that store/release K+ from internal stores (internal balance) and those that retain/excrete K+ (external balance).


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