Articoli di riviste: "Reticular stress"

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Anyanwu, GE, e CA Agbor. "Correlation Between Oxidative Stress Generation, Reticular Fiber Density and Testicular Histomorphometric Parameters Of Streptozotocin-Induced Diabetic Wistar Rat". Journal of Bio-Science 29, n. 2 (4 agosto 2021): 1–8. http://dx.doi.org/10.3329/jbs.v29i2.54949.

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The actual underlying mechanism of alterations in testicular histomorphometric parameters resulting from diabetes-induced oxidative stress is still not well understood because of the absence of supporting evidence from scientific experiments. This study was conducted to investigate the correlation between serum oxidative stress markers with testicular histomorphometric parameters and reticular fiber density of Streptozotocin-induced diabetic Wistar rat. The experiment included twenty eight adult male rats sorted into four groups, Group A (Control), other animals were sorted into treatment groups based on their blood glucose levels after inducing diabetes with 65 mg/kg/bw of streptozotocin, Groups B (100 - 200 mmol/l), Group C (210 - 250 mmol/l), Group D (260 - 300 mmol/l). At termination, Serum superoxide dimutase (SOD), catalase and melondialdehyde where evaluated using reagent based antioxidant enzyme assay while reticulum stain kits was used to demonstrate for reticular fiber density. Histomorphometric measurements were carried out using ocular micrometer after calibration on a light microscope. Statistical analysis was done using analysis of variance with p<0.05 considered significant. Results reveal that the higher the blood glucose levels in diabetic animals, the higher the serum concentration of oxidative stress markers. Density of reticular fiber increased with increase in blood glucose levels, while tubular diameter and epithelial height decreased with increase in increase in hyperglycaemic levels. In conclusion, there was a progressive increase in reticular fiber density and decrease in tubular diameter and epithelial height as a consequence of increase oxidative stress generation in diabetic model. J. Bio-Sci. 29(2): 01-08, 2021 (December)

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Groenendyk, Jody, Xiao Fan, Zhenling Peng, Lukasz Kurgan e Marek Michalak. "Endoplasmic reticulum and the microRNA environment in the cardiovascular system". Canadian Journal of Physiology and Pharmacology 97, n. 6 (giugno 2019): 515–27. http://dx.doi.org/10.1139/cjpp-2018-0720.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in the biology of the cardiac myocyte, and are involved in pathological cardiac function and remodeling. In this paper, we review a link between endoplasmic reticulum homeostasis and microRNA with an emphasis on the impact on stress responses in the cardiovascular system.

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Carew, Nolan, Ashley Nelson, Zhitao Liang, Sage Smith e Christine Milcarek. "Linking Endoplasmic Reticular Stress and Alternative Splicing". International Journal of Molecular Sciences 19, n. 12 (7 dicembre 2018): 3919. http://dx.doi.org/10.3390/ijms19123919.

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RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 (eleven-nineteen lysine-rich leukemia gene 2) induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response comprising a highly conserved set of genes crucial for cell survival; among these is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 mRNA and yet degrades other cellular mRNAs with related motifs. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2, a transcription elongation factor. ELL2 is necessary for immunoglobulin secretion and does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes.

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Kim, Min Hwan, Yeon Hee Kim, Woobong Choi e Jong-Hwan Lee. "Alteration of Stress Fiber in Fibroblastic Reticular Cells via Lymphotoxin β Receptor Stimulation is Associated with Myosin". Journal of Life Science 25, n. 5 (30 maggio 2015): 585–93. http://dx.doi.org/10.5352/jls.2015.25.5.585.

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Milcarek, Christine. "Linking Endoplasmic Reticular Stress, ELL2, and Alternative Splicing". Journal of Immunology 202, n. 1_Supplement (1 maggio 2019): 123.9. http://dx.doi.org/10.4049/jimmunol.202.supp.123.9.

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Abstract RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 transcription elongation factor induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response; among these stress proteins is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 and yet degrades other cellular mRNAs with related motifs, in a cell-specific manner. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2 which is necessary for immunoglobulin secretion; it does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes. unexpectedly, ubiquitination of c-myc by the ELL family members also plays a role in plasma-blast survival.

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Griendling, Kathy K., Livia L. Camargo, Francisco J. Rios, Rhéure Alves-Lopes, Augusto C. Montezano e Rhian M. Touyz. "Oxidative Stress and Hypertension". Circulation Research 128, n. 7 (2 aprile 2021): 993–1020. http://dx.doi.org/10.1161/circresaha.121.318063.

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A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.

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Aghili-Mehrizi, Sina, Eric Williams, Sandra Yan, Matthew Willman, Jonathan Willman e Brandon Lucke-Wold. "Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence". Diseases 10, n. 2 (23 maggio 2022): 30. http://dx.doi.org/10.3390/diseases10020030.

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Traumatic central nervous system injury is a leading cause of neurological injury worldwide. While initial neuroresuscitative efforts are focused on ameliorating the effects of primary injury through patient stabilization, secondary injury in neurotrauma is a potential cause of cell death, oxidative stress, and neuroinflammation. These secondary injuries lack defined therapy. The major causes of secondary injury in neurotrauma include endoplasmic reticular stress, mitochondrial dysfunction, and the buildup of reactive oxygen or nitrogenous species. Stress to the endoplasmic reticulum in neurotrauma results in the overactivation of the unfolded protein response with subsequent cell apoptosis. Mitochondrial dysfunction can lead to the release of caspases and the buildup of reactive oxygen species; several characteristics make the central nervous system particularly susceptible to oxidative damage. Together, endoplasmic reticulum, mitochondrial, and oxidative stress can have detrimental consequences, beginning moments and lasting days to months after the primary injury. Understanding these causative pathways has led to the proposal of various potential treatment options.

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Pecoraro, Michela, Adele Serra, Maria Pascale e Silvia Franceschelli. "Vx-809, a CFTR Corrector, Acts through a General Mechanism of Protein Folding and on the Inflammatory Process". International Journal of Molecular Sciences 24, n. 4 (20 febbraio 2023): 4252. http://dx.doi.org/10.3390/ijms24044252.

