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To elucidate the variations in quality and volatile component changes in different forms of stored indica-japonica hybrid rice, a study was conducted with Yongyou 1540 rice as the test material. Under storage conditions of paddy, brown rice, and milled rice, compared to conventional warehousing, an investigation was conducted to assess the influence of low-temperature storage (15±1 ℃, RH 60%) on its quality (fatty acid value, sensory evaluation) and volatile components. Results showed that storing rice at low temperatures significantly enhanced sensory quality when comparing with conventional storage after six months, and the fatty acid value was notably superior after 12 months. Moreover, storing rice as paddy or brown rice significantly outperformed milled rice storage (at 12 months). Analysis using gas chromatography-ion mobility spectrometry (GC-IMS) to examine the volatile components of the rice under different treatments, aldehyde and ketone substances in rice stored for 6~12 months increased in comparison of fresh rice. Among these, the differences in volatile components were relatively minor between samples stored for 6 months and notably greater between samples stored for 12 months. Substances like 2-methyl-1-butanol, pentanal, hexanal, 3-methylbutanal were found in higher concentrations in room temperature samples compared to low-temperature storage, while cyclohexanone, 2-butanone, butanal, 3-hydroxy-2-butanone were lower in concentration. In conclusion, low-temperature storage of paddy or brown rice maintained the quality and volatile components of indica-japonica hybrid rice better than those of conventional storage. This research can provide essential data and theoretical foundations for post-harvest storage and production of indica-japonica hybrid rice.

Agricultural products usually contain a large number of spoilage bacteria and endogenous enzymes, which can adversely affect the quality of agricultural products. Radio frequency is a kind of dielectric heating technology, which has fast heating speed and high efficiency, can effectively inactivate microorganisms and endogenous enzymes in agricultural products and has little influence on the quality of agricultural products， such as color, texture and nutritional composition, etc. This review summarized the mechanism of action of radiofrequency sterilization blunt enzyme technology and its application in agricultural products processing in recent years, and the shortcomings and solutions of radiofrequency sterilization blunt enzyme technology was pointed out. Moreover, the future application of radiofrequency sterilization blunt enzyme technology in agricultural products and food was also prospected.

Purpose: To develop and validate a clinical-radiomic nomogram for the preoperative prediction of the aldosterone-producing adenoma (APA) risk in patients with unilateral adrenal adenoma. Patients and Methods: Ninety consecutive primary aldosteronism (PA) patients with unilateral adrenal adenoma who underwent adrenal venous sampling (AVS) were randomly separated into training (n = 62) and validation cohorts (n = 28) (7:3 ratio) by a computer algorithm. Data were collected from October 2017 to June 2020. The prediction model was developed in the training cohort. Radiomic features were extracted from unenhanced computed tomography (CT) images of unilateral adrenal adenoma. The least absolute shrinkage and selection operator (LASSO) regression model was used to reduce data dimensions, select features, and establish a radiomic signature. Multivariable logistic regression analysis was used for the predictive model development, the radiomic signature and clinical risk factors integration, and the model was displayed as a clinical-radiomic nomogram. The nomogram performance was evaluated by its calibration, discrimination, and clinical practicability. Internal validation was performed. Results: Six potential predictors were selected from 358 texture features by using the LASSO regression model. These features were included in the Radscore. The predictors included in the individualized prediction nomogram were the Radscore, age, sex, serum potassium level, and aldosterone-to-renin ratio (ARR). The model showed good discrimination, with an area under the receiver operating characteristic curve (AUC) of 0.900 [95% confidence interval (CI), 0.807 to 0.993], and good calibration. The nomogram still showed good discrimination [AUC, 0.912 (95% CI, 0.761 to 1.000)] and good calibration in the validation cohort. Decision curve analysis presented that the nomogram was useful in clinical practice. Conclusions: A clinical-radiomic nomogram was constructed by integrating a radiomic signature and clinical factors. The nomogram facilitated accurate prediction of the probability of APA in patients with unilateral adrenal nodules and could be helpful for clinical decision making. [ABSTRACT FROM AUTHOR]

The present study was undertaken to examine the association between intermittent hypoxia and left ventricular (LV) remodeling and explore which parameter of intermittent hypoxia is most relevant to LV remodeling in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). Two hundred eighty six patients underwent polysomnographic examination were enrolled. Based on apnea-hypoxia index (AHI), patients were divided into no, mild, moderate and severe OSAHS groups. Between-group differences in LV remodeling and the association between parameters of intermittent hypoxia and LV remodeling was evaluated. Patients with severe OSAHS were more likely to have hypertension, and higher values of LV mass (LVM) and LVM index (LVMI). In univariate regression analysis, male, body mass index (BMI), systolic and diastolic blood pressure (BP), statins, antihypertensive drugs, creatinine, and parameters of intermittent hypoxia (AHI, obstructive apnea index [OAI], lowest oxygen saturation [LSpO2], oxygen desaturation index [ODI], time spent below oxygen saturation of 90% [TS90%], and mean nocturnal oxygen saturation [MSpO2]) were associated with LVMI. After multivariate regression analyses, only male gender, BMI, systolic BP, creatinine, and ODI remained significantly associated with LVMI. Compared to those without LV hypertrophy (LVH), patients with LVH had higher ODI. Compared to patients with normal LV, concentric remodeling and eccentric LVH, those with concentric LVH had higher ODI. In conclusion, intermittent hypoxia was significantly associated with left ventricular remodeling; and among various parameters of intermittent hypoxia, ODI was the most relevant to LV remodeling. [ABSTRACT FROM AUTHOR]

Previous studies indicate a preliminary association between age and circadian blood pressure (BP) variation. This association would be affected by confounding factors in real-world populations. The authors investigated whether this is a convincingly independent association in a real-world population of adults with hypertension. Clinical data and findings of 24-hour ambulatory BP monitoring were obtained from 297 consecutive adults with hypertension (60.19±0.77 years). BP dipping patterns were categorized based on the percentage of nocturnal BP drop. Multivariate linear regression analysis identified an independent correlation between age and percentage of nocturnal systolic BPdrop (β=-7.296; 95% CI, -10.430 to -4.162 [P<.001]). Reverse dippers were the oldest and extreme dippers were the youngest. A significant age difference was noted among patients grouped into four BP dipping patterns with and without adjustments for sex, body mass index, drugs, diabetes mellitus, smoking, 24-hour mean heart rate, and 24-hour mean systolic and diastolic BP. [ABSTRACT FROM AUTHOR]

It is not known whether combination of hypertension and high homocysteine (HHcy) impacts on stroke-related neurological severity. Our aim was to determine whether there is an interaction of hypertension and HHcy on neurological severity in first-ever ischemic stroke patients. We analyzed neurological severity among 189 consecutive first-ever ischemic stroke patients with or without hypertension or HHcy. Hypertension (odds ratio [OR]: 8.086, 95% confidence interval [CI]: 3.596–18.181, P < .001) and total homocysteine (OR: 1.403, 95% CI: 1.247–1.579, P < .001) were independently associated with neurological severity. In receiver-operating characteristic analysis, total homocysteine was a significant predictor of neurological severity (area under curve: 0.794; P < .001). A multiplicative interaction of hypertension and HHcy on more severe neurological severity was revealed by binary logistic regression (OR: 13.154, 95% CI: 5.293–32.691, P < .001). Analysis further identified a more than multiplicative interaction of hypertension and HHcy on neurological severity compared with patients without each condition (OR: 50.600, 95% CI: 14.775–173.285, P < .001). Interaction effect measured on an additive scale showed that 76.4% patients with moderate/severe neurological severity were attributed to interaction of hypertension and HHcy. Significant interaction of hypertension and HHcy on neurological severity was found on multiplicative and additive scale in first-ever Chinese ischemic stroke patients. [ABSTRACT FROM AUTHOR]

BackgroundThe pharmacological advantage of combination of an angiotensin receptor blocker (ARB) and a calcium-channel blocker (CCB) is not fully defined. This study was undertaken to elucidate the potential benefit of their combination in metabolic syndrome.MethodsSHR/NDmcr-cp (SHRcp), a rat model of human metabolic syndrome, were divided into four groups, and were administered (i) vehicle, (ii) candesartan (an ARB) 0.3 mg/kg/day, (iii) amlodipine (a CCB) 3 mg/kg/day, and (iv) candesartan 0.3 mg/kg/day plus amlodipine 3 mg/kg/day, for 4 weeks.ResultsCandesartan, amlodipine, or their combination significantly ameliorated the impairment of vascular endothelium-dependent relaxation with acetylcholine in SHRcp. However, the impairment of insulin-induced vasodilation in SHRcp was partially improved by candesartan alone, but not by amlodipine alone. Interestingly, amlodipine added to candesartan synergistically enhanced the improvement of impaired insulin-induced vasodilation by candesartan, indicating the synergistic improvement of vascular insulin resistance by the combination of these drugs. Candesartan alone, but not amlodipine alone, significantly attenuated vascular superoxide and NADPH oxidase subunit p22phox in SHRcp. Amlodipine added to candesartan synergistically enhanced the reduction of vascular p22phox levels and superoxide by candesartan in SHRcp, suggesting the association of vascular insulin resistance with oxidative stress. Furthermore, the combination of candesartan with amlodipine synergistically decreased the increase in visceral adipocyte size, serum free-fatty acid, and tumor necrosis factor-α in SHRcp.ConclusionsARB and CCB combination synergistically ameliorated vascular insulin resistance in metabolic syndrome, being associated with the synergistic attenuation of vascular oxidative stress and metabolic disorders.American Journal of Hypertension, (2012);. doi:10.1038/ajh.2012.26 [ABSTRACT FROM AUTHOR]

The role of the renin-angiotensin system in cognitive impairment is unclear. This work was undertaken to test our hypothesis that renin-angiotensin system may contribute to cognitive decline and brain damage caused by chronic cerebral ischemia. C57BL/6J mice were subjected to bilateral common carotid artery stenosis with microcoil to prepare mice with chronic cerebral hypoperfusion, a model of subcortical vascular dementia. The effects of aliskiren, a direct renin inhibitor, or Tempol, a superoxide scavenger, on brain damage and working memory in these mice were examined. Chronic cerebral hypoperfusion significantly increased brain renin activity and angiotensinogen expression in C57BL/6J mice, which was attributed to the increased renin in activated astrocytes and microvessels and the increased angiotensinogen in activated astrocytes in white matter. Aliskiren pretreatment significantly inhibited brain renin activity and ameliorated brain p67(phox)-related NADPH oxidase activity, oxidative stress, glial activation, white matter lesion, and spatial working memory deficits in C57BL/6J mice with bilateral common carotid artery stenosis. To elucidate the role of oxidative stress in brain protective effects of aliskiren, we also examined the effect of Tempol in the same mice with bilateral common carotid artery stenosis. Tempol pretreatment mimicked the brain protective effects of aliskiren in this mouse model. Posttreatment of mice with aliskiren or Tempol after bilateral common carotid artery stenosis also prevented cognitive decline. In conclusion, chronic cerebral hypoperfusion induced the activation of the brain renin-angiotensin system. Aliskiren ameliorated brain damage and working memory deficits in the model of chronic cerebral ischemia through the attenuation of oxidative stress. Thus, direct renin inhibition seems to be a promising therapeutic strategy for subcortical vascular dementia. [ABSTRACT FROM AUTHOR]

The protective effect of aliskiren, a direct renin inhibitor, against hypertensive cardiovascular and renal injury remains to be defined. This study was undertaken to examine the protective effects of the combination of aliskiren and valsartan, an angiotensin receptor blocker, against cardiovascular and renal injury. Endothelial NO synthase-deficient mice, subjected to cuff injury of femoral artery, were divided into 5 groups and were treated with the following: (1) vehicle; (2) aliskiren (25 mg/kg per day); (3) valsartan (8 mg/kg per day); (4) combined aliskiren (12.5 mg/kg per day) and valsartan (4 mg/kg per day); and (5) hydralazine (10 mg/kg per day) for 4 weeks. Aliskiren and valsartan alone markedly and similarly suppressed cardiac hypertrophy, inflammation and fibrosis, and coronary remodeling; prevented cuff injury-induced arterial intimal thickening; and reduced urinary albumin excretion, glomerular inflammation, and glomerulosclerosis in endothelial NO synthase-deficient mice. These beneficial effects of aliskiren and valsartan were associated with the significant attenuation of oxidative stress in these tissues. Hence, aliskiren and valsartan markedly exert the protective effects against cardiovascular and renal injury through the reduction of oxidative stress. Furthermore, compared with monotherapy with aliskiren or valsartan, the combination of a half dose of these drugs more greatly improved the above-mentioned cardiovascular and renal injuries of endothelial NO synthase-deficient mice, which were associated with greater attenuation of tissue oxidative stress by the combination therapy. Thus, the combination of aliskiren and valsartan exerts the synergistic organ-protective effects through synergistic attenuation of oxidative stress. The combination of aliskiren and valsartan seems to be a promising therapeutic strategy for hypertensive organ injury caused by endothelial NO synthase dysfunction. [ABSTRACT FROM AUTHOR]

The molecular mechanism underlying aldosterone/salt-induced cardiovascular injury remains to be defined. This work was undertaken to determine the role of apoptosis signal-regulating kinase 1 (ASK1) in the mechanism underlying aldosterone-induced cardiac injury in vivo. We compared the in vivo effects of 4 weeks of aldosterone/salt treatment on wild-type and ASK1-deficient mice. Aldosterone infusion plus high salt intake in wild-type mice significantly increased blood pressure and urinary albumin excretion and decreased plasma potassium concentrations, and these effects of aldosterone/salt were not affected by ASK1 deficiency. Thus, ASK1 seems to play a minor role in aldosterone-induced hypertension and renal injury. ASK1 deficiency also failed to affect aldosterone-induced cardiac hypertrophy. However, ASK1 deficiency markedly ameliorated aldosterone-induced cardiac injury, eg, the enhancement of cardiac macrophage infiltration, monocyte chemotactic protein 1 expression, interstitial fibrosis, perivascular fibrosis, and transforming growth factor-beta1 and collagen type I expressions. Thus, ASK1 participates in aldosterone-induced cardiac inflammation and fibrosis. Furthermore, the enhancement of NADPH oxidase-mediated cardiac oxidative stress caused by aldosterone infusion was markedly lessened by ASK1 deficiency, which was associated with the significant amelioration by ASK1 deficiency of aldosterone-induced cardiac Nox2 upregulation. Furthermore, aldosterone/salt treatment significantly enhanced cardiac expression of the angiotensin-converting enzyme and angiotensin II type 1 receptor in wild-type mice, whereas the enhancement of these proteins by aldosterone/salt was abolished by ASK1 deficiency. Our results demonstrate that ASK1 is implicated in aldosterone/salt-induced cardiac inflammation and fibrosis through the enhancement of NADPH oxidase-mediated oxidative stress and the upregulation of the cardiac renin-angiotensin system. [ABSTRACT FROM AUTHOR]

Dietary obesity is associated with type 2 diabetes and cardiovascular diseases, although the underlying mechanism is unknown. This study was undertaken to elucidate the role of angiotensin II and apoptosis signal regulating kinase-1 (ASK1) in obesity/diabetes-associated cardiovascular complications and hepatic steatosis. Mice fed a high-fat diet were treated with olmesartan, an angiotensin II type 1 receptor blocker, to elucidate the role of angiotensin II in diabetic mice. Treatment of mice fed a high-fat diet with olmesartan markedly suppressed cardiac inflammation and fibrosis, as well as vascular endothelial dysfunction and remodeling, induced by obesity/diabetes. Moreover, olmesartan suppressed the disruption of the vascular endothelial NO synthase dimer in diabetic mice. Olmesartan also significantly prevented hepatic steatosis and fibrosis in diabetic mice. These beneficial effects of olmesartan on diabetic mice were associated with the attenuation of ASK1 activation in these mice. ASK1-deficient mice and wild-type mice were compared, regarding the effects of a high-fat diet. A comparison between ASK1-deficient and wild-type mice showed that ASK1 deficiency attenuated cardiac inflammation and fibrosis, as well as vascular endothelial dysfunction and remodeling induced by obesity/diabetes. The amelioration of vascular endothelial impairment by ASK1 deficiency was attributed to the prevention of endothelial NO synthase dimer disruption. ASK1 deficiency also significantly lessened hepatic steatosis in diabetic mice. In conclusion, our work provided the evidence that ASK1 is significantly activated in diet-induced diabetic mice and contributes to cardiovascular diseases and hepatic steatosis in diabetic mice. Moreover, the beneficial effects of angiotensin II inhibition on dietary diabetic mice seem to be mediated by the inhibition of ASK1 activation. [ABSTRACT FROM AUTHOR]

The effect of pioglitazone, a peroxisome proliferator-activated receptor gamma agonist, on hypertensive cardiovascular injury is unknown. We examined the effect of pioglitazone on hypertensive cardiovascular injury and the significance of combination of pioglitazone with angiotensin type 1 receptor blocker. Stroke-prone spontaneously hypertensive rats (SHRSP) were orally given pioglitazone, candesartan, or combined pioglitazone and candesartan for 4 weeks to compare their effects on cardiovascular injury. Pioglitazone, without lowering blood pressure, significantly suppressed cardiac inflammation and fibrosis and reduced vascular endothelial dysfunction, and these beneficial effects were associated with the reduction of superoxide by inhibition of cardiovascular NADPH oxidase. Thus, pioglitazone protects against hypertensive cardiovascular injury, by inhibiting reactive oxygen species (ROS). Combination of pioglitazone and candesartan suppressed cardiac hypertrophy, inflammation, and interstitial fibrosis of SHRSP to a greater extent than either monotherapy, and reduced vascular endothelial dysfunction of SHRSP more than either monotherapy. Furthermore, more beneficial effects of their combination on cardiovascular injury were associated with more reduction of NADPH oxidase-mediated cardiovascular ROS. To elucidate the underlying molecular mechanism, we examined cardiovascular NADPH oxidase subunits. Pioglitazone monotherapy significantly attenuated cardiovascular p22(phox) and Rac1 in SHRSP, whereas pioglitazone combined with candesartan more attenuated p22(phox) and significantly reduced Nox1. Thus, additive suppression of cardiovascular NADPH oxidase by the combination was attributed to its additive attenuation of p22(phox) and Nox1 protein levels. In conclusion, we showed that pioglitazone protected against hypertensive cardiovascular damage, and the combination of pioglitazone and candesartan exerted more beneficial effects on hypertensive cardiovascular injury by more suppressing ROS. [ABSTRACT FROM AUTHOR]

The role of angiotensin II and reactive oxygen species in the exacerbation of diastolic heart failure is unknown. We examined the therapeutic effect of angiotensin blockade on hypertensive diastolic heart failure, focusing on the role of xanthine oxidoreductase and reduced nicotinamide-adenine dinucleotide phosphate oxidase, major enzymes producing reactive oxygen species. Dahl salt-sensitive hypertensive rats (DS rats) with established diastolic heart failure were given vehicle, candesartan (an angiotensin II receptor subtype 1 receptor blocker), oxypurinol (a xanthine oxidoreductase inhibitor), apocynin (a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor), or hydralazine (a vasodilator), and their therapeutic effects on diastolic heart failure were compared. Candesartan treatment of DS rats with established diastolic heart failure reversed cardiac remodeling, improved cardiac relaxation abnormality, and prolonged survival, being accompanied by the attenuation of the increase in cardiac superoxide, reduced nicotinamide-adenine dinucleotide phosphate oxidase, and xanthine oxidoreductase activities. Thus, the beneficial effect of candesartan in DS rats appears to be mediated by the inhibition of cardiac reactive oxygen species. Cardiac xanthine oxidoreductase inhibition with oxypurinol significantly reduced cardiac superoxide, prevented the progression of cardiac remodeling, and delayed the mortality in DS rats. Apocynin, which significantly inhibited cardiac reduced nicotinamide-adenine dinucleotide phosphate oxidase activity, prevented the exacerbation of diastolic heart failure more than hydralazine. However, compared with candesartan or oxypurinol, apocynin did not improve cardiac reactive oxygen species, remodeling, and function in DS rats. In conclusion, candesartan slowed the exacerbation of hypertensive diastolic heart failure in DS rats by causing reverse cardiac remodeling. Cardiac xanthine oxidoreductase contributed to these beneficial effects of candesartan. [ABSTRACT FROM AUTHOR]

Long-term treatment with N(omega)-nitro-l-arginine methylester (l-NAME), an NO synthase inhibitor, induces hypertension and cardiovascular injury. However, its precise mechanism is unknown. Using apoptosis signal-regulating kinase-1 (ASK1)-deficient mice, we investigated the role of ASK1 in cardiovascular injury caused by l-NAME treatment. l-NAME was orally administered to ASK1-deficient and C57BL/6J (wild) mice for 8 weeks. l-NAME treatment increased blood pressure of wild and ASK1-deficient mice to a similar extent, indicating no role of ASK1 in NO-deficient hypertension. l-NAME treatment significantly impaired acetylcholine-induced carotid arterial relaxation in wild mice (P<0.01), being associated with the decreased endothelial NO synthase (eNOS) activity (P<0.01) and the increased disruption of eNOS dimer (P<0.01), whereas these changes by l-NAME were substantially attenuated in ASK1-deficient mice. Thus, ASK1 is involved in the impairment of vascular endothelial function by reducing eNOS activity and disrupting eNOS dimer. l-NAME treatment increased vascular reduced nicotinamide-adenine dinucleotide phosphate oxidase activity and superoxide in wild mice to a greater extent than in ASK1 deficient mice. l-NAME treatment in wild mice caused cardiac hypertrophy, myocyte apoptosis, macrophage infiltration, coronary arterial remodeling, interstitial fibrosis, and the expression of monocyte chemoattractant protein-1 and transforming growth factor-beta1, whereas these cardiac changes by l-NAME were absent in ASK1-deficient mice. Cardiac reduced nicotinamide-adenine dinucleotide phosphate oxidase activation and superoxide elevation by l-NAME were much less in ASK1-deficient mice than in wild mice. Our work provided the first evidence that ASK1 is implicated in vascular endothelial dysfunction and cardiovascular remodeling induced by NO deficiency by regulating eNOS and reduced nicotinamide-adenine dinucleotide phosphate oxidase. [ABSTRACT FROM AUTHOR]

Previous studies have confirmed the clinical efficacy of sacubitril/valsartan (Sac/Val) for the treatment of heart failure with reduced ejection fraction (HFrEF). However, the role of Sac/Val in heart failure with preserved ejection fraction (HFpEF) remains unclear. Sac/Val is a combination therapeutic medicine comprising sacubitril and valsartan that acts as a first angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor (ARNI)). Here, we investigated the role of Sac/Val in high-salt diet-induced HFpEF coupled with vascular injury as well as the underlying mechanism. Rats were fed with high-salt feed, followed by intragastric administration of Sac/Val (68 mg/kg; i.g.). The results of functional tests revealed that a high-salt diet caused pathological injuries in the heart and vascular endothelium, which were significantly reversed by treatment with Sac/Val. Moreover, Sac/Val significantly decreased the levels of fibrotic factors, including type I collagen and type Ⅲ collagen, thus, reducing the ratio of MMP2/TIMP2 while increasing Smad7 levels. Further investigation suggested that Sac/Val probably reversed the effects of high-salt diet-induced HFpEF by inhibiting the activation of the TGF-β1/Smad3 signaling pathway. Thus, treatment with Sac/Val effectively alleviated the symptoms of high-salt diet-induced HFpEF, probably by inhibiting fibrosis via the TGF-β1/Smad3 signaling pathway, supporting the therapeutic potential of Sac/Val for the treatment of HFpEF. [ABSTRACT FROM AUTHOR]

This investigation elucidates the impact of sophocarpine treatment on lipopolysaccharide (LPS) stimulated sepsis-induced cardiomyopathy (SIC) via in vivo and in vitro experiments. Echocardiography, ELISA, TUNEL, Western blotting experiments, and Hematoxylin/Eosin, Dihydroethidium, and Immunohistochemistry staining assays, were carried out to identify associated indicators. The echocardiography revealed that sophocarpine treatment alleviated LPS-induced cardiac dysfunction as indicated by fractional shortening shortened and improved ejection fraction. Heart injury biomarkers, such as creatine kinase, lactate dehydrogenase, and creatine kinase-MB, were assessed, and indicated that sophocarpine treatment could alleviate LPS-induced upregulation of these indices. Furthermore, different experimental protocols revealed that sophocarpine treatment inhibits LPS-induced pathological alterations and decreases LPS-stimulated inflammatory cytokines, IL-1β, monocyte chemoattractant protein-1, IL-6, NOD-like receptor protein-3, and TNF-α, increase. Apoptotic proteins such as cytochrome-c, Bax, and cleaved-caspase-3 were increased, and Bcl-2 was alleviated after LPS stimulation; however, these effects were inhibited by sophocarpine treatment. Decreased antioxidant proteins [superoxide dismutase-1 (SOD-1) and SOD-2] induced by LPS stimulation were upregulated by sophocarpine treatment. LPS upregulated autophagic proteins such as Beclin-1 and the ratio of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I and downregulated sequestosome 1 (SQSTM1, or P62), sophocarpine therapy reversed these effects. Moreover, it was indicated that sophocarpine treatment inhibited the Toll-like receptor-4 (TLR-4)/nuclear transcription factor-kappa B (NF-κB) signaling pathway and activated nuclear factor erythroid 2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In conclusion, sophocarpine treatment could alleviate LPS-trigger SIC by repressing oxidative stress, autophagy, inflammation, and apoptosis via TLR-4/NF-κB inhibition and Nrf2/HO-1 signaling pathway activation, implicating the potential of sophocarpine as a new therapeutic approach against SIC. [ABSTRACT FROM AUTHOR]

Identifying and protecting refugia is a priority for conservation management under projected anthropogenic climate change. We have two main objectives: the first is to explore the spatial (East Asia) and temporal (Last Glacial Maximum to year 2070) distribution patterns of dominant Castanopsis species of evergreen broad-leaved forests, also the relation with their niche breadths; the second is to identify long-term stable refugia for preserving these species and provide a framework of conservation strategies. We find that there is an extraordinary richness with 32 dominant Castanopsis species, and they form both a geographically and climatically almost unbroken connection from ca. 5°N to 38°N, having thus ecological significance. During the Mid-Holocene and, particularly, the Last Glacial Maximum, the predicted suitable areas of the species as a whole were larger than those in the present. By 2070, potentially suitable areas with high richness of dominant Castanopsis species will be reduced by 94.5 % on average. No correlation between species niche breadths and distribution ranges is found, which could be due to regional climate stability. Mountains of southwestern and southern Yunnan in China are identified as climatically long-term stable refugia for 7–9 Castanopsis species. We recommend that these refugia have the highest priority of conservation to prevent their extinction. Our suggested urgent measures include improving the effectiveness of currently protected Castanopsis species and expanding the network of protected areas to cover a larger fraction of the refugia, as well as ensuring Castanopsis species natural regeneration potential in fragmented and natural secondary forest areas. [ABSTRACT FROM AUTHOR]

Abstract: Experimental and clinical data support the notion that peroxisome proliferator-activated receptor γ (PPARγ) activation is associated with anti-atherosclerosis as well as anti-diabetic effect. Telmisartan, an angiotensin receptor blocker (ARB), acts as a partial PPARγ agonist. We hypothesized that telmisartan protects against diabetic vascular complications, through PPARγ activation. We compared the effects of telmisartan, telmisartan combined with GW9662 (a PPARγ antagonist), and losartan with no PPARγ activity on vascular injury in obese type 2 diabetic db/db mice. Compared to losartan, telmisartan significantly ameliorated vascular endothelial dysfunction, downregulation of phospho-eNOS, and coronary arterial remodeling in db/db mice. More vascular protective effects of telmisartan than losartan were associated with greater anti-inflammatory effects of telmisartan, as shown by attenuation of vascular nuclear factor kappa B (NFκB) activation and tumor necrosis factor α. Coadministration of GW9662 with telmisartan abolished the above mentioned greater protective effects of telmisartan against vascular injury than losartan in db/db mice. Thus, PPARγ activity appears to be involved in the vascular protective effects of telmisartan in db/db mice. Moreover, telmisartan, but not losartan, prevented the downregulation of vascular PPARγ in db/db mice and this effect of telmisartan was cancelled by the coadministration of GW9662. Our data provided the first evidence indicating that PPARγ activity of telmisartan contributed to the protective effects of telmisartan against diabetic vascular complication. PPARγ activity of telmisartan was involved in the normalization of vascular PPARγ downregulation in diabetic mice. Thus, telmisartan seems to exert vascular protective effects in hypertensive patients with diabetes. [Copyright &y& Elsevier]

Abstract: The effect of calcium channel blockers (CCBs) on type 2 diabetes is still unclear. The present study was undertaken to examine the efficacy of nifedipine, a dihydropyridine CCB, on obesity, glucose intolerance and vascular endothelial dysfunction in db/db mice (a mouse model of obesity and type 2 diabetes). db/db mice, fed high-fat diet (HFD) were treated with vehicle, nifedipine (10mgkg−1 day−1) or hydralazine (5mgkg−1 day−1) for 4weeks, and the protective effects were compared. Although nifedipine and hydralazine exerted similar blood pressure lowering in db/db mice, neither affected body weight, fat weight, and glucose intolerance of db/db mice. However, nifedipine, but not hydralazine, significantly improved vascular endothelial function in db/db mice, being accompanied by more attenuation of vascular superoxide by nifedipine than hydralazine. These protective effects of nifedipine were attributed to the attenuation of eNOS uncoupling as shown by the prevention of vascular endothelial nitric oxide synthase (eNOS) dimer disruption, and the prevention of dihydrofolate reductase (DHFR) downregulation, the key enzyme responsible for eNOS uncoupling. Moreover, nifedipine, but not hydralazine, significantly prevented the decreases in phosphorylation of vascular akt and eNOS in db/db mice. Our work provided the first evidence that nifedipine prevents vascular endothelial dysfunction, through the inhibition of eNOS uncoupling and the enhancement of eNOS phosphorylation, independently of blood pressure-lowering effect. We propose that nifedipine may be a promising therapeutic agent for cardiovascular complications in type 2 diabetes. [Copyright &y& Elsevier]

Background: Doxorubicin (DOX) is a potent anti-cancer medication that is associated with numerous adverse effects, particularly concerning damage to the heart., Methods: This study aimed to investigate the impact of sophocarpine (SOP) on DOX-induced heart injury through both in vivo and in vitro experiments. The experimental techniques employed encompassed echocardiography, hematoxylin/eosin (H&E) staining, Masson staining, immunohistochemical staining, western blotting, and so on., Results: Echocardiography showed that SOP alleviated DOX-induced cardiac dysfunction, as evidenced by the improvements in both left ventricle ejection fraction and left ventricle fractional shortening. DOX caused upregulations of creatine kinase-MB and lactate dehydrogenase, while SOP decreased these indices. Staining methods such as H&E and Masson showed that SOP reversed the pathological changes induced by DOX. DOX elevated the expression levels of fibrosis-associated proteins such as Collagen I, Collagen III, α-SMA, Fibronectin, MMP-2, and MMP-9. However, SOP reversed these changes. Moreover, the study further revealed that SOP inhibited the TGF-β1/Smad3 signaling pathway., Conclusions: These findings imply that SOP has the potential to mitigate DOX-induced heart injury by suppressing fibrosis. The underlying molecular mechanism may involve the inhibition of the TGF-β1/Smad3 signaling pathway.

Purpose: Obstructive sleep apnea (OSA) is common in hypertrophic cardiomyopathy (HCM) patients and is related to worse adverse prognosis in HCM patients. However, there are no acknowledged warning characteristics to help to identify OSA in HCM patients., Methods: Seventy-one HCM patients and forty-nine hypertensive (HTN) patients as control group underwent polysomnography (PSG) examination at the Second Affiliated Hospital of Nanchang University from January 2015 to December 2019 patients were consecutively enrolled. The characteristics were analyzed and compared between HCM patients with OSA and without OSA., Results: A total of 37 (52%) HCM patients and 25 (51%) HTN patients were diagnosed with OSA. High body mass index (BMI) (OR = 1.228, 95% CI: 1.032,1.461, P = 0.020) and low estimated glomerular filtration rate (eGFR) (OR = 0.959, 95% CI: 0.931,0.989, P = 0.007) independently correlated with the occurrence of OSA in HCM patients, respectively. Multiplicative interaction was shown between high BMI and low eGFR on the risk of OSA in HCM patients (OR: 6.050, 95% CI: 1.598, 22.905, P = 0.008). The additive interaction analysis further suggested that 70.1% of HCM patients developed OSA due to the additive interaction between BMI and eGFR. The identification ability of OSA in HCM patients was significantly enhanced by using both BMI and eGFR (area under receiver-operating characteristic analysis curve 0.785; P = 0.000038) as compared with BMI (area under curve 0.683, P = 0.008) or eGFR (area under curve 0.700, P = 0.004), respectively., Conclusion: High BMI or low eGFR independently related to the occurrence of OSA in HCM patients, and the multiplicative and additive interactions between BMI and eGFR increased the identification ability of OSA in HCM patients., Competing Interests: The authors report no conflicts of interest in this work., (© 2022 Zhou et al.)

Exercising was reported by several studies to bring great benefits to heart failure with preserved ejection fraction (HFpEF), which reduced the hospitalization and the mortality of heart failure. However, the underlying mechanism of exercising on HFpEF remains unclear. In the present study, we designed and constructed a device that can perform early passive leg movement (ePLM) in rats and further observed whether treatment of ePLM exerts protective effects on HFpEF of rats. Rats were fed with high salt feed to establish an animal model of pre-clinical diastolic dysfunction (PDD), which would eventually develop into HFpEF, and then treated rats with ePLM. We conducted several experiments to evaluate the conditions of heart and blood vessel. The results show that diastolic functions of heart and blood vessel in rats were significantly improved by treatment of ePLM. We also found that pathological injuries of heart and blood vessel were ameliorated after treatment of ePLM. Moreover, treatment of ePLM decreased the protein levels of Collagen type I, Collagen type III, MMP2, and MMP9 in heart and blood vessel, indicating that cardiac and vascular fibrosis were reduced apparently by treatment of ePLM. Further investigation suggested that treatment of ePLM probably inhibit the activation of TGF-β1/Smad3 signaling pathway as well as promote the activation of Akt/eNOS signaling pathway in high salt diet induced HFpEF. In conclusion, treatment of ePLM alleviated high salt diet induced HFpEF by inhibiting fibrosis via suppressing TGF-β1/Smad3 signaling pathway as well as activating Akt/eNOS signaling pathway, implicating treatment of ePLM as a promising novel non-pharmacological approach for HFpEF., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Liu, Ji, Fu, Zhang, Ji, Liu, Cheng and Dong.)

The Chinese water pine Glyptostrobus pensilis is the sole surviving species of the genus Glyptostrobus . It is endemic to southern China, central Vietnam, and eastern Laos, and today it is nearly extinct in the wild. Forest community characteristics and population structure of G. pensilis in China have remained unknown up to now. We investigated six swamp forest stands and analyzed their forest community characteristics (i.e. vertical stratification, species composition, and diversity) and population structure, including the frequency distribution of DBH (diameter at breast height) and age-classes as found in Fujian Province, southeastern China. The vertical stratifications of all the forest stands were rather simple. The remaining wild specimens ranged from roughly 15 to some 357 years for an average of ca. 85 years, with only a few individuals less than 20 years old. Compared with the stands and populations of G. pensilis in Vietnam, the taxonomic compositions of the stands in the two regions were different, except for the dominant species- G. pensilis . The Shannon-Wiener index showed the overstory of each stand had much lower diversity (0.26 on average) in Fujian Province than that (1.97 on average) in Vietnam, whereas the diversity indices were about the same (around 2.41) for the understories in the two regions. Furthermore, we discovered 18 G. pensilis seedlings at the study sites in Fujian Province. This discovery demonstrates that G. pensilis regeneration is extremely poor and its populations are declining, although these populations are relatively healthier than those in Vietnam.