Sentences with phrase «in hypoxia response»

«One major adaptation is a positive selection for genes involved in hypoxia response and skeletal development, similar to those expressed in other organisms in high - altitude environments such as Tibet and the Andes,» Dr Subramanian said.

Not exact matches

Arousal and ventilatory responses to hypoxia in sleeping infants: effects of maternal smoking

Deficient hypoxia awakening response in infants of smoking mothers: possible relationship to sudden infant death syndrome

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

The production of the HIF - 1 inhibitor occurs in response to hypoxia in these cells.

Identification of these genes provides support for previously hypothesized mechanisms of high - altitude adaptation and illuminates the complexity of hypoxia - response pathways in humans.

Several of the identified genes were representative of pathways previously described in other tissues exposed to hypoxia, including genes in the stress response, apoptotic, proliferation, and synaptic transmission pathways.

Insight into the novel role that NMDA receptors play in retinal responses to hypoxia may be derived from study of the coordinated expression patterns of genes that interact, either directly or indirectly, with the NMDA receptor; namely, the NMDA interactome.

Thus, interactome hubs such as NR1 may exhibit low levels of change in individual gene expression following hypoxia, but, based on analysis of interaction networks, are likely to play an important role in regulating the biologic response.

He is best known for his ground - breaking discovery of the HIF - 1 (hypoxia - inducible factor 1) protein, which controls genes in response to changes in oxygen availability.

A major aspect of this process is the production of multiple angiogenic cytokines and growth factors in response to hypoxia / ischemia, which is mediated by the transcription factor HIF - 1 (hypoxia - inducible factor 1).

Large - scale transcriptional response to hypoxia in Aspergillus fumigatus observed using RNAseq identifies a novel hypoxia regulated ncRNA.

Compensatory behaviour in response to sulfide - induced hypoxia affects time budgets, feeding efficiency, and predation risk.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

Hypoxia - inducible factor - 1alpha expression predicts a poor response to primary chemoendocrine therapy and disease - free survival in primary human breast cancer

Endogenous markers of two separate hypoxia response pathways (hypoxia inducible factor 2 alpha and carbonic anhydrase 9) are associated with radiotherapy failure in head and neck cancer patients recruited in the CHART randomized trial

Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1 / TSC2 tumor suppressor complex

Lu is a medical student interested in the role of epigenetic regulation in high altitude adaptation and hypoxia response.

Cytoplasmic in normoxia, nuclear translocation in response to hypoxia.

To mimic the in vitro hypoxic response in vivo, we developed a xenograft model based on the hypothesis that with increasing xenograft sizes, there will be a parallel increase in hypoxia due to rapid cell proliferation and restricted blood supply to the xenograft cells.

To assess whether this is occurring within breast cancer cells in response to hypoxia - induced activation of ER - α, EGFR signaling was blocked with the inhibitor gefitinib.

AOPCP also modified cardiovascular responses to hypoxia, as evidenced by reduced elevations in heart rate and exaggerated changes in femoral vascular conductance and mean arterial blood pressure.

Autophagy, a cellular cleaning process, gets activated in response to certain types of metabolic stress, including nutrient deprivation, growth factor depletion and hypoxia.

That response was even better during certain stages of the menstrual cycle in younger female rats, suggesting female hormones play a role in the response to hypoxia during sleep.

In indigenous Australians and Papua New Guineans, mingling with the Denisovans (the «other Neanderthal,» an ancestral human living primarily in Asia) introduced genes related to «spermatogenesis, fertilization, cold acclimation, circadian rhythm, development of brain, neural tube, face, and olfactory pit, immunity,» as well as «female pregnancy, development of face, lung, heart, skin, nervous system, and male gonad, visual and smell perception, response to heat, pain, hypoxia, and UV, lipid transport, metabolism, blood coagulation, wound healing, aging.&raquIn indigenous Australians and Papua New Guineans, mingling with the Denisovans (the «other Neanderthal,» an ancestral human living primarily in Asia) introduced genes related to «spermatogenesis, fertilization, cold acclimation, circadian rhythm, development of brain, neural tube, face, and olfactory pit, immunity,» as well as «female pregnancy, development of face, lung, heart, skin, nervous system, and male gonad, visual and smell perception, response to heat, pain, hypoxia, and UV, lipid transport, metabolism, blood coagulation, wound healing, aging.&raquin Asia) introduced genes related to «spermatogenesis, fertilization, cold acclimation, circadian rhythm, development of brain, neural tube, face, and olfactory pit, immunity,» as well as «female pregnancy, development of face, lung, heart, skin, nervous system, and male gonad, visual and smell perception, response to heat, pain, hypoxia, and UV, lipid transport, metabolism, blood coagulation, wound healing, aging.»

· Cancer Growth and Spread — Healing Angiogenesis and Metastasis, discussing blood vessel development and growth factors, dysregulation including hypoxia and other blood supply stress responses in cancer and other diseases and how cancer cells travel and invade — metastasis via the complex tumour microenvironment — TME — comprised of immune cells, cytokines, growth factors, reactive oxygen species (ROS) and cancer - associated fibroblast (CAF);