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Correct protein folding is the basis of cellular well-being; thus, accumulation of misfolded proteins within the endoplasmic reticulum (ER) leads to an imbalance of homeostasis that causes stress to the ER. Various studies have shown that protein misfolding is a significant factor in the etiology of many human diseases, including cancer, diabetes, and cystic fibrosis. Misfolded protein accumulation in the ER triggers a sophisticated signal transduction pathway, the unfolded protein response (UPR), which is controlled by three proteins, resident in ER: IRE1α, PERK, and ATF6. Briefly, when ER stress is irreversible, IRE1α induces the activation of pro-inflammatory proteins; PERK phosphorylates eIF2α which induces ATF4 transcription, while ATF6 activates genes encoding ER chaperones. Reticular stress causes an alteration of the calcium homeostasis, which is released from the ER and taken up by the mitochondria, leading to an increase in the oxygen radical species production, and consequently, to oxidative stress. Accumulation of intracellular calcium, in combination with lethal ROS levels, has been associated with an increase of pro-inflammatory protein expression and the initiation of the inflammatory process. Lumacaftor (Vx-809) is a common corrector used in cystic fibrosis treatment which enhances the folding of mutated F508del-CFTR, one of the most prevalent impaired proteins underlying the disease, promoting a higher localization of the mutant protein on the cell membrane. Here, we demonstrate that this drug reduces the ER stress and, consequently, the inflammation that is caused by such events. Thus, this molecule is a promising drug to treat several pathologies that present an etiopathogenesis due to the accumulation of protein aggregates that lead to chronic reticular stress.

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Pogrebnyak, Tatyana, Elena Khorolskaya, Anzhelika Gorbacheva e Irina Sagalaeva. "The dynamics of EEG correlates of activity of subcortical structures of the bird brain in conditions of chronic stress". BIO Web of Conferences 40 (2021): 01012. http://dx.doi.org/10.1051/bioconf/20214001012.

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In birds, acute stress (a three-day 12-hour inversion of the photomode) is associated with the dominant activity of the sympathetic hypothalamus and hippocampus, which suppress the tone of the parasympathetic section and the reticular formation of the midbrain. The effect of hyperglycemia on the background of a negative chronotropic effect indicates a mismatch of the functions of the autonomic sections of the hypothalamus on the 30th day. Chronic stress in birds (30-days crowding) causes persistent pathological stress of the functions of the anterior hypothalamus and reticular formation of the middle brain with the suppression of parasympathetic tone of the posterior hypothalamus and high functional activity of the hippocampus, determining the switching of the ventricles of the heart to a more economical mode of functioning by the 30th day. Using central cholinoblockers or tranquilizers, having a cholinoblocking component in the mechanism of its influence during neurogenic stress and in the post-stress period is excluded, but it is possible to use stressprotektors.

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Jafarova, A. M., A. M. Mammadov, A. G. Gaziyev e Sh R. Eyvazova. "Functional relationships of the cerebral cortex with subcortical structures in emotionally stressful conditions". Azerbaijan Journal of Physiology 38, n. 2 (31 dicembre 2023): 26–31. http://dx.doi.org/10.59883/ajp.7.

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Multidirectional and stable changes in phase shifts and cross-correlation coefficients of the cortical and subcortical stress rhythms occur under conditions of repeated irregular photostimulation, especially in the initial periods. Thus, cross-correlation functional connections, characterized by changes in the spatio-temporal relationships of the brain structures (posterior nuclei of the hypothalamus, reticular formation, and visual projection zones of the cerebral cortex), can be one of the indicators of the formation of stress. By using the parameters mentioned above, we can solve many issues related to the central mechanisms of stress. Our results show that functional connections between the cortical projection area and subcortical structures decrease under stress conditions, while connections between subcortical structures increase. We furthermore found that these EEG changes correlated with autonomic reactions in animals. Thus, these changes may lie based on central mechanisms of stress, and the results of changes in the EEG activity of the cerebral cortex and the cross-correlation parameters in the posterior nuclei of the hypothalamus and the reticular formation may allow preventive measures to be taken to affect these structures to reduce emotional stress.

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Chen, Yu-Chen, Guang-Di Chen, Benjamin D. Auerbach, Senthilvelan Manohar, Kelly Radziwon e Richard Salvi. "Tinnitus and hyperacusis: Contributions of paraflocculus, reticular formation and stress". Hearing Research 349 (giugno 2017): 208–22. http://dx.doi.org/10.1016/j.heares.2017.03.005.

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Gundamaraju, Rohit, Ravichandra Vemuri, Wai Chin Chong, Stephen Myers, Shaghayegh Norouzi, Madhur D. Shastri e Rajaraman Eri. "Interplay between Endoplasmic Reticular Stress and Survivin in Colonic Epithelial Cells". Cells 7, n. 10 (15 ottobre 2018): 171. http://dx.doi.org/10.3390/cells7100171.

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Sustained endoplasmic reticular stress (ERS) is implicated in aggressive metastasis of cancer cells and increased tumor cell proliferation. Cancer cells activate the unfolded protein response (UPR), which aids in cellular survival and adaptation to harsh conditions. Inhibition of apoptosis, in contrast, is a mechanism adopted by cancer cells with the help of the inhibitor of an apoptosis (IAP) class of proteins such as Survivin to evade cell death and gain a proliferative advantage. In this study, we aimed to reveal the interrelation between ERS and Survivin. We initially verified the expression of Survivin in Winnie (a mouse model of chronic ERS) colon tissues by using immunohistochemistry (IHC) and immunofluorescence (IF) in comparison with wild type Blk6 mice. Additionally, we isolated the goblet cells and determined the expression of Survivin by IF and protein validation. Tunicamycin was utilized at a concentration of 10 µg/mL to induce ERS in the LS174T cell line and the gene expression of the ERS markers was measured. This was followed by determination of inflammatory cytokines. Inhibition of ERS was carried out by 4Phenyl Butyric acid (4PBA) at a concentration of 10 mM to assess whether there was a reciprocation effect. The downstream cell death assays including caspase 3/7, Annexin V, and poly(ADP-ribose) polymerase (PARP) cleavage were evaluated in the presence of ERS and absence of ERS, which was followed by a proliferative assay (EdU click) with and without ERS. Correspondingly, we inhibited Survivin by YM155 at a concentration of 100 nM and observed the succeeding ERS markers and inflammatory markers. We also verified the caspase 3/7 assay. Our results demonstrate that ERS inhibition not only significantly reduced the UPR genes (Grp78, ATF6, PERKandXBP1) along with Survivin but also downregulated the inflammatory markers such as IL8, IL4, and IL6, which suggests a positive correlation between ERS and the inhibition of apoptosis. Furthermore, we provided evidence that ERS inhibition promoted apoptosis in LS174T cells and shortened the proliferation rate. Moreover, Survivin inhibition by YM155 led to a comparable effect as that of ERS inhibition, which includes attenuation of ERS genes and inflammatory markers as well as the promotion of programmed cell death via the caspase 3/7 pathway. Together, our results propose the interrelation between ERS and inhibition of apoptosis assigning a molecular and therapeutic target for cancer treatment.

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Obut, T. A. "Effect of stress on the reticular zone of the adrenal cortex". Bulletin of Experimental Biology and Medicine 118, n. 1 (luglio 1994): 685–88. http://dx.doi.org/10.1007/bf02444356.

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Belova, T. I. "Structural damage to the mesencephalic reticular formation induced by immobilization stress". Bulletin of Experimental Biology and Medicine 108, n. 1 (luglio 1989): 1026–30. http://dx.doi.org/10.1007/bf00839803.

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Ghosh, Pratiti, Abhishek Jana e Jincy Thomas. "Erosive oral lichen planus inflicts higher cellular stress than reticular type". Journal of Oral and Maxillofacial Pathology 25, n. 2 (2021): 279. http://dx.doi.org/10.4103/0973-029x.325127.

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Sachdev, Rohan, Kriti Garg e Sekhar Mukherjee. "Reticular Lichen planus in young female: Rare case study". Current Dental Research Journal 1, Issue 1 (3 agosto 2019): 22–25. http://dx.doi.org/10.12944/cdrj.01.o1.04.

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Lichen planus is a chronic autoimmune disorder of mucosa and skin, mainly females in their forty to sixty years and rare in young age group. Etiology is still unknown; certain triggering factors include mental stress, medicines and systemic disorders. Oral Lichen planus is a painful disorder; mainly involve the buccal mucosa of the oral cavity. The reticular pattern is most common while atrophic and erosive type of oral lichen planus are less common. Here we present a rare case of a reticular lichen planus involving the right buccal mucosa and tongue of 18 years old female patient without any cutaneous lesions.

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Fu, Ge Yan, e Shi Hong Shi. "A Mechanics Analysis of Formation and Expansion of Fatigue Crack in Laser Cladding on Repeated Impact Load". Key Engineering Materials 392-394 (ottobre 2008): 109–15. http://dx.doi.org/10.4028/www.scientific.net/kem.392-394.109.

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Coating samples prepared by laser cladding were subjected to repeated impact fatigue experiment. It is observed through phenomenological analysis that most coating cracks are original from the surface. And then, the cracks extend by the combined action of coating inner stress and repeated impact compression stress. The formation of crack is close related to performance of coating material. It can be divided to traversed crack and reticular crack from surface side; it also can be divided to vertical extend crack and reticular extend crack from the cross section side. Rigid and brickle coating has a shorter repeated impact life because a kind of linear crack is formed easily in it. On the other hand, tougher coating has a long life. Mechanics of nucleation and expansion of crack was explained by using stress concentration theory and vacancy concentration theory. The anti-repeated impact fatigue performance of laser cladding part could be improved by increasing toughness and reducing hardness of the coating material. Furthermore, suitable dispersion strengthening and fine-crystal strengthening can obtain the same purpose.

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Skrinjar, Ivana, Valentina Vidranski, Bozana Loncar Brzak, Danica Vidovic Juras, Ana Andabak Rogulj, Vlaho Brailo e Vanja Vucicevic Boras. "Salivary Cortisol Levels in Patients with Oral Lichen Planus—A Pilot Case-Control Study". Dentistry Journal 7, n. 2 (1 giugno 2019): 59. http://dx.doi.org/10.3390/dj7020059.

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It is known that cortisol level increases in stress situations. The aim of the study was to measure the levels of salivary cortisol in patients with oral lichen planus (OLP) and healthy controls. This was a case-control pilot study which included seven patients with reticular (non-symptomatic) OLP, eight patients with atrophic/erosive (symptomatic) OLP, and nine healthy controls. We hypothesized that patients with an atrophic/erosive type of OLP have higher levels of cortisol compared to patients with the reticular type of OLP and healthy controls. In each participant, unstimulated saliva was collected in order to determine cortisol levels by using commercially available ELISA kit. Our results have shown no differences between levels of salivary cortisol in OLP patients and healthy controls. We can conclude that further research with a larger number of OLP patients is needed to determine the correlation between OLP and stress.

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Ten Cate, Wouter J. F., e Kyle E. Rarey. "Planum Semilunatum of the Rat: New Light and Electron Microscopy Observations". Annals of Otology, Rhinology & Laryngology 101, n. 7 (luglio 1992): 601–6. http://dx.doi.org/10.1177/000348949210100711.

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Planum semilunatum (PSL) cells of the rat ampullae were studied by light, transmission, and scanning electron microscopy. The observed ultrastructure of rat PSL cells was similar to that described in other species, but is in disagreement with earlier reports of rat PSL cells, most probably because of previous divergent definitions of the PSL. Regions of PSL cells were easily distinguished from other nonsensory epithelia at the lateral ends of the crista ampullaris. The PSL region consisted of irregular-shaped columnar to cuboidal pentagonal or hexagonal cells that interdigitated with one another by lateral membrane infoldings. In the PSL region the subepithelial reticular layer appeared thickened and formed wartlike impressions in the basal surface of the PSL cells. These morphological characteristics of the subepithelial reticular layer were unique to the PSL region in the ampulla and may reflect special adaptations of the PSL region to mechanical stress. Furthermore, the thick subepithelial reticular layer may have implications for transport across the PSL region.

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YANG, Yuan-yuan, Jin SHANG e Hui-guo LIU. "Role of endoplasmic reticular stress in aortic endothelial apoptosis induced by intermittent/persistent hypoxia". Chinese Medical Journal 126, n. 23 (5 dicembre 2013): 4517–23. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20130602.

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Background Accumulated evidence shows that hypoxia can induce endothelial apoptosis, however the mechanism is still unknown. We hypothesized whether intermittent or persistent hypoxia could induce endoplasmic reticular stress, leading to endothelial apoptosis. Methods Twenty-four 8-week male Sprague Dawley (SD) rats were divided into three groups: normoxia (NC) group, intermittent hypoxia (IH) group and persistent hypoxia (PH) group. TUNEL staining was performed to detect aortic arch endotheliar apoptosis, and immunohistochemistry for BIP, CHOP and caspase12 to test protein expression; human umbilical vein endothelial cells (HUVECs) of the line ECV304 were cultured (with or without taurodeoxycholic acid (TUDCA) 10 mmol/L, 100 mmol/L) and divided into four groups: NC group (20.8% O2 for 4 hours), PH1 group (5% O2 for 4 hours), PH2 group (5% O2 for 12 hours) and IH group (20.8% O2 and 5% O2 alternatively for 8 hours). Annexin V-fluorescein-isothiocyanate/propidium iodide flow cytometry was used to assess apoptosis in each group. The expressions of GRP78, CHOP and caspase12 were detected by real-time quantitative reverse-transcription PCR. Result Intermittent and persistent hypoxia could increase the rate of endothelium apoptosis and the expressions of GRP78, CHOP and caspase12 compared with the control, induction by intermittent hypoxia was slightly higher than persistent hypoxia. In the HUVEC experiment, TUDCA significantly reduced apoptosis and the expressions of GRP78, CHOP and caspase12. Conclusion Hypoxia, especially intermittent, can induce endothelial cell apoptosis possibly through endoplasmic reticulum stress pathway, which can be attenuated by taurodeoxycholic acid.

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Suk, Fat-Moon, Gi-Shih Lien, Wei-Jan Huang, Chia-Nan Chen, Shao-Yu Lu, Ying-Chen Yang, Ming-De Yan e Yu-Chih Liang. "A Taiwanese Propolis Derivative Induces Apoptosis through Inducing Endoplasmic Reticular Stress and Activating Transcription Factor-3 in Human Hepatoma Cells". Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/658370.

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Activating transcription factor-(ATF-) 3, a stress-inducible transcription factor, is rapidly upregulated under various stress conditions and plays an important role in inducing cancer cell apoptosis. NBM-TP-007-GS-002 (GS-002) is a Taiwanese propolin G (PPG) derivative. In this study, we examined the antitumor effects of GS-002 in human hepatoma Hep3B and HepG2 cellsin vitro. First, we found that GS-002 significantly inhibited cell proliferation and induced cell apoptosis in dose-dependent manners. Several main apoptotic indicators were found in GS-002-treated cells, such as the cleaved forms of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP). GS-002 also induced endoplasmic reticular (ER) stress as evidenced by increases in ER stress-responsive proteins including glucose-regulated protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153), phosphorylated eukaryotic initiation factor 2α(eIF2α), phosphorylated protein endoplasmic-reticular-resident kinase (PERK), and ATF-3. The induction of ATF-3 expression was mediated by mitogen-activated protein kinase (MAPK) signaling pathways in GS-002-treated cells. Furthermore, we found that GS-002 induced more cell apoptosis in ATF-3-overexpressing cells. These results suggest that the induction of apoptosis by the propolis derivative, GS-002, is partially mediated through ER stress and ATF-3-dependent pathways, and GS-002 has the potential for development as an antitumor drug.

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Ammer, S., C. Lambertz e M. Gauly. "Is reticular temperature a useful indicator of heat stress in dairy cattle?" Journal of Dairy Science 99, n. 12 (dicembre 2016): 10067–76. http://dx.doi.org/10.3168/jds.2016-11282.

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Tseng, Sung-Hui, Ting-Yun Chang, Chun-Kuang Shih, Rong-Hong Hsieh, Chia-Wen Chen, Yi-Chun Chen, Mei-Hsiang Lin e Jung-Su Chang. "Effect of Endoplasmic Reticular Stress on Free Hemoglobin Metabolism and Liver Injury". International Journal of Molecular Sciences 19, n. 7 (6 luglio 2018): 1977. http://dx.doi.org/10.3390/ijms19071977.

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Muskat, J. C., V. L. Rayz, C. J. Goergen e C. F. Babbs. "Hemodynamic modeling of the circle of Willis reveals unanticipated functions during cardiovascular stress". Journal of Applied Physiology 131, n. 3 (1 settembre 2021): 1020–34. http://dx.doi.org/10.1152/japplphysiol.00198.2021.

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Hemodynamic modeling reveals potential evolutionary benefits of the intact circle of Willis (CW) during fear and aerobic exercise. The CW equalizes pulse waveforms due to bidirectional shunting of blood flow through communicating arteries, which boosts vertebrobasilar blood flow velocity and acceleration. These phenomena may enhance perfusion of the brainstem and cerebellum via nitric oxide-mediated vasodilation, improving performance of the reticular-activating system and motor coordination in survival situations.

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Delcroix, Vanessa, Olivier Mauduit, Nolwenn Tessier, Anaïs Montillaud, Tom Lesluyes, Thomas Ducret, Frédéric Chibon, Fabien Van Coppenolle, Sylvie Ducreux e Pierre Vacher. "The Role of the Anti-Aging Protein Klotho in IGF-1 Signaling and Reticular Calcium Leak: Impact on the Chemosensitivity of Dedifferentiated Liposarcomas". Cancers 10, n. 11 (14 novembre 2018): 439. http://dx.doi.org/10.3390/cancers10110439.

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By inhibiting Insulin-Like Growth Factor-1-Receptor (IGF-1R) signaling, Klotho (KL) acts like an aging- and tumor-suppressor. We investigated whether KL impacts the aggressiveness of liposarcomas, in which IGF-1R signaling is frequently upregulated. Indeed, we observed that a higher KL expression in liposarcomas is associated with a better outcome for patients. Moreover, KL is downregulated in dedifferentiated liposarcomas (DDLPS) compared to well-differentiated tumors and adipose tissue. Because DDLPS are high-grade tumors associated with poor prognosis, we examined the potential of KL as a tool for overcoming therapy resistance. First, we confirmed the attenuation of IGF-1-induced calcium (Ca2+)-response and Extracellular signal-Regulated Kinase 1/2 (ERK1/2) phosphorylation in KL-overexpressing human DDLPS cells. KL overexpression also reduced cell proliferation, clonogenicity, and increased apoptosis induced by gemcitabine, thapsigargin, and ABT-737, all of which are counteracted by IGF-1R-dependent signaling and activate Ca2+-dependent endoplasmic reticulum (ER) stress. Then, we monitored cell death and cytosolic Ca2+-responses and demonstrated that KL increases the reticular Ca2+-leakage by maintaining TRPC6 at the ER and opening the translocon. Only the latter is necessary for sensitizing DDLPS cells to reticular stressors. This was associated with ERK1/2 inhibition and could be mimicked with IGF-1R or MEK inhibitors. These observations provide a new therapeutic strategy in the management of DDLPS.

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KATO, Shiro, Seishi YAMADA, Hideyuki TAKASHIMA e Ryoichi SHIBATA. "STUDY ON THE BUCKLING STRESS OF A RIGIDLY JOINTED SINGLE-LAYER RETICULAR DOME". Journal of Structural and Construction Engineering (Transactions of AIJ) 428 (1991): 97–105. http://dx.doi.org/10.3130/aijsx.428.0_97.

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Kumano, Masafumi, Junya Furukawa, Masaki Shiota, Anousheh Zardan, Fan Zhang, Eliana Beraldi, Romina M. Wiedmann, Ladan Fazli, Amina Zoubeidi e Martin E. Gleave. "Cotargeting Stress-Activated Hsp27 and Autophagy as a Combinatorial Strategy to Amplify Endoplasmic Reticular Stress in Prostate Cancer". Molecular Cancer Therapeutics 11, n. 8 (6 giugno 2012): 1661–71. http://dx.doi.org/10.1158/1535-7163.mct-12-0072.

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Marker, Ryan J., Serge Campeau e Katrina S. Maluf. "Psychosocial stress alters the strength of reticulospinal input to the human upper trapezius". Journal of Neurophysiology 117, n. 1 (1 gennaio 2017): 457–66. http://dx.doi.org/10.1152/jn.00448.2016.

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Psychosocial stress has been shown to influence several aspects of human motor control associated with the fight-or-flight response, including augmentation of upper trapezius muscle activity. Given the established role of the reticular formation in arousal, this study investigated the contribution of reticulospinal activation to trapezius muscle activity during exposure to an acute psychosocial stressor. Twenty-five healthy adults were exposed to startling acoustic stimuli (SAS) while performing a motor task during periods of low and high psychosocial stress. Acoustic startle reflexes (ASRs) were recorded in the upper trapezius during low intensity contractions using both surface and intramuscular electromyography. Exposure to the stressor increased subjective and physiological measures of arousal ( P < 0.01). The majority of participants demonstrated inhibitory ASRs, whereas a small subgroup with significantly higher trait anxiety ( n = 5) demonstrated excitatory ASRs in the low stress condition. Changes in synaptic input for inhibitory ASRs were confirmed by decreases in the discharge rate of single motor units in response to the SAS. ASRs decreased in magnitude for all participants during exposure to the acute psychosocial stressor. These findings suggest that the reticular formation has predominately inhibitory effects on the human upper trapezius during an ongoing motor task and that disinhibition caused by psychosocial stress may contribute to augmentation of trapezius muscle activity. Further research is required to investigate mechanisms underlying the complex ASRs characterized by this study, particularly the phase reversal to excitatory responses observed among more anxious individuals. NEW & NOTEWORTHY This study is the first to quantify stress-evoked changes in the acoustic startle reflex in the upper trapezius muscle of humans, and our findings reveal a complex pattern of inhibitory and facilitatory responses consistent with observations in nonhuman primates. We further demonstrate that psychosocial stress consistently reduces the amplitude of these responses. These findings have implications for the control of motor behaviors in response to stress.

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Gundamaraju, Rohit, Ravichandra Vemuri, Wai Chin Chong, Dominic P. Geraghty e Rajaraman Eri. "Cell Stress Signaling Cascades Regulating Cell Fate". Current Pharmaceutical Design 24, n. 27 (3 dicembre 2018): 3176–83. http://dx.doi.org/10.2174/1381612824666180711122753.

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Initiating anti-apoptotic signaling or triggering cell death depends to a great extent on the nature or source of cellular stress and cell type. Interplay between each stress response eventually determines the fate of stressed cell. Numerous factors induce cell death by a number of pathways including apoptosis, autophagy and necrosis. Not surprisingly, some of the pathways are interrelated to each other through a mediator that could articulate the entire mechanism. The present review attempts to consolidate all the pathways included in intrinsic cellular stress such as oxidative stress and autophagy, endoplasmic reticular stress (ERS) and mitophagy and apoptosis as fate in cell stress. These stress responses are a hallmark of numerous diseases including neurodegenerative diseases, diabetes and cancer. Understanding the cross-talk between different intrinsic cell stress responses will help to develop new therapeutic targets and hence lead to the development of new therapeutics.

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Berger, Marie, Delphine Daubin, Jeremy Charriot, Kada Klouche, Vincent Le Le Moing, David Morquin, Laurence Halimi et al. "Mid-Term Sequelae of Surviving Patients Hospitalized in Intensive Care Unit for COVID-19 Infection: The REHCOVER Study". Journal of Clinical Medicine 12, n. 3 (28 gennaio 2023): 1000. http://dx.doi.org/10.3390/jcm12031000.

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Objectives: The objective of this prospective, single-center study was to explore the mid-term outcomes 6 to 9 months after hospitalization in an Intensive Care Unit (ICU) for severe COVID-19 infection. Methods: Patients systematically underwent biological tests, pulmonary function tests, chest computed tomography (CT) scan, and psychological tests. Results: Among 86 patients, including 71 (82.6%) men, median age of 65.8 years (56.7; 72.4), 57 (71.3%) patients presented post-COVID-19 asthenia, 39 (48.1%) muscle weakness, and 30 (36.6%) arthralgia. Fifty-two (64.2%) patients had a decreased diffusion capacity for carbon monoxide (DLCO) < 80% and 16 (19.8%) had DLCO < 60%. Chest CT-scans showed ground glass opacities in 35 (40.7%) patients, and reticular changes in 28 patients (33.7%), including fibrosis-like changes in 18 (21.7%) patients. Reticular changes and DLCO < 60% were associated with length of stay in ICU, and reticular changes with higher maximal CRP level. The psychological questionnaires found 37.7% suffered from depression, 23.5% from anxiety, 42.4% from insomnia, and 9.4% from post-traumatic stress. Being female was associated with a higher frequency of depression and anxiety, with depression scores being associated with obesity. Conclusions: Many patients hospitalized in ICU for severe COVID-19 infection have mid-term sequelae. Additional studies on the prognostic factors seem necessary.

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Rissone, Alberto, Katja Gabriele Weinacht, Giancarlo la Marca, Kevin Bishop, Elisa Giocaliere, Jayashree Jagadeesh, Kerstin Felgentreff et al. "Reticular dysgenesis–associated AK2 protects hematopoietic stem and progenitor cell development from oxidative stress". Journal of Cell Biology 210, n. 2 (20 luglio 2015): 2102OIA141. http://dx.doi.org/10.1083/jcb.2102oia141.

