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Mollisols are rich in organic matter, which makes them suitable for cultivation and for enhancing global food security. Mollisols are experiencing severe soil erosion due to overfarming and a lack of maintenance. Thus, suitable soil and water conservation measures (SWCMs) are needed to protect Mollisols. However, how SWCMs respond to changes in slope gradient and rainfall and their effective application area remain ambiguous. Using a long-term field observation dataset, meta-analysis, and statistical test methods, we reveal the typical erosion reduction effect of SWCMs and their responses to changes in slope gradient and rainfall. Next, we calculated a coupling factor, P·S, by slope gradient and rainfall in flood season to determine the effective SWCMs application threshold. Compared with bare land, no-tillage (NT), contour ridge tillage (CT), ridge hedgerows (RH), and terraced fields (TF) had an average erosion reduction coefficient of 91.5%. There was a significant exponential increase in the correlation between P·Sand the soil erosion amount in plots with typical measures. According to this correlation and soil loss tolerance (200 t/km2), the upper limits of P·S(NT: 564 mm; CT: 885 mm; RH: 1135 mm) were determined and utilized to determine the effective application areas (NT: 311.40 103 km2; CT: 320.86 103 km2; RH: 323.72 103 km2) at the plot scale. In wet years, the applicable area of SWCMs declined toward the low-elevation foothills and flat terrain. All the results are applicable when slope length within 20 m. These results provide a basis for the precise allocation of SWCMs in Mollisols area and promote the scientific utilization of Mollisols resources.

This study aimed to explore the effect of κ-carrageenan on the stability of WSPfrom the muscle of Pinctada martensiiand provide data reference for the use of P. martensiimeat and improvement of the functional properties and application expansion of different types of aquatic proteins.The effect of κ-carrageenan (2 mg/mL)on WSP (1 mg/mL)stability before and after heat treatment (50~100 °C) in the range of pH 5.0~8.0was explored using differential scanning (DSC), Fourier transform infrared spectroscopy (FT-IR) and circular dichroism (CD). Turbidity, ζ-potential, particle size, hydrophobicity, and presence of free sulfhydryl groups and total sulfhydryl groups of WSP and κ-WSPwere measured. Compared with WSP, light transmittance of κ-WSP decreased after heat treatments at various temperatures (50~100 °C) under the same pH conditions, and the difference of transmittance reached maximum at pH 5.0 and 80 °C.DSC showed that the denaturation temperature of κ-WSP was slightly higher (an average increase of 4.4 ± 1.2 °C)than that of WSP except at pH 4.0 and pH 5.5. At pH 5.0, the ζ-potential value of κ-WSP was higher than (an average increase value of 2.7 ± 0.9) that of WSP with lower particle size distribution, and the hydrophobic content of WSP and κ-WSP showed different trends with increasing temperature. The total thiol groups of both WSP and κ-WSP increased with increasing temperature, except the decrease at 100 °C, while the content of free thiol groups of either WSP or κ-WSP did not change significantly.The FT-IR and CD results showed that the electrostatic combination of WSP and κ-carrageenan did not produce new functional groups, and κ-carrageenan significantly affected the secondary structure of WSP under heat treatment in the range of 80~100°C. These results suggest that κ-carrageenan has a protective effect on the thermal denaturation of WSP of pearl shellfish, and this protective effect is most obvious at isoelectric point (pH 5.0).

Oyster hydrolysates exhibit promising potential as a zinc supplement for its significant amounts of zinc, however, the zinc chemical speciation which determines zinc nutrition in oyster hydrolysates has not been investigated. This study optimized the oyster hydrolysis conditions using the Response surface methodology (RSM) method, and the zinc chemical speciation, the sequence of zinc-containing peptides, and the binding sites of zinc and peptides were further investigated. Results showed that inorganic and organic zinc in oysters were 60.15% and 36.53% of total zinc respectively, while organic zinc in oysters aqueous extract was 4.54% of which 3.56% was present in the polysaccharide fraction. The zinc yield was 84.20% of total zinc under optimal hydrolysis conditions, while the organic zinc increased to 52.93% of which 38.14% existed in the protein/peptides fraction. Zinc in protein/peptide fraction primarily was bound to low-molecular-weight peptides (Mw < 1000 Da). Further, 42 shared zinc-containing peptides (mainly 3–4 peptides) were identified. Molecular docking indicated that Glu, Leu, and Tyr might be the binding sites for zinc and peptides. These findings provided a theoretical basis for the development of novel and safe zinc dietary supplements.

