scholarly journals CATALASE INHIBITION BY NORMAL AND NEOPLASTIC TISSUE EXTRACTS

1957 ◽  
Vol 227 (2) ◽  
pp. 975-985
Author(s):  
Nicholas M. Alexander
Virology ◽  
1959 ◽  
Vol 7 (3) ◽  
pp. 348-351 ◽  
Author(s):  
A.R. Taylor ◽  
Anne Gillen ◽  
F.B. Brandon

2001 ◽  
pp. 161-164 ◽  
Author(s):  
AK Velin ◽  
A Herder ◽  
KJ Johansson ◽  
LM Trulsson ◽  
S Smeds

BACKGROUND: Telomerase is a specific enzyme that appears to have a key role in cellular senescence and the progression of neoplastic tissue. High telomerase activity has been found in several cancers, but not in most normal and benign tissue. Little is known about the influence of telomerase on the abnormal growth associated with hyperparathyroidism. OBJECTIVE: To analyse telomerase activity in parathyroid tissue obtained from 29 patients undergoing surgery for primary hyperparathyroidism. DESIGN: Tissue for telomerase activity measurements was collected from six hyperplastic, 20 adenomatous and 22 normal parathyroid glands. METHODS: The highly sensitive PCR-based telomeric repeat amplification protocol, TRAP, combined with ELISA, was used to detect telomerase activity in tissue extracts containing 3.0 microg protein. RESULT: Telomerase was not activated in any of the analysed tissue by 3 microg protein. Reassay of 12 samples containing 6.0 microg protein verified these negative TRAP results. CONCLUSION: Our findings indicate that telomerase is not a part of the mechanism promoting parathyroid proliferation and the underlying conditions remain to be determined.


1979 ◽  
Vol 42 (02) ◽  
pp. 726-733 ◽  
Author(s):  
Utako Okamoto ◽  
Jun-ichiro Yamamoto ◽  
Yoko Nagamatsu ◽  
Noboru Horie

SummaryProtease-like activity which split plasminogen-free fibrin was demonstrated in 2 M KSCN extracts of the lung and spleen of conventional rats. The activity was virtually undetectable in tissue extracts from germ-free rats. The extracts from the conventional rat tissues split fibrin and fibrinogen remarkably at neutral pH, but not casein, when examined using fibrin, fibrinogen-agar and casein-agar plates. The fibrinolytic activity was inhibited by STI and DFP, indicating a serine protease nature. The activity was not inhibited by TLCK, t-AMCHA or dansyl-L-arginine-methylpiperidine amide (a selective synthetic thrombin inhibitor, OM189). It was neither activated nor inhibited by cysteine, KCN or iodoacetic acid. The results obtained indicate that the protease-like activity of the lung and spleen extracted with 2 M KSCN from conventional rats has properties which differ from those of trypsin, plasmin, plasminogen-activator, thrombin, and cathepsin A, B and C.


2020 ◽  
Vol 27 (29) ◽  
pp. 4840-4854 ◽  
Author(s):  
Chrysoula-Evangelia Karachaliou ◽  
Hubert Kalbacher ◽  
Wolfgang Voelter ◽  
Ourania E. Tsitsilonis ◽  
Evangelia Livaniou

Prothymosin alpha (ProTα) is a highly acidic polypeptide, ubiquitously expressed in almost all mammalian cells and tissues and consisting of 109 amino acids in humans. ProTα is known to act both, intracellularly, as an anti-apoptotic and proliferation mediator, and extracellularly, as a biologic response modifier mediating immune responses similar to molecules termed as “alarmins”. Antibodies and immunochemical techniques for ProTα have played a leading role in the investigation of the biological role of ProTα, several aspects of which still remain unknown and contributed to unraveling the diagnostic and therapeutic potential of the polypeptide. This review deals with the so far reported antibodies along with the related immunodetection methodology for ProTα (immunoassays as well as immunohistochemical, immunocytological, immunoblotting, and immunoprecipitation techniques) and its application to biological samples of interest (tissue extracts and sections, cells, cell lysates and cell culture supernatants, body fluids), in health and disease states. In this context, literature information is critically discussed, and some concluding remarks are presented.


1941 ◽  
Vol 137 (1) ◽  
pp. 343-356
Author(s):  
Sidney P. Colowick ◽  
Herman M. Kalckar ◽  
Carl F. Cori

Biomolecules ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 8
Author(s):  
Paulina Lewandowska ◽  
Jaroslaw Wierzbicki ◽  
Marek Zawadzki ◽  
Anil Agrawal ◽  
Małgorzata Krzystek-Korpacka

Facilitating resolution of inflammation using atypical chemokine receptors (ACKR) as an anticancer strategy is considered but requires a deeper understanding of receptor role in carcinogenesis. We aimed at transcriptional analysis (RTqPCR) of ACKR2 and ACKR4 expression in colorectal adenoma-adenocarcinoma sequence in paired normal-neoplastic tissues from 96 polyps and 51 cancers. On average, ACKR2 was downregulated in neoplastic as compared to non-affected tissue in polyp (by 2.7-fold) and cancer (by 3.1-fold) patients. The maximal downregulation (by 8.2-fold) was observed in adenomas with the highest potential for malignancy and was gradually lessening through cancer stages I-IV, owing to increased receptor expression in tumors. On average, ACKR4 was significantly downregulated solely in adenocarcinomas (by 1.5-fold), less so in patients with lymph node metastasis, owing to a gradual decrease in ACKR4 expression among N0-N1-N2 cancers in non-affected tissue without changes in tumors. In adenomas, ACKR4 downregulation in neoplastic tissue increased with increasing potential for malignancy and contribution of villous growth pattern. ACKR4 expression increased in non-affected tissue with a concomitant decrease in pathological mucosa. In conclusion, the changes in ACKRs expression occur already in precancerous colorectal lesions, culminating in the adenomas with the highest potential for malignancy. Therefore, chemoprevention by manipulating ACKRs’ expression is worth exploration.


1946 ◽  
Vol 19 (2) ◽  
pp. 148-154 ◽  
Author(s):  
Harold R. Wolfe ◽  
Mary Jane Bradford ◽  
Chester A. Herrick
Keyword(s):  

1956 ◽  
Vol 222 (1) ◽  
pp. 399-414
Author(s):  
Charles E. Wenner ◽  
Sidney Weinhouse
Keyword(s):  

2021 ◽  
pp. 0271678X2199617
Author(s):  
Narayan D Soni ◽  
Akila Ramesh ◽  
Dipak Roy ◽  
Anant B Patel

Alzheimer’s disease (AD) is a very common neurodegenerative disorder. Although a majority of the AD cases are sporadic, most of the studies are conducted using transgenic models. Intracerebroventricular (ICV) administered streptozotocin (STZ) animals have been used to explore mechanisms in sporadic AD. In this study, we have investigated memory and neurometabolism of ICV-STZ-administered C57BL6/J mice. The neuronal and astroglial metabolic activity was measured in 1H-[13C]-NMR spectrum of cortical and hippocampal tissue extracts of mice infused with [1,6-13C2]glucose and [2-13C]acetate, respectively. STZ-administered mice exhibited reduced (p = 0.00002) recognition index for memory. The levels of creatine, GABA, glutamate and NAA were reduced (p ≤ 0.04), while that of myo-inositol was increased (p < 0.05) in STZ-treated mice. There was a significant (p ≤ 0.014) reduction in aspartate-C3, glutamate-C4/C3, GABA-C2 and glutamine-C4 labeling from [1,6-13C2]glucose. This resulted in decreased rate of glucose oxidation in the cerebral cortex (0.64 ± 0.05 vs. 0.77 ± 0.05 µmol/g/min, p = 0.0008) and hippocampus (0.60 ± 0.04 vs. 0.73 ± 0.07 µmol/g/min, p = 0.001) of STZ-treated mice, due to similar reductions of glucose oxidation in glutamatergic and GABAergic neurons. Additionally, reduced glutamine-C4 labeling points towards compromised synaptic neurotransmission in STZ-treated mice. These data suggest that the ICV-STZ model exhibits neurometabolic deficits typically observed in AD, and its utility in understanding the mechanism of sporadic AD.


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