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Rissone, Alberto, Katja Gabriele Weinacht, Giancarlo la Marca, Kevin Bishop, Elisa Giocaliere, Jayashree Jagadeesh, Kerstin Felgentreff et al. "Reticular dysgenesis–associated AK2 protects hematopoietic stem and progenitor cell development from oxidative stress". Journal of Experimental Medicine 212, n. 8 (6 luglio 2015): 1185–202. http://dx.doi.org/10.1084/jem.20141286.

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Adenylate kinases (AKs) are phosphotransferases that regulate the cellular adenine nucleotide composition and play a critical role in the energy homeostasis of all tissues. The AK2 isoenzyme is expressed in the mitochondrial intermembrane space and is mutated in reticular dysgenesis (RD), a rare form of severe combined immunodeficiency (SCID) in humans. RD is characterized by a maturation arrest in the myeloid and lymphoid lineages, leading to early onset, recurrent, and overwhelming infections. To gain insight into the pathophysiology of RD, we studied the effects of AK2 deficiency using the zebrafish model and induced pluripotent stem cells (iPSCs) derived from fibroblasts of an RD patient. In zebrafish, Ak2 deficiency affected hematopoietic stem and progenitor cell (HSPC) development with increased oxidative stress and apoptosis. AK2-deficient iPSCs recapitulated the characteristic myeloid maturation arrest at the promyelocyte stage and demonstrated an increased AMP/ADP ratio, indicative of an energy-depleted adenine nucleotide profile. Antioxidant treatment rescued the hematopoietic phenotypes in vivo in ak2 mutant zebrafish and restored differentiation of AK2-deficient iPSCs into mature granulocytes. Our results link hematopoietic cell fate in AK2 deficiency to cellular energy depletion and increased oxidative stress. This points to the potential use of antioxidants as a supportive therapeutic modality for patients with RD.

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Carew, J. S., C. M. Espitia, K. R. Kelly, M. Coffey, J. W. Freeman e S. T. Nawrocki. "537 Reovirus Therapy Induces Endoplasmic Reticular Stress and Apoptosis in RAS-activated Pancreatic Cancer". European Journal of Cancer 48 (novembre 2012): 165. http://dx.doi.org/10.1016/s0959-8049(12)72334-1.

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Ivanova, T. M., e T. I. Belova. "Effect of emotional stress on lactate dehydrogenase isozyme spectrum in the rat reticular formation". Bulletin of Experimental Biology and Medicine 102, n. 4 (ottobre 1986): 1331–34. http://dx.doi.org/10.1007/bf00851037.

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Chuang, Mao-Te, Feng-Ming Ho, Chien-Chih Wu, Shao-Yu Zhuang, Shyr-Yi Lin, Fat-Moon Suk e Yu-Chih Liang. "15,16-Dihydrotanshinone I, a Compound ofSalvia miltiorrhizaBunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma Cells". Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/865435.

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5,16-dihydrotanshinone I (DHTS) is extracted fromSalvia miltiorrhizaBunge (tanshen root) and was found to be the most effective compound of tanshen extracts against breast cancer cells in our previous studies. However, whether DHTS can induce apoptosis through an endoplasmic reticular (ER) stress pathway was examined herein. In this study, we found that DHTS significantly inhibited the proliferation of human prostate DU145 carcinoma cells and induced apoptosis. DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 (GRP78/Bip) and CAAT/enhancer binding protein homologous protein/growth arrest- and DNA damage-inducible gene 153 (CHOP/GADD153), as well as increases in phosphorylated eukaryotic initiation factor 2α (eIF2α), c-jun N-terminal kinase (JNK), and X-box-binding protein 1 (XBP1) mRNA splicing forms. DHTS treatment also caused significant accumulation of polyubiquitinated proteins and hypoxia-inducible factor (HIF)-1α, indicating that DHTS might be a proteasome inhibitor that is known to induce ER stress or enhance apoptosis caused by the classic ER stress-dependent mechanism. Moreover, DHTS-induced apoptosis was reversed by salubrinal, an ER stress inhibitor. Results suggest that DHTS can induce apoptosis of prostate carcinoma cells via induction of ER stress and/or inhibition of proteasome activity, and may have therapeutic potential for prostate cancer patients.

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Huttner, Inken G., Celine F. Santiago, Arie Jacoby, Delfine Cheng, Gunjan Trivedi, Stephen Cull, Jasmina Cvetkovska et al. "Loss of Sec-1 Family Domain-Containing 1 (scfd1) Causes Severe Cardiac Defects and Endoplasmic Reticulum Stress in Zebrafish". Journal of Cardiovascular Development and Disease 10, n. 10 (22 settembre 2023): 408. http://dx.doi.org/10.3390/jcdd10100408.

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Dilated cardiomyopathy (DCM) is a common heart muscle disorder that frequently leads to heart failure, arrhythmias, and death. While DCM is often heritable, disease-causing mutations are identified in only ~30% of cases. In a forward genetic mutagenesis screen, we identified a novel zebrafish mutant, heart and head (hahvcc43), characterized by early-onset cardiomyopathy and craniofacial defects. Linkage analysis and next-generation sequencing identified a nonsense variant in the highly conserved scfd1 gene, also known as sly1, that encodes sec1 family domain-containing 1. Sec1/Munc18 proteins, such as Scfd1, are involved in membrane fusion regulating endoplasmic reticulum (ER)/Golgi transport. CRISPR/Cas9-engineered scfd1vcc44 null mutants showed severe cardiac and craniofacial defects and embryonic lethality that recapitulated the phenotype of hahvcc43 mutants. Electron micrographs of scfd1-depleted cardiomyocytes showed reduced myofibril width and sarcomere density, as well as reticular network disorganization and fragmentation of Golgi stacks. Furthermore, quantitative PCR analysis showed upregulation of ER stress response and apoptosis markers. Both heterozygous hahvcc43 mutants and scfd1vcc44 mutants survived to adulthood, showing chamber dilation and reduced ventricular contraction. Collectively, our data implicate scfd1 loss-of-function as the genetic defect at the hahvcc43 locus and provide new insights into the role of scfd1 in cardiac development and function.

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Braun, U., e S. Rauch. "Ultrasonographic evaluation of reticular motility during rest, eating, rumination and stress in 30 healthy cows". Veterinary Record 163, n. 19 (8 novembre 2008): 571–74. http://dx.doi.org/10.1136/vr.163.19.571.

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Kelly, K. R., C. M. Espitia, E. C. Medina, D. Mahalingam, B. O. Oyajobi, M. Coffey, F. J. Giles, J. S. Carew e S. T. Nawrocki. "580 Reolysin induces endoplasmic reticular stress in multiple myeloma and enhances the activity of bortezomib". European Journal of Cancer Supplements 8, n. 7 (novembre 2010): 183. http://dx.doi.org/10.1016/s1359-6349(10)72287-4.

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Clark, R. A., R. Alon e T. A. Springer. "CD44 and hyaluronan-dependent rolling interactions of lymphocytes on tonsillar stroma." Journal of Cell Biology 134, n. 4 (15 agosto 1996): 1075–87. http://dx.doi.org/10.1083/jcb.134.4.1075.

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Little is known about how lymphocytes migrate within secondary lymphoid organs. Stromal cells and their associated reticular fibers form a network of fibers that radiate from high endothelial venules to all areas of the lymph node and may provide a scaffold for lymphocyte migration. We studied interactions of lymphocytes with cultured human tonsillar stromal cells and their extracellular matrix using shear stress to distinguish transient interactions from firm adhesion. Tonsillar lymphocytes and SKW3 T lymphoma cells tethered and rolled on monolayers of cultured tonsillar stromal cells and their matrix. A significant proportion of these rolling interactions were independent of divalent cations and were mediated by CD44 binding to hyaluronan, as shown by inhibition with mAb to CD44, soluble hyaluronan, as hyaluronidase treatment of the substrate, and O-glycoprotease treatment of the rolling cells. O-glycoprotease treatment of the substrate also blocked binding completely to stromal matrix and partially to stromal monolayers. SKW3 cells tethered and rolled on plastic-immobilized hyaluronan, confirming the specificity of this interaction. By contrast, monolayers of resting or stimulated human umbilical vein endothelial cells failed to support CD44- and hyaluronan-dependent rolling. SKW3 cells added under flow conditions to frozen sections of human tonsil bound and rolled along reticular fibers in the presence of EDTA. Rolling was blocked by either CD44 mAb or hyaluronan. We propose that lymphocytes migrating through secondary lymphoid organs may use CD44 to bind to hyaluronan immobilized on stromal cells and reticular fibers.

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Rembold, C. M., e R. A. Murphy. "Histamine concentration and Ca2+ mobilization in arterial smooth muscle". American Journal of Physiology-Cell Physiology 257, n. 1 (1 luglio 1989): C122—C128. http://dx.doi.org/10.1152/ajpcell.1989.257.1.c122.

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Smooth muscle contraction is dependent on Ca2+ entry from the extracellular space or release from intracellular stores. The sensitivity of these Ca2+ sources to agonist concentration was evaluated by measuring myoplasmic [Ca2+] (as estimated by aequorin), myosin phosphorylation, and isometric stress in the swine carotid media. High histamine concentrations produced transient elevations in [Ca2+] and phosphorylation with rapid generation of near maximal stress. Lower histamine concentrations produced much smaller [Ca2+] and phosphorylation transients, and stress development was slower. Peak [Ca2+] was proportional to the rate of stress development. Steady-state [Ca2+], phosphorylation, and stress values (which are dependent on extracellular Ca2+) were more sensitive to histamine concentration than was the peak [Ca2+] response both in the presence and absence of extracellular CaCl2 (measures of intracellular Ca2+ release). This result suggests that the mechanism for Ca2+ influx from the extracellular space is more sensitive to histamine than intracellular Ca2+ release. These results are also consistent with the hypothesis that agonist-releasable sarcoplasmic reticular Ca2+ is the major contributor to initial phosphorylation transients that enhance the rate of stress development.

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Farías, Mónica A., Benjamín Diethelm-Varela, Areli J. Navarro, Alexis M. Kalergis e Pablo A. González. "Interplay between Lipid Metabolism, Lipid Droplets, and DNA Virus Infections". Cells 11, n. 14 (17 luglio 2022): 2224. http://dx.doi.org/10.3390/cells11142224.

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Lipid droplets (LDs) are cellular organelles rich in neutral lipids such as triglycerides and cholesterol esters that are coated by a phospholipid monolayer and associated proteins. LDs are known to play important roles in the storage and availability of lipids in the cell and to serve as a source of energy reserve for the cell. However, these structures have also been related to oxidative stress, reticular stress responses, and reduced antigen presentation to T cells. Importantly, LDs are also known to modulate viral infection by participating in virus replication and assembly. Here, we review and discuss the interplay between neutral lipid metabolism and LDs in the replication cycle of different DNA viruses, identifying potentially new molecular targets for the treatment of viral infections.

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Thome, Janine, Maria Densmore, Georgia Koppe, Braeden Terpou, Jean Théberge, Margaret C. McKinnon e Ruth A. Lanius. "Back to the Basics: Resting State Functional Connectivity of the Reticular Activation System in PTSD and its Dissociative Subtype". Chronic Stress 3 (gennaio 2019): 247054701987366. http://dx.doi.org/10.1177/2470547019873663.

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Background Brainstem and midbrain neuronal circuits that control innate, reflexive responses and arousal are increasingly recognized as central to the neurobiological framework of post-traumatic stress disorder (PTSD). The reticular activation system represents a fundamental neuronal circuit that plays a critical role not only in generating arousal but also in coordinating innate, reflexive responding. Accordingly, the present investigation aims to characterize the resting state functional connectivity of the reticular activation system in PTSD and its dissociative subtype. Methods We investigated patterns of resting state functional connectivity of a central node of the reticular activation system, namely, the pedunculopontine nuclei, among individuals with PTSD (n = 77), its dissociative subtype (PTSD+DS; n = 48), and healthy controls (n = 51). Results Participants with PTSD and PTSD+DS were characterized by within-group pedunculopontine nuclei resting state functional connectivity to brain regions involved in innate threat processing and arousal modulation (i.e., midbrain, amygdala, ventromedial prefrontal cortex). Critically, this pattern was most pronounced in individuals with PTSD+DS, as compared to both control and PTSD groups. As compared to participants with PTSD and controls, individuals with PTSD+DS showed enhanced pedunculopontine nuclei resting state functional connectivity to the amygdala and the parahippocampal gyrus as well as to the anterior cingulate and the ventromedial prefrontal cortex. No group differences emerged between PTSD and control groups. In individuals with PTSD+DS, state derealization/depersonalization was associated with reduced resting state functional connectivity between the left pedunculopontine nuclei and the anterior nucleus of the thalamus. Altered connectivity in these regions may restrict the thalamo-cortical transmission necessary to integrate internal and external signals at a cortical level and underlie, in part, experiences of depersonalization and derealization. Conclusions The present findings extend the current neurobiological model of PTSD and provide emerging evidence for the need to incorporate brainstem structures, including the reticular activation system, into current conceptualizations of PTSD and its dissociative subtype.

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Janni, Kevin A., Chad R. Nelson, Bradley J. Heins e Kirsten Sharpe. "Dairy Cow Thermal Balance Model During Heat Stress: Part 2. Model Assessment". Journal of the ASABE 66, n. 2 (2023): 461–68. http://dx.doi.org/10.13031/ja.15191.

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Highlights The thermal balance model body temperature and respiration rate results compared well with published data. Model results were commonly within one standard deviation of reported averages. Research that measures more model inputs, coefficients, and results is needed. The thermal balance model can be used to identify heat stress factors and assess mitigation practices. Abstract. A steady-state process-based lactating cow thermal balance spreadsheet model developed by Nelson and Janni (in press) was compared to mean measured body temperatures, respiration rates, and skin temperatures from two published studies (Gebremedhin et al., 2010; Chen et al., 2015). Model body temperatures were also compared with reticular temperatures from cows standing in unshaded paddocks that were part of a solar shade study (Sharpe et al., 2021). Gebremedhin et al. (2010) reported measured mean rectal temperatures, 39.4 ± 0.5 C and 40.6 ± 0.4 C for hot and dry conditions with and without a solar load; model body temperatures for similar hot and dry conditions were 39.7 C and 40.6 C with and without a solar load, respectively. Model respiration rates were within one standard deviation of measured mean respiration rates (Gebremedhin et al., 2010). The model body temperature for a baseline condition was 39.1°C, which was within 0.1°C of the mean baseline temperature of 39.2 ± 0.6°C (Chen et al., 2015). The model respiration rate was 63 breaths per minute (bpm); much lower than the reported baseline respiration rate of 88 bpm (Chen et al., 2015). Model body temperatures were 0.1°C to 0.7°C lower than the measured mean reticular temperatures of standing cows in non-shaded paddocks with solar loads when ambient temperatures ranged from 24.4°C to 26.5°C. Model results compared well with mean measured parameters from three studies. The model can be used to assess the impact of factors affecting heat exchange (e.g., body mass, milk yield, solar load, air dry-bulb temperature, dew-point temperature, and air velocity) on heat exchange flux, cow respiration rate, and body temperature. Keywords: Body temperature, Dairy, Heat stress, Lactating cow, Respiration rate, Thermal balance model.

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Kelly, K. R., C. M. Espitia, D. Mahalingam, B. O. Oyajobi, M. Coffey, F. J. Giles, J. S. Carew e S. T. Nawrocki. "Reovirus therapy stimulates endoplasmic reticular stress, NOXA induction, and augments bortezomib-mediated apoptosis in multiple myeloma". Oncogene 31, n. 25 (17 ottobre 2011): 3023–38. http://dx.doi.org/10.1038/onc.2011.478.

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Butler, P. D., D. P. Ly, M. T. Longaker, A. C. Koong, E. J. Huang e G. P. Yang. "QS206. Targeted Deletion of HIPK2 Leads to Improved Cell Survival in Response to Endoplasmic Reticular Stress". Journal of Surgical Research 151, n. 2 (febbraio 2009): 291. http://dx.doi.org/10.1016/j.jss.2008.11.507.

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Shukla, Nilima, Song Wan, Gianni D. Angelini e Jamie Y. Jeremy. "Low nanomolar thapsigargin inhibits the replication of vascular smooth muscle cells through reversible endoplasmic reticular stress". European Journal of Pharmacology 714, n. 1-3 (agosto 2013): 210–17. http://dx.doi.org/10.1016/j.ejphar.2013.05.036.

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Wu, Ming‐Shun, Chih‐Chiang Chien, Jungshan Chang e Yen‐Chou Chen. "Pro‐apoptotic effect of haem oxygenase‐1 in human colorectal carcinoma cells via endoplasmic reticular stress". Journal of Cellular and Molecular Medicine 23, n. 8 (14 giugno 2019): 5692–704. http://dx.doi.org/10.1111/jcmm.14482.

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Cao, Longxiang, Xiaoshuai Yuan, Feichao Bao, Wang Lv, Zhehao He, Jie Tang, Jia Han e Jian Hu. "Downregulation of HSPA2 inhibits proliferation via ERK1/2 pathway and endoplasmic reticular stress in lung adenocarcinoma". Annals of Translational Medicine 7, n. 20 (ottobre 2019): 540. http://dx.doi.org/10.21037/atm.2019.10.16.

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Aksel'rod, L. B., V. I. Kresyun, I. N. Moiseev, D. M. Sukolovskaya, L. S. Kravchenko, D. G. Rasina e L. L. Kadyrova. "Functional changes in the myocardium and medullary reticular formation in cardiogenic stress treated with lithium nicotinate". Bulletin of Experimental Biology and Medicine 105, n. 4 (aprile 1988): 542–44. http://dx.doi.org/10.1007/bf00841199.

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Yan, Ruzhong, Liaoyuan Wang e Shengze Wang. "Investigating the influences of pressure-equalizing grooves on characteristics of aerostatic bearings based on CFD". Industrial Lubrication and Tribology 71, n. 7 (9 settembre 2019): 853–60. http://dx.doi.org/10.1108/ilt-11-2018-0411.

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Purpose The purpose of this study is to reveal the influence law of pressure-equalizing grooves on aerostatic bearings and improve the static performance of bearings by optimizing the distribution form of grooves. Design/methodology/approach In view of two kinds of common restrictor distribution forms on the thrust surface, the linear and the rectangular, six kinds of pressure-equalizing groove schemes were proposed – the line-shape, the extended-shape, the S-shape, the oblong-shape, the X-shape and the reticular-shape. Based on the analysis of lubrication theory of the orifice-type aerostatic bearing, the numerical simulations of different bearings were carried out. The pressure distributions and static characteristic curves of different bearings were obtained. Findings The study reveals that the adoption of the pressure-equalizing grooves can substantially improve the load capacity and static stiffness of the bearing and make the bearing maintain a uniform stress, which enhances operating accuracy and life of the bearing. The superior function of the reticular-shape groove is highlighted. Originality/value The research results can effectively guide the optimization design of aerostatic bearings and provide a crucial technical reference for application of ultra-precision aerostatic supporting system.

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