Purpose:To investigate the difference in the optic canal diameter between children with autosomal recessive malignant infantile osteopetrosis and normal children, and to assess the influence of hematopoietic stem cell transplantation on the optic canal diameter.Methods:Twenty pediatric patients with malignant infantile osteopetrosis and 22 normal control children were included in this study. Eleven patients with malignant infantile osteopetrosis underwent hematopoietic stem cell transplantation. The measurements included optical canal diameter and flash visual evoked potential. Comparisons of these measurements between patients with malignant infantile osteopetrosis and normal controls as well as before and after hematopoietic stem cell transplantation were performed. The correlation between age and optic canal diameter was analyzed using Pearson correlation analysis.Results:The mean optic canal diameter before hematopoietic stem cell transplantation was 1.65 ± 0.54 mm in patients with malignant infantile osteopetrosis and 3.38 ± 0.60 mm in the control group (The mean optic canal diameter before hematopoietic stem cell transplantation was 1.65 ± 0.54 mm in patients with malignant infantile osteopetrosis and 3.38 ± 0.60 mm in the control group (P< .001). The mean optic canal diameter after hematopoietic stem cell transplantation was 2.72 ± 0.66 mm, which was significantly different from the pre-transplantation measurement (P< .001). The P2 latency for the flash visual evoked potential after hematopoietic stem cell transplantation (152.3 ± 36.4 ms) was significantly less than that before transplantation (165.5 ± 27.7 ms; P= .051). Pearson correlation analysis revealed a significant correlation between age and optic canal diameter (r= 0.722, P< .001).Conclusions:The optic canal was narrower in pediatric patients with malignant infantile osteopetrosis than in age-matched normal controls. This condition can be relieved through hematopoietic stem cell transplantation and the impaired conductibility of the optic nerve can be improved in some cases.[[J Pediatr Ophthalmol Strabismus.2019;56(1):35–42.]

Salinization is one of the most serious land degradation problems facing world. Salinity results in poor plant growth and low soil microbial activity due to osmotic stress and toxic ions. Soil microorganisms play a pivotal role in soils through mineralization of organic matter into plant available nutrients. Therefore it is important to maintain high microbial activity in soils. Salinity tolerant soil microbes counteract osmotic stress by synthesizing osmolytes which allows them to maintain their cell turgor and metabolism. Osmotic potential is a function of the salt concentration in the soil solution and therefore affected by both salinity (measured as electrical conductivity at a certain water content) and soil water content. Soil salinity and water content vary in time and space. Understanding the effect of changes in salinity and water content on soil microorganisms is important for crop production, sustainable land use and rehabilitation of saline soils. In this review, the effects of soil salinity and water content on microbes are discussed to guide future research into management of saline soils.

The main goal of this review is to provide more specific and effective targets for prevention and treatment of insulin resistance and associated atherosclerosis. Modern technologies and medicine have vastly improved human health and prolonged the average life span of humans primarily by eliminating various premature deaths and infectious diseases. The modern technologies have also provided us abundant food and convenient transportation tools such as cars. As a result, more people are becoming overfed and sedentary. People are generally ingesting more calories than their bodies' need, leading to the so-called “positive energy imbalance”, which is inseparable from the development of insulin resistance and its associated atherosclerosis. A direct consequence of insulin resistance is hyperinsulinemia. The current general view is that insulin is not functional properly in the presence of insulin resistance. Thus, the role of insulin itself in the development of insulin resistance and associated atherosclerosis has not been recognized. We have recently observed that the basal level of insulin signaling is increased in the presence of insulin resistance and hyperinsulinemia. In this review, we will explain how the increased basal insulin signaling contributes to the development of insulin resistance and associated atherosclerosis. We will first explain how insulin causes insulin resistance through two arbitrary stages (before and after the presence of obvious insulin resistance), and, then, explain how the excess exposure to insulin and the relative insulin insufficiency contributes to the atherosclerotic diseases. We propose that blockade of the excess insulin signaling is a viable approach to prevent and/or reverse insulin resistance and its associated atherosclerosis.

Type 2 diabetes is associated with insulin resistance, endothelial dysfunction and accelerated atherosclerotic diseases. Though underlying mechanisms remain to be unraveled, p38 mitogen-activated protein kinase (MAPK) appears to play important roles in their pathogenesis. As a member of the MAPK family, it regulates the activities of many transcription factors and proteins/enzymes and thus has a wide-spectrum of biological effects. Patients with insulin resistance and/or type 2 diabetes have high levels of plasma free fatty acids, inflammatory cytokines, and/or glucose, and overactivation of the cardiovascular renin-angiotensin system, all are capable of activating p38 MAPK. p38 MAPK plays a central role in hepatic glucose and lipid metabolism, leading to increased hepatic glucose production and decreased hepatic lipogenesis. The roles of p38 MAPK in insulin-mediated glucose uptake in skeletal muscle and adipose tissue remain controversial. p38 MAPK also mediates inflammatory processes and cell apoptosis. Recent evidence suggests that p38 MAPK may be the key node linking cardiovascular insulin resistance, endothelial dysfunction and the pathogenesis of atherosclerotic diseases through its influences on monocytes/macrophages, vascular endothelial cells, and vascular smooth muscle cells in type 2 diabetes. In addition, p38 MAPK also contributes significantly to cardiac injury during ischemiareperfusion.

