Association between Low Ambient Temperature and the Severity of Acute Ischemic Stroke

Objective:To explore the relationships among ambient temperature,ischemic stroke severity,and blood pressure.Methods:Meteorological data(2005–2015)were collected from the Guangzhou Meteorological Data Service.Ischemic stroke patients from the Department of Neurology of the First Affiliated Hospital,Sun Yat-sen University were retrospectively evaluated,each winter from 2005 to 2015.Patient demographics,baseline measurements,and National Institute of Health Stroke Scale(NIHSS)score were evaluated.Results:Three hundred sixty-two patients were included.The median latency from symptom onset to admission was 2 d(IQR:1–3 d).During recruitment,the highest and lowest temperatures were 39℃and 1.3℃,respectively.Hypertension was the most common comorbidity(75.1%).NIHSS scores at admission and discharge were higher in the cold-exposed group than in the controls regardless of the average temperature at admission.In addition,systolic and diastolic blood pressure values at admission were higher in the cold-exposed group than in the controls.When stratified by hypertensive status,the average and minimum temperatures at admission were negatively associated with systolic and diastolic blood pressure values in hypertensive patients.Reductions in the average and minimum temperatures at symptom onset were associated with more severe stroke.Conclusion:Ischemic stroke patients with symptom onset in winter had higher systolic blood pressure values and more serious neurologic deficits upon admission.

The impact of low ambient temperature on cardiovascular health

Extreme weather events and climate change have witnessed a substantial increase in recent years,leading to heightened concerns.The rise in abnormal ambient temperatures,both in intensity and frequency,directly and indirectly impacts cardiovascular health.While the impact of high ambient temperatures on cardiovascular response is a common concern in the context of global warming,the significance of low temperatures cannot be overlooked.The challenges posed by low temperatures contribute to increased cardiovascular morbidity and mortality,posing a significant threat to global public health.This review aims to provide an overview of the relationship between low ambient temperature and cardiovascular health,encompassing the burden of cardiovascular outcomes and underlying mechanisms.Additionally,the review explores strategies for cold adaptation and cardioprotection.We posit that to optimize cold adaptation strategies,future research should delve deeper into the underlying mechanisms of cardiovascular health in response to low ambient temperature exposure.

Effects of low ambient temperatures and dietary vitamin C supplementation on pulmonary vascular remodeling and hypoxic gene expression of 21-d-old broilers

The objective of this study was to evaluate the effects of low ambient temperature （LAT） and dietary vitamin C （VC） sup- plementation on pulmonary vascular remodeling （PVR） and the relative expression of hypoxia inducible factor-la （HIF-la）, vascular endothelial growth factor （VEGF） and its receptor 2 （VEGFR-2） mRNA of lungs in 21-d-old broilers. 400 1-d-old male Cobb broilers were assigned randomly to 4 treatments as follows for 21 d： 1 ） LAT and a basal diet; 2） LAT and a basal diet supplemented with 1 000 mg kg-1 VC （LAT＋VC）; 3） normal ambient temperature （NAT） and a basal diet; 4） NAT and a basal diet supplemented with 1 000 mg kg-1 VC （NAT＋VC）. Each treatment was composed of 10 replicates of 10 birds per replicate. Samples of lung were collected after the broilers were killed at d 21. LAT increased the ratio of vessel wall area to vessel total area （WA/TA, %） and mean media thickness in pulmonary arterioles （mMTPA, %） （P〈0.05）. Dietary VC supplementation decreased mMTPA （P〈0.05）, but had no effect on the WA/TA. LAT increased （P〈0.05） the relative mRNA expression of HIF-la, VEGF and VEGFR-2, while adding VC to the diet could decrease （P〈0.05） their relative mRNA expression. A significant positive correlation existed between the level of VEGF mRNA expression and the value of WA/WT （P〈0.05） or mMTPA （P〈0.05）. These results suggested LAT resulted in pulmonary vascular remodeling, and the increase of HIF-la, VEGF and VEGFR-2 mRNA expression, and dietary VC supplementation can alleviate pulmonary vascular remodeling in broiler by affecting these gene expression.

Targeting PPARαin low ambient temperature exposure-induced cardiac dysfunction and remodeling

The present study demonstrates that the down-regulation of peroxisome proliferator-activated receptor-α(PPARα)results in chronic low ambient temperature(LT)exposure-induced cardiac dysfunction and remodeling,emphasizing the therapeutic potential of PPARαactivation strategies(e.g.,fenofibrate treatment)in LT-associated cardiac injury.

Effects of Imidapril on Venous Blood Gas Values in Broiler Chickens Exposed to Low Ambient Temperature

ObjectiveThis study was designed to evaluate the effects of imidapril on blood gas parameters in broiler chickens. MethodTwenty-four chickens were randomly divided into three groups (n=8), control group, low temperature group and imidapril group. Chickens in low temperature group and imidapril group were exposed to low ambient temperature (12-18 ℃) from age at 14 d to 45 d, whereas the control group was exposed to 24-30 ℃; chickens in imidapril group were gavaged with imidapril (3 mg/kg) once daily for 30 d. At age of 45 d, blood was taken from wing vein and blood gas parameters were evaluated by blood gas analyzer in Luoyang Central Hospital Affiliated to Zhengzhou University. ResultImidapril significantly increased hematocrit (HCT) and total hemoglobin content (T HBC ) and blood Na concentration in broiler chickens exposed to low ambient temperature. No significant differences were observed in pH, P CO 2 , P O 2 , K + , Ca 2+ , HCO 3-, HCO 3std , T CO 2 , BE and SO 2c . ConclusionImidapril increases hematocrit, total hemoglobin content and blood Na + concentration in chickens exposed to low ambient temperature.

Cardiac-specific knockout of ET_(A)receptor mitigates low ambient temperature-induced cardiac hypertrophy and contractile dysfunction

Cold exposure is associated with oxidative stress and cardiac dysfunction.The endothelin(ET)system,which plays a key role in myocardial homeostasis,may participate in cold exposure-induced cardiovascular dysfunction.This study was designed to examine the role of ET-1 in cold stress-induced cardiac geometric and contractile responses.Wild-type(WT)and ETA receptor knockout(ETAKO)mice were assigned to normal or cold exposure(48C)environment for 2 and 5 weeks prior to evaluation of cardiac geometry,contractile,and intracellular Ca21 properties.Levels of the temperature sensor transient receptor potential vanilloid(TRPV1),mitochondrial proteins for biogenesis and oxidative phosphorylation,including UCP2,HSP90,and PGC1a were evaluated.Cold stress triggered cardiac hypertrophy,depressed myocardial contractile capacity,including fractional shortening,peak shortening,and maximal velocity of shortening/relengthening,reduced intracellular Ca21 release,prolonged intracellular Ca21 decay and relengthening duration,generation of ROS and superoxide,as well as apoptosis,the effects of which were blunted by ETAKO.Western blotting revealed downregulated TRPV1 and PGC1a as well as upregulated UCP2 and activation of GSK3b,GATA4,and CREB in cold-stressed WT mouse hearts,which were obliterated by ETAKO.Levels of HSP90,an essential regulator for thermotolerance,were unchanged.The TRPV1 agonist SA13353 attenuated whereas TRPV1 antagonist capsazepine mimicked cold stress-or ET-1-induced cardiac anomalies.The GSK3b inhibitor SB216763 ablated cold stress-induced cardiac contractile(but not remodeling)changes and ET-1-induced TRPV1 downregulation.These data suggest that ETAKO protects against cold exposure-induced cardiac remodeling and dysfunction mediated through TRPV1 and mitochondrial function.

Revealing the intrinsic mechanisms for accelerating nitrogen removal efficiency in the Anammox reactor by adding Fe(Ⅱ)at low temperature

Fe(Ⅱ)is an essential trace element for anaerobic ammonium oxidation bacteria(AAOB)metabolism,and can improve the nitrogen removal efficiency of anaerobic ammonia oxidation(Anammox).Here we oper-ated two identical expanded granular sludge bed(EGSB)reactors at low temperature(15±3℃)for 154 days.Reactor 1(R_(1))received additional Fe(Ⅱ)(0.12 mmol/L)during the late startup phase,while reactor 0(R_(0))served as the control and did not receive extra Fe(Ⅱ).Nitrogen removal in R_(1)became stable at 55 d of operation,ten days earlier than R_(0).The nitrogen removal rate(NRR)of R_(1) was 1.64 kg N m^(−3)d^(−1)and its TN removal rate was as high as 89%,while R_(0)only reached 75%.The addition of Fe(Ⅱ)was fur-ther beneficial to aggregation and stability of the granular sludge,and the used sludge of both reactors showed enrichment for AAOB populations compared to the inoculum,for instance,increased abundance of Candidatus-Kuenenia and in particular of Candidatus-Brocadia(from 0.17%to 10.10%in R_(0)and 7.79%in R_(1)).Diverse microbial species and complex microbial network structure in R_(1)compared to R_(0)promoted the coupled denitrogenation by Anammox,dissimilatory nitrate reduction to ammonium(DNRA),nitrate-dependent Fe oxidation(NDFO),and ferric ammonium oxidation(Feammox).In addition,the microbial community in R_(1)was more resistant to short-term low temperature(2-7℃)starvation,illustrating a further positive effect of adding Fe(Ⅱ)during the startup phase of an Anammox reactor.

HOS15 represses flowering by promoting GIGANTEA degradation in response to low temperature in Arabidopsis

Flowering is the primary stage of the plant developmental transition and is tightly regulated by environmental factors such as light and temperature.However,the mechanisms by which temperature signals are integrated into the photoperiodic flowering pathway are still poorly understood.Here,we demonstrate that HOS15,which is known as a GI transcriptional repressor in the photoperiodic flowering pathway,controls flowering time in response to low ambient temperature.At 16℃,the hos15 mutant exhibits an early flowering phenotype,and HOS15 acts upstream of photoperiodic flowering genes(GI,CO,and FT).GI protein abundance is increased in the hos15 mutant and is insensitive to the proteasome inhibitor MG132.Furthermore,the hos15 mutant has a defect in low ambient temperature-mediated GI degradation,and HOS15 interacts with COP1,an E3 ubiquitin ligase for GI degradation.Phenotypic analyses of the hos15 cop1 double mutant revealed that repression of flowering by HOS15 is dependent on COP1 at 16℃.However,the HOS15-COP1 interaction was attenuated at 16℃,and GI protein abundance was additively increased in the hos15 cop1 double mutant,indicating that HOS15 acts independently of COP1 in GI turnover at low ambient temperature.This study proposes that HOS15 controls GI abundance through multiple modes as an E3 ubiquitin ligase and transcriptional repressor to coordinate appropriate flowering time in response to ambient environmental conditions such as temperature and day length.