Integrating proximal soil sensing data and environmental variables to enhance the prediction accuracy for soil salinity and sodicity in a region of Xinjiang Province, China.

Soil salinization and sodification, the primary causes of land degradation and desertification in arid and semi-arid regions, demand effective monitoring for sustainable land management. This study explores the utility of partial least square (PLS) latent variables (LVs) derived from visible and near-infrared (Vis-NIR) spectroscopy, combined with remote sensing (RS) and auxiliary variables, to predict electrical conductivity (EC) and sodium absorption ratio (SAR) in northern Xinjiang, China. Using 90 soil samples from the Karamay district, machine learning models (Random Forest, Support Vector Regression, Cubist) were tested in four scenarios. Modeling results showed that RS and Land use alone were unreliable predictors, but the addition of topographic attributes significantly improved the prediction accuracy for both EC and SAR. The incorporation of PLS LVs derived from Vis-NIR spectroscopy led to the highest performance by the Random Forest model for EC (CCC = 0.83, R2 = 0.80, nRMSE = 0.48, RPD = 2.12) and SAR (CCC = 0.78, R2 = 0.74, nRMSE = 0.58, RPD = 2.25). The variable importance analysis identified PLS LVs, certain topographic attributes (e.g., valley depth, elevation, channel network base level, diffuse insolation), and specific RS data (i.e., polarization index of VV + VH) as the most influential predictors in the study area. This study affirms the efficiency of Vis-NIR data for digital soil mapping, offering a cost-effective solution. In conclusion, the integration of proximal soil sensing techniques and highly relevant topographic attributes with the RF model has the potential to yield a reliable spatial model for mapping soil EC and SAR. This integrated approach allows for the delineation of hazardous zones, which in turn enables the consideration of best management practices and contributes to the reduction of the risk of degradation in salt-affected and sodicity-affected soils.

IP3R2-mediated Ca2+ release promotes LPS-induced cardiomyocyte pyroptosis via the activation of NLRP3/Caspase-1/GSDMD pathway.

Pyroptosis plays a crucial role in sepsis, and the abnormal handling of myocyte calcium (Ca2+) has been associated with cardiomyocyte pyroptosis. Specifically, the inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) is a Ca2+ release channel in the endoplasmic reticulum (ER). However, the specific role of IP3R2 in sepsis-induced cardiomyopathy (SIC) has not yet been determined. Thus, this study aimed to investigate the underlying mechanism by which IP3R2 channel-mediated Ca2+ signaling contributes to lipopolysaccharide (LPS)-induced cardiac pyroptosis. The SIC model was established in rats by intraperitoneal injection of LPS (10 mg/kg). Cardiac dysfunction was assessed using echocardiography, and the protein expression of relevant signaling pathways was analyzed using ELISA, RT-qPCR, and western blot. Small interfering RNAs (siRNA) and an inhibitor were used to explore the role of IP3R2 in neonatal rat cardiomyocytes (NRCMs) stimulated by LPS in vitro. LPS-induced NLRP3 overexpression and GSDMD-mediated pyroptosis in the rats' heart. Treatment with the NLRP3 inhibitor MCC950 alleviated LPS-induced cardiomyocyte pyroptosis. Furthermore, LPS increased ATP-induced intracellular Ca2+ release and IP3R2 expression in NRCMs. Inhibiting IP3R activity with xestospongin C (XeC) or knocking down IP3R2 reversed LPS-induced intracellular Ca2+ release. Additionally, inhibiting IP3R2 reversed LPS-induced pyroptosis by suppressing the NLRP3/Caspase-1/GSDMD pathway. We also found that ER stress and IP3R2-mediated Ca2+ release mutually regulated each other, contributing to cardiomyocyte pyroptosis. IP3R2 promotes NLRP3-mediated pyroptosis by regulating ER Ca2+ release, and the mutual regulation of IP3R2 and ER stress further promotes LPS-induced pyroptosis in cardiomyocytes.

High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy.

Mitochondrial dysfunction and impaired Ca2+ handling are involved in the development of diabetic cardiomyopathy (DCM). Dynamic relative protein 1 (Drp1) regulates mitochondrial fission by changing its level of phosphorylation, and the Orai1 (Ca2+ release-activated calcium channel protein 1) calcium channel is important for the increase in Ca2+ entry into cardiomyocytes. We aimed to explore the mechanism of Drp1 and Orai1 in cardiomyocyte hypertrophy caused by high glucose (HG). We found that Zucker diabetic fat rats induced by administration of a high-fat diet develop cardiac hypertrophy and impaired cardiac function, accompanied by the activation of mitochondrial dynamics and calcium handling pathway-related proteins. Moreover, HG induces cardiomyocyte hypertrophy, accompanied by abnormal mitochondrial morphology and function, and increased Orai1-mediated Ca2+ influx. Mechanistically, the Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1) prevents cardiomyocyte hypertrophy induced by HG by reducing phosphorylation of Drp1 at serine 616 (S616) and increasing phosphorylation at S637. Inhibition of Orai1 with single guide RNA (sgOrai1) or an inhibitor (BTP2) not only suppressed Drp1 activity and calmodulin-binding catalytic subunit A (CnA) and phosphorylated-extracellular signal-regulated kinase (p-ERK1/2) expression but also alleviated mitochondrial dysfunction and cardiomyocyte hypertrophy caused by HG. In addition, the CnA inhibitor cyclosporin A and p-ERK1/2 inhibitor U0126 improved HG-induced cardiomyocyte hypertrophy by promoting and inhibiting phosphorylation of Drp1 at S637 and S616, respectively. In summary, we identified Drp1 as a downstream target of Orai1-mediated Ca2+ entry, via activation by p-ERK1/2-mediated phosphorylation at S616 or CnA-mediated dephosphorylation at S637 in DCM. Thus, the Orai1-Drp1 axis is a novel target for treating DCM.

The enhancement of TXA2 receptors-mediated contractile response in intrarenal artery dysfunction in type 2 diabetic mice.

Thromboxane A2 (TXA2) has been implicated in the pathogenesis of diabetic vascular complications, although the underlying mechanism remains unclear. The present study investigated the alterations in TXA2 receptor signal transduction in type 2 diabetic renal arteries. The contraction of renal arterial rings in control (db/m+) mice and type 2 diabetic (db/db) mice was measured by a Multi Myograph System. Intracellular calcium concentration ([Ca2+]i) in vascular smooth muscle cells was measured by Fluo-4/AM dye and confocal laser scanning microscopy. Quantitative real-time PCR and Western blot analysis were used to determine gene and protein expression levels, respectively. A stable TXA2 mimic U46619 caused markedly stronger dose-dependent contractions in the renal arteries of db/db mice than in those of db/m+ mice. This response was completely blocked by a TXA2 receptor antagonist GR32191 and significantly inhibited by U73122. U46619-induced vasoconstriction was increased in the presence of nifedipine in db/db mice compared with that in db/m+ mice, whereas the response to U46619 did not differ between the two groups in the presence of SKF96365. Sarcoplasmic reticulum Ca2+ release-mediated and CaCl2-induced contractions did not differ between the two groups. In db/db mice, store-operated Ca2+(SOC) entry-mediated contraction in the renal arteries and SOC entry-mediated Ca2+ influx in smooth muscle cells were significantly increased. And the gene and protein expressions of TXA2 receptors, Orai1 and Stim1 were upregulated in the diabetic renal arteries. Therefore the enhancement of U46619-induced contraction was mediated by the upregulation of TXA2 receptors and downstream signaling in the diabetic renal arteries.

Hypertonic saline alleviates cerebral edema by inhibiting microglia-derived TNF-α and IL-1ß-induced Na-K-Cl Cotransporter up-regulation.

BACKGROUND: Hypertonic saline (HS) has been successfully used clinically for treatment of various forms of cerebral edema. Up-regulated expression of Na-K-Cl Cotransporter 1 (NKCC1) and inflammatory mediators such as tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß) has been demonstrated to be closely associated with the pathogenesis of cerebral edema resulting from a variety of brain injuries. This study aimed to explore if alleviation of cerebral edema by 10% HS might be effected through down-regulation of inflammatory mediator expression in the microglia, and thus result in decreased NKCC1 expression in astrocytes in the cerebral cortex bordering the ischemic core. METHODS: The Sprague-Dawley (SD) rats that underwent right-sided middle cerebral artery occlusion (MCAO) were used for assessment of NKCC1, TNF-α and IL-1ß expression using Western blotting, double immunofluorescence and real time RT-PCR, and the model also was used for evaluation of brain water content (BWC) and infarct size. SB203580 and SP600125, specific inhibitors of the p38 and JNK signaling pathways, were used to treat primary microglia cultures to determine whether the two signaling pathways were required for the inhibition of HS on microglia expressing and secreting TNF-α and IL-1ß using Western blotting, double immunofluorescence and enzyme-linked immunosorbent assay (ELISA). The effect of TNF-α and IL-1ß on NKCC1 expression in primary astrocyte cultures was determined. In addition, the direct inhibitory effect of HS on NKCC1 expression in primary astrocytes was also investigated by Western blotting, double immunofluorescence and real time RT-PCR. RESULTS: BWC and infarct size decreased significantly after 10% HS treatment. TNF-α and IL-1ß immunoexpression in microglia was noticeably decreased. Concomitantly, NKCC1 expression in astrocytes was down-regulated. TNF-α and IL-1ß released from the primary microglia subjected to hypoxic exposure and treatment with 100 mM HS were decreased. NKCC1 expression in primary astrocytes was concurrently and progressively down-regulated with decreasing concentration of exogenous TNF-α and IL-1ß. Additionally, 100 mM HS directly inhibited NKCC1 up-regulation in astrocytes under hypoxic condition. CONCLUSIONS: The results suggest that 10% HS alleviates cerebral edema through inhibition of the NKCC1 Cotransporter, which is mediated by attenuation of TNF-α and IL-1ß stimulation on NKCC1.

A comparative study on the efficacy of 10% hypertonic saline and equal volume of 20% mannitol in the treatment of experimentally induced cerebral edema in adult rats.

BACKGROUND: Hypertonic saline and mannitol are commonly used in the treatment of cerebral edema and elevated intracranial pressure (ICP) at present. In this connection, 10% hypertonic saline (HS) alleviates cerebral edema more effectively than the equal volume of 20% mannitol. However, the exact underlying mechanism for this remains obscure. This study aimed to explore the possible mechanism whereby 10% hypertonic saline can ameliorate cerebral edema more effectively than mannitol. RESULTS: Adult male Sprague-Dawley (SD) rats were subjected to permanent right-sided middle cerebral artery occlusion (MCAO) and treated with a continuous intravenous infusion of 10% HS, 20% mannitol or D-[1-3H(N)]-mannitol. Brain water content (BWC) as analyzed by wet-to-dry ratios in the ischemic hemisphere of SD rats decreased more significantly after 10% HS treatment compared with 20% mannitol. Concentration of serum Na+ and plasma crystal osmotic pressure of the 10% HS group at 2, 6, 12 and 18 h following permanent MCAO increased significantly when compared with 20% mannitol treated group. Moreover, there was negative correlation between the BWC of the ipsilateral ischemic hemisphere and concentration of serum Na+, plasma crystal osmotic pressure and difference value of concentration of serum Na+ and concentration of brain Na+ in ipsilateral ischemic hemisphere in the 10% HS group at the various time points after MCAO. A remarkable finding was the progressive accumulation of mannitol in the ischemic brain tissue. CONCLUSIONS: We conclude that 10% HS is more effective in alleviating cerebral edema than the equal volume of 20% mannitol. This is because 10% HS contributes to establish a higher osmotic gradient across BBB and, furthermore, the progressive accumulation of mannitol in the ischemic brain tissue counteracts its therapeutic efficacy on cerebral edema.

[Relationship between flash visual evoked potential and severity and prognosis in critically ill patients].

OBJECTIVE: To explore the relationship between flash visual evoked potential (fVEP) and severity and prognosis in critically ill patients in intensive care unit (ICU). METHODS: Sixty-nine critically ill patients were divided into two groups according to survival (35 cases) or death (34 cases) in 28 days. fVEP, Glasgow coma scale (GCS) score, acute physiology and chronic health evaluation II (APACHE II) score and sepsis-related organ failure assessment (SOFA) score of survivors were compared with those of nonsurvivors. Also, according to primary disease, the patients were divided into a group of patients with primary intracranial disease and patients with mental disturbance but without primary intracranial lesion. Above mentioned indexes were compared, and clinical outcome was predicted with their correlation with fVEP in each patient. RESULTS: The latent period of fVEP peak appeared later in nonsurvivors than those in survivors [(228.6+/-41.7) ms vs. (190.5+/-49.2) ms, P<0.01]. APACHE II score (25.9+/-6.4 vs. 22.5+/-6.7) and SOFA score (6.7+/-2.0 vs. 5.4+/-2.5) were higher in nonsurvivors than those in survivors (both P<0.05 ), while the changes in GCS score was in contrary (6.3+/-2.4 vs. 7.0+/-3.0, P<0.05). fVEP peak latency showed a negative correlation with GCS score (r=-0.332, P<0.01). The death rate of the group of patients with primary intracranial lesion was similar to that of the total. fVEP peak latency of the group with no primary intracranial lesion but with mental impairment in nonsurvivors was significantly longer than that of survivors [(226.0+/-46.7) ms vs. (168.8+/-54.1) ms, P<0.05], fVEP peak latency was positively correlated with SOFA score (r=0.526, P<0.05). Area under receiver operator characteristic (ROC) curve of fVEP peak latency was 0.800+/-0.104 (P<0.05) for predicting outcome of patients, while that of SOFA score was 0.650+/-0.131 (P>0.05). The former could be used for predicting death. CONCLUSION: fVEP reflects the prognosis and severity of critically ill patients in ICU. Especially, it maybe used as a tool for predicting death and multiple organ dysfunction syndrome (MODS) in the patients with no primary intracranial lesion but with mental impairment.

[Influence of different treatment patterns on cost-effectiveness in treatment of acute myocardial infarction].

OBJECTIVE: To investigate the influences of different treatment patterns on the cost-effectiveness in treating acute myocardial infarction (AMI). METHODS: Data about referral of AMI patients who called for help because of chest pain to the nearby hospitals from October 2003 to December 2005 were collected from the Guangzhou 120 Call Center. All these patients were followed up 6 months after discharge to survey the cost during hospitalization, major treatment, prognosis (death, re-infarction, stroke etc. ), and secondary prevention for coronary heart disease. We used SF-36 scale was used to quantify the health status. RESULTS: 101 AMI patients referred to grade 2 A hospitals (Group A) and 137 patients referred to grade 3 A hospitals (Group B) were successfully followed up. The cost during hospitalization of Group B was (33965 +/- 963) yuan RMB, significantly higher than that of Group A (18943 +/- 893) yuan, P = 0.021). 11 patients of Group B died, and 5 patients suffered from stroke with the mortality and stroke rate both significantly lower than those of Group A (18/101 and 12/101, P = 0.022, P = 0.015). There was no significant difference in the re-infarction rate between the 2 groups. The scores in physical function, general health status, vitality, social function, role-emotional, mental health of Group B were all significantly higher than those of Group A (all P < 0.05) , however, there were not significant differences in body pain and role-physical between these 2 groups. The smoking cessation rate, specialist outpatient department follow-up rate, statins use rate of Group B were significantly higher than those of Group A (P = 0.017, P = 0.016, P = 0.038). CONCLUSION: The 120-grade 3 A hospital CCU pattern is more cost-effective in treatment of AMI.

[The feasibility study of using the dual stylet method as a bedside measure in facilitating insertion of the spiral distal end nasal-enteral feeding tube in critically ill patients].

OBJECTIVE: To evaluate the feasibility of using the dual stylet method as a bedside measure after unsuccessful of the spiral distal end nasal-enteral feeding tubes into the duodenum in critically ill patients. METHODS: Spiral distal end nasal-enteral feeding tubes were introduced into the stomach of 50 critically ill patients but unable to pass through the pylorus from July 2005 to March 2007. Under electrocardiographic monitoring, the dual stylet method was used as a bedside measure to facilitate the passage. The duration, successful ratio, and complication of the procedure were recorded. RESULTS: This procedure took an average time of (24.5+/-4.9) minutes. The success rate of passing through the pylorus was 82.0% (41/50). The success rate of the latter 25 cases treated from July 2006 to March 2007 was significantly higher than that of the former 25 cases treated from July 2005 to July 2006 [96.0% (24/25) vs. 68.0% (17/25), P<0.05]. The average insertion distance of the 41 successful cases was (85.3+/-2.9)cm. Heart rate(HR) during the procedure was (116.7+/-18.5) beats per minute, that before insertion was (107.6+/-14.2) beats per minute (P<0.01), respiratory rate (RR) was (22.4+/-4.6)breaths per minute during the procedure and (21.3+/-3.9)breaths per minute (P<0.01) before the procedure and mean arterial pressure (MAP) (86.7+/-10.7) mm Hg during and (82.0+/-7.7)mm Hg (1 mm Hg=0.133 kPa, P<0.01) before the procedure. But there was no change in arterial oxygen saturation (SaO(2)). No severe complication was noted. CONCLUSION: The dual stylet method can be used effectively and safely in critically ill patients as a bedside measure after placement of the spiral distal end nasal-enteral feeding tubes.

[Use W303-1A/hER-ERE-Lac Z to determine estrogenic compounds in traditional Chinese materia medica].

OBJECTIVE: To study the content of phytoestrogen in dissimilarity herbs. METHOD: The activity of phytoestrogen in heat-clearing drugs, drugs for relieving exterior syndrome, diuretic, anastaltics, tonics and astringents were detected based on the recombinant yeast cell (W303-1A/hER-ERE-Lac Z). The estrogenic activity in traditional Chinese materia medica were assayed quantitatively by determining the expression of beta-galactosidase. RESULT: The phytoestrogen concentration (6.35 x 10(-3) nmol x g(-1) E2 equivalent) in heat-clearing drugs was the highest while that in anastaltic and tonic drugs was the lowest, which was less than the detected limit. CONCLUSION: Compared with the other traditional Chinese materia medica, the content of phytoestrogen, which can bind to estrogen receptor, in giant knotweed rhizome, forsythia suspense, ash bark, baical skullcap root and ophiopogonis tuber were higher.