The simulation of hyper-concentrated sediment transport is very important in managing rivers with high sediment concentrations. Based on the theory of non-equilibrium transport of non-uniform sediment, a 1-D mathematical model is developed to simulate long-term and long-distance sediment transport and channel bed variation for both ordinary and hyper-concentrated flows. The model considers the effect of lateral inflow on flow movement by adding an extra term in the momentum equation. Also considered is the effect of high concentration on the flow density, sediment settling velocity and particle volume. The coefficients used in the model can be easily estimated by data analyses and empirical expressions. Therefore the uncertainty in finding coefficients may be avoided and the applicability is greatly increased. The use of a general formula for sediment-carrying capacity insures the model is capable of simulating sediment transport in both low- and hyper-concentrated flows. After calibration and verification by using large quantities of measured data from the Yellow River and Weihe River, the model is finally used to satisfactorily simulate the channel bed variation processes in the lowerYellow River since the operation of the Xiaolangdi Reservoir.

Current evidence suggests that uncoupling protein-2 (UCP2) is a regulator of insulin secretion. It is also known that chronic exposure of pancreatic islets to free fatty acids (FFAs) blunts glucose-stimulated insulin secretion and is accompanied by elevated levels of UCP2. However, the mechanisms regulating expression of UCP2 in beta-cells are unknown. Here, we show that UCP2 mRNA and protein levels were increased after a 48-h exposure of INS-1(832/13) beta-cells to oleic acid (0.5 mm) by activation of the UCP2 promoter. Furthermore, progressive deletions of the mouse UCP2 promoter (from -7.3 kb to +12 bp) indicated that an enhancer region (-86/-44) was responsible for both basal and FFA-stimulated UCP2 gene transcription. This enhancer contains tightly clustered Sp1, sterol regulatory element (SRE), and double E-Box elements. While all three sequence motifs were required for basal activity of the UCP2 promoter, the mutations in either the SRE or the E-Box elements eliminated the response to FFAs. The SRE and sterol regulatory element binding protein-1 (SREBP1) appear to be crucial for the response of the UCP2 gene to FFAs, since overexpression of the nuclear forms of the SREBPs increased UCP2 promoter activity by 7-10-fold and restored the ability of E-Box mutants to respond to oleic acid. These data support a model in which SREBP is the major modulator of UCP2 gene transcription by FFA, while E-Box binding factors play a supportive role.

Interest in the biology of adipose tissue has undergone a revival in recent years with the discovery of a host of genes that contribute to the regulation of satiety and metabolic rate. The catecholamines have long been known to be key modulators of adipose tissue lipolysis and the hydrolysis of triglyceride energy stores. However, more recent efforts to understand the role of Individual adrenergic receptor subtypes expressed in adipocytes and their signal transduction pathways have revealed a complexity not previously appreciated. Combined with this interest in the modulation of adipocyte metabolism is a renewed focus upon brown adipose tissue and the mechanisms of whole body thermogenesis in general. The discovery of novel homologs of the brown fat uncoupling protein (UCP) such as UCP2 and UCP3 has provoked intensive study of these mitochondrial proteins and the role that they play in fuel metabolism. The story of the novel UCPs has proven to be intriguing and still incompletely understood. Here, we review the status of adipose tissue from inert storage depot to endocrine organ, Interesting signal transduction pathways triggered by β-adrenergic receptors in adipocytes, the potential of these receptors for discriminating and coordinated metabolic regulation, and current views on the role of UCP2 and UCP3 based on physiological studies and gene knockout models.

Because of increasing evidence that G protein-coupled receptors activate multiple signaling pathways, it becomes important to determine the coordination of these pathways and their physiological significance. Here we show that the β3-adrenergic receptor (β3AR) stimulates p38 mitogen-activated protein kinase (p38 MAPK) via PKA in adipocytes and that cAMP-dependent transcription of the mitochondrial uncoupling protein 1 (UCP1) promoter by β3AR requires p38 MAPK. The selective β3AR agonist CL316,243 (CL) stimulates phosphorylation of MAP kinase kinase 3/6 and p38 MAPK in a time- and dose-dependent manner in both white and brown adipocytes. Isoproterenol and forskolin mimicked the effect of CL on p38 MAPK. In all cases activation was blocked by the specific p38 MAPK inhibitor SB202190 (SB; 1–10 µm). The involvement of PKA in β3AR-dