scholarly journals Role of plant physiology and dynamic vegetation feedbacks in the climate response to low GHG concentrations typical of late stages of previous interglacials

2010 ◽  
Vol 37 (8) ◽  
Author(s):  
Gwenaëlle Philippon-Berthier ◽  
Stephen J. Vavrus ◽  
John E. Kutzbach ◽  
William F. Ruddiman
Keyword(s):  
Plant Physiology ◽  
Climate Response ◽  
Vegetation Feedbacks ◽  
Late Stages

PTTG has a Dual Role of Promotion-Inhibition in the Development of Pituitary Adenomas

2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang
Keyword(s):  
Cell Cycle ◽  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Cell Cycle Progression ◽  
Key Factors ◽  
Cycle Progression ◽  
Sister Chromatids ◽  
Regulation Of Cell Cycle ◽  
Late Stages

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.

scholarly journals A STUDY OF THE POSSIBLE RÔLE OF ALUMINUM COMPOUNDS IN ANIMAL AND PLANT PHYSIOLOGY

1928 ◽  
Vol 77 (2) ◽  
pp. 753-769 ◽  
Author(s):  
E.V. McCollum ◽  
O.S. Rask ◽  
J. Ernestine Becker
Keyword(s):  
Plant Physiology ◽  
Aluminum Compounds

scholarly journals The differential role of reactive oxygen species in early and late stages of cancer

2017 ◽  
Vol 313 (6) ◽  
pp. R646-R653 ◽  
Author(s):  
Mohamad Assi
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Reactive Oxygen ◽  
Pentose Phosphate ◽  
Oxygen Species ◽  
Redox Biology ◽  
Oxidative Damages ◽  
Late Stages

The large doses of vitamins C and E and β-carotene used to reduce reactive oxygen species (ROS) production and oxidative damages in cancerous tissue have produced disappointing and contradictory results. This therapeutic conundrum was attributed to the double-faced role of ROS, notably, their ability to induce either proliferation or apoptosis of cancer cells. However, for a ROS-inhibitory approach to be effective, it must target ROS when they induce proliferation rather than apoptosis. On the basis of recent advances in redox biology, this review underlined a differential regulation of prooxidant and antioxidant system, respective to the stage of cancer. At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in prooncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Whereas in late stages of cancer progression, tumor cells escape apoptosis by producing high levels of intracellular antioxidants, like NADPH and GSH, via the pentose phosphate pathway to buffer the excessive production of ROS and related intratumor oxidative injuries. Therefore, antioxidants should be prohibited in patients with advanced stages of cancer and/or undergoing anticancer therapies. Interestingly, the biochemical and biophysical properties of some polyphenols allow them to selectively recognize tumor cells. This characteristic was exploited to design and deliver nanoparticles coated with low doses of polyphenols and containing chemotherapeutic drugs into tumor-bearing animals. First results are encouraging, which may revolutionize the conventional use of antioxidants in cancer.

Serum Calprotectin as a Blood-Based Biomarker for Monitoring Knee Osteoarthritis at Early but Not Late Stages

Cartilage ◽  
2020 ◽  
pp. 194760352096116
Author(s):  
Amin Safa ◽  
Abolfazl Bagherifard ◽  
Hamadalla Hadi Al-Baseesee ◽  
Azade Amini Kadijani ◽  
Hooman Yahyazadeh ◽  
...  
Keyword(s):  
Disease Duration ◽  
Early Stage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
Knee Oa ◽  
Calprotectin Level ◽  
Healthy Control ◽  
Grade Ii ◽  
Late Stages

Objective The identification of early-stage osteoarthritis (OA) is crucial for the deceleration of its progression; however, no reliable biomarker is available for this purpose. The current study aimed to determine the role of serum calprotectin in the detection of early-stage knee OA. Design In a case-control study, serum samples were collected from 84 patients with primary bilateral knee OA and 52 healthy controls. The radiographic grading of knee OA was performed using the Kellgren-Lawrence classification system. Serum concentrations of calprotectin were measured using an enzyme-linked immunosorbent assay. Results The mean serum calprotectin level was 2908 ± 2516 ng/mL in OA patients and 901 ± 875 ng/mL in healthy control subjects ( P < 0.001). Mean serum calprotectin levels were significantly higher in the lower stages of OA: 3740 ± 2728 ng/mL in OA grade I, 3100 ± 2084 ng/mL in OA grade II, 2246 ± 1418 ng/mL in OA grade III, and 2035 ± 765 ng/mL in OA grade IV ( P = 0.047). Serum calprotectin levels were significantly higher in patients with a disease duration <42 months compared with those with a disease duration >42 months ( P = 0.043). Conclusion Serum calprotectin level increases significantly in the early stages of OA and shows a reverse association with disease severity. Therefore, it could be suggested as a promising blood-based marker for early-stage knee OA.

scholarly journals SIRT7-mediated ATM deacetylation is essential for its deactivation and DNA damage repair

