scholarly journals Physiological Consequence of Disruption of theVMA1Gene in the Riboflavin OverproducerAshbya gossypii

1999 ◽  
Vol 274 (14) ◽  
pp. 9442-9448 ◽  
Author(s):  
Carola Förster ◽  
Maria A. Santos ◽  
Susanne Ruffert ◽  
Reinhard Krämer ◽  
José L. Revuelta
2021 ◽  
pp. 1-8
Author(s):  
Marwa Brahmi ◽  
Moufida Atigui ◽  
Ihmen Hammadi ◽  
Jacques Portanguen ◽  
Mohamed Hammadi ◽  
...  

Abstract This research paper addresses the hypothesis that oxytocin (OT) could be released during suckling and during milking with and without the presence of a calf and that this release could be regulated by maternal behaviour. Plasma concentration patterns of OT and cortisol (CORT) were measured in six Tunisian dromedary camels during 2 suckling episodes, 2 manual milking episodes with calves beside the mother and 2 machine milking episodes without calves present. Various patterns of OT release were observed between each camel including specific two peak release patterns. Higher plasma OT concentrations were found during the suckling and hand-milking episodes with simultaneous suckling of calves, than during the machine milking episodes without calves. Exclusive mechanical milking episodes also evoked significant mean OT release, although greatly reduced compared to suckling and hand milking. The low basal levels and classical CORT release patterns suggested non-stressful management practices were used and there were very limited differences in udder stimulation between managements. The OT release induced by exclusive suckling and suckling together with hand-milking gives a reference point for what a good milk ejection stimulation is in camels. The important and specific reduction of OT release during machine milking without the calf present could be a physiological consequence of the maternal behaviour (selectivity for the own young) and to a lesser extent explained by a lower stimulation by machine milking.


1970 ◽  
Vol 1 (1) ◽  
pp. 43-59 ◽  
Author(s):  
SM Raj ◽  
AR Vasavada ◽  
SR Kaid Johar ◽  
VA Vasavada ◽  
VA Vasavada

Post-operative capsular opacification (PCO) is a multifactorial physiological consequence of cataract surgery. Opacification involving the central posterior capsule has a significant impact on high and low contrast acuity and low contrast sensitivity. The assessment of PCO on cadaver eyes, experimental studies and culture models and in clinical studies has provided an understanding of its pathogenesis. The proliferation, migration and abnormal differentiation of residual lens epithelial cells and fibers in the capsular bag have been implicated in the pathogenesis of PCO. The incidence and severity of PCO correlates to the use of surgical techniques, intraocular lens (IOL) optic edge designs and IOL materials. This article summarizes the clinical studies with recommendations for retarding the development of central PCO. It discusses experiments with pharmacological agents broadly categorized as anti-inflammatory, immuno-modulating, antiproliferative, antiadhering and antitransdifferentiating agents for the prevention of PCO. These studies will remain critical for future endeavors undertaken for the eradication of PCO. Key words: posterior capsular opacification; capsular opacification; cataract; crystalline lens; phacoemulsification DOI: 10.3126/nepjoph.v1i1.3673 Nep J Oph 2009;1(1):43-59


Fire Ecology ◽  
2010 ◽  
Vol 6 (1) ◽  
pp. 80-94 ◽  
Author(s):  
Kathleen L. Kavanagh ◽  
Matthew B. Dickinson ◽  
Anthony S. Bova

2017 ◽  
Author(s):  
Alexey V. Revtovich ◽  
Ryan Lee ◽  
Natalia V. Kirienko

SummaryDiet is a crucial determinant of organismal biology. Here we demonstrate the dramatic impact of a subtle shift in diet on the ability ofCaenorhabditis elegansto survive pathogenic or abiotic stress. Interestingly, this shift occurs independently of canonical host defense pathways, arising instead from improvements in mitochondrial health. Using a variety of assays, we reveal that the most commonC. elegansfood source (E. coliOP50) results in a vitamin B12 deficiency that compromises mitochondrial homeostasis. Increasing B12 supply by feeding onE. coliHT115 or by supplementing bacterial media with methylcobalamin restored mitochondrial function, even if the bacteria were dead. B12 supplementation also efficiently increased host health without adversely affecting lifespan. Our study forges a molecular link between a dietary deficiency (nutrition/microbiota) and a physiological consequence (host sensitivity), using the host-microbiota-diet framework. The ubiquity of B12 deficiency (~10-40% of US adults) highlights the importance of our findings.


1971 ◽  
Vol 66 (4) ◽  
pp. 648-652
Author(s):  
A. K. Medda

ABSTRACT Antithyroglobulin (antigammaglobulin) isolated from thyroglobulin immunized rabbit sera inhibited the thyroxine-induced urea excretion and tail resorption in tadpoles. Albumin produced similar effects. Normal gammaglobulin fraction from rabbit sera or gammaglobulin, Fr. II, did not inhibit the action of T4 in tadpoles. The physiological consequence of thyroxine-protein binding is discussed.


1993 ◽  
Vol 39 (4-5) ◽  
pp. 537-540 ◽  
Author(s):  
Bernhard Fischer ◽  
Barry Perry ◽  
Gareth Phillips ◽  
Ian Sumner ◽  
Peter Goodenough

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Neal J. Dawson ◽  
Ryan A. V. Bell ◽  
Kenneth B. Storey

Lactate dehydrogenase (LDH; E.C. 1.1.1.27) is a crucial enzyme involved in energy metabolism in muscle, facilitating the production of ATP via glycolysis during oxygen deprivation by recycling NAD+. The present study investigated purified LDH from the muscle of 20 h anoxic and normoxic T. s. elegans, and LDH from anoxic muscle showed a significantly lower (47%) Km for L-lactate and a higher Vmax value than the normoxic form. Several lines of evidence indicated that LDH was converted to a low phosphate form under anoxia: (a) stimulation of endogenously present protein phosphatases decreased the Km of L-lactate of control LDH to anoxic levels, whereas (b) stimulation of kinases increased the Km of L-lactate of anoxic LDH to normoxic levels, and (c) dot blot analysis shows significantly less serine (78%) and threonine (58%) phosphorylation in anoxic muscle LDH as compared to normoxic LDH. The physiological consequence of anoxia-induced LDH dephosphorylation appears to be an increase in LDH activity to promote the reduction of pyruvate in muscle tissue, converting the glycolytic end product to lactate to maintain a prolonged glycolytic flux under energy-stressed anoxic conditions.


2019 ◽  
Author(s):  
Jessica Tittelmeier ◽  
Carl Alexander Sandhof ◽  
Heidrun Maja Ries ◽  
Silke Druffel-Augustin ◽  
Axel Mogk ◽  
...  

ABSTRACTThe gradual accumulation and prion-like propagation of α-synuclein and other amyloidogenic proteins is associated with devastating neurodegenerative diseases. The metazoan disaggregation machinery, a specific combination of HSP70 and its co-chaperones, is able to disassemble α-synuclein fibrils in vitro, but the physiological consequence in vivo is unknown. To explore this, we used Caenorhabditis elegans models that exhibit pathological features of α-synuclein, such as misfolding, intercellular spreading and toxicity. We inhibited the HSP70 disaggregase by depleting the crucial component HSP-110 and monitored the effect on α-synuclein related phenotypes. The knockdown of HSP-110 not only impaired HSP70 disaggregation activity and prevented the resolubilization of amorphous heat shock induced firefly luciferase aggregates, but also compromised the cellular folding capacity. In stark contrast, HSP-110 depletion reduced α-synuclein foci formation, cell-to-cell transmission and toxicity. Similar effects were observed for a polyQ model substrate, confirming that inhibition of HSP70 disaggregation function mitigates amyloid toxicity. These data demonstrate that the metazoan HSP70 disaggregation complex plays a critical role in the prion-like propagation of amyloid-type conformers. Therefore, the HSP70 disaggregation activity is a double-edged sword as it is essential for the maintenance of cellular proteostasis while being involved in the generation of toxic amyloid-type protein species.


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