2019 ◽  
Vol 5 (3) ◽  
pp. eaav1118 ◽  
Author(s):  
Ming Tang ◽  
Zhiming Li ◽  
Chaohua Zhang ◽  
Xiaopeng Lu ◽  
Bo Tu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Class Iii ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Repair ◽  
Damage Response ◽  
Late Stages

The activation of ataxia-telangiectasia mutated (ATM) upon DNA damage involves a cascade of reactions, including acetylation by TIP60 and autophosphorylation. However, how ATM is progressively deactivated after completing DNA damage repair remains obscure. Here, we report that sirtuin 7 (SIRT7)–mediated deacetylation is essential for dephosphorylation and deactivation of ATM. We show that SIRT7, a class III histone deacetylase, interacts with and deacetylates ATM in vitro and in vivo. In response to DNA damage, SIRT7 is mobilized onto chromatin and deacetylates ATM during the late stages of DNA damage response, when ATM is being gradually deactivated. Deacetylation of ATM by SIRT7 is prerequisite for its dephosphorylation by its phosphatase WIP1. Consequently, depletion of SIRT7 or acetylation-mimic mutation of ATM induces persistent ATM phosphorylation and activation, thus leading to impaired DNA damage repair. Together, our findings reveal a previously unidentified role of SIRT7 in regulating ATM activity and DNA damage repair.

scholarly journals Alterations of Plasmin Activity, Plasminogen Levels and Activity of Anti-Plasmins During Endotoxin Shock in Dogs

1977 ◽  
Author(s):  
A. O. Aasen ◽  
M. J. Gallimore ◽  
K. Ohlsson ◽  
E. Amundsen
Keyword(s):  
Intravenous Infusion ◽  
Lethal Dose ◽  
Endotoxin Shock ◽  
Time Dependent ◽  
Plasmin Activity ◽  
Endotoxin Infusion ◽  
E Coli ◽  
Research Division ◽  
Late Stages

Endotoxin shock was induced in dogs by intravenous infusion of a lethal dose of E. coli endotoxin over a period of 3 hours. Typical changes of cardiovascular parameters were found and evidence of an intravascular clotting process was observed. Spontaneous plasmin activity and “immediate” and “time dependent” antiplasmin activities were determined by means of assays utilizing the chromogenic tripeptide derivative S-2251(Kabi Peptide Research Division, Mölndal, Sweden). Levels of plasminogen, α2-macrolobulin (α2-M) , and ai-antitrypsin(α1-AT) were determined immunochemically. During shock, gradually decreasing values of “immediate” antiplasmin and α2M were observed. During the late stages of shock “immediate” antiplasmin was found to be reduced by up to 89 per cent and α2M up to 50 per cent of pre endotoxin infusion values. A less marked lowering of “time dependent” antiplasmin and α1-AT also occurred during shock. These changes of plasma antiplasmins were accompanied by decreasing values of plasminogen and evidence of plasmin activity. These findings indicate that plasminogen is converted to plasmin during endotoxin shock and emphasize the role of antiplasmins in the pathophysiology of endotoxin shock.

An Erythroid-Specific Transcript Generates the Soluble Form of NADH-Cytochrome b5 Reductase in Humans

Blood ◽  
1998 ◽  
Vol 92 (1) ◽  
pp. 310-319 ◽  
Author(s):  
Alessandra Bulbarelli ◽  
Alessandra Valentini ◽  
Marcella DeSilvestris ◽  
M. Domenica Cappellini ◽  
Nica Borgese
Keyword(s):  
Cytochrome B5 ◽  
K562 Cells ◽  
Soluble Form ◽  
Rnase Protection ◽  
Cytochrome B5 Reductase ◽  
Erythroid Maturation ◽  
Nadh Cytochrome ◽  
Internal Initiation ◽  
Late Stages

Two forms of NADH-cytochrome b5 reductase (b5R), an erythrocyte-restricted soluble form, active in methemoglobin reduction, and a ubiquitous membrane-associated form involved in lipid metabolism, are produced from one gene. In the rat, the two forms are generated from alternative transcripts differing in the first exon, however, biogenesis of human b5R was less understood. Recently, two different transcripts (M and S), differing in the first exon were also described in humans. Here, we have investigated the tissue-specificity and the role of the S-transcript in the generation of soluble b5R. By RNase protection assays designed to simultaneously detect alternative b5R transcripts in the same sample, the S transcript was undetectable in nonerythroid and in erythroleukemic K562 cells induced to differentiate, but was present in terminal erythroblast cultures, and represented a major b5R transcript in reticulocytes. Analysis of the translation products of the M- and S-transcripts in HeLa cells transfected with the corresponding cDNAs demonstrated that the S-transcript generates soluble b5R, presumably from an internal initiation codon. Our results indicate that the S-transcript is expressed at late stages of erythroid maturation to generate soluble b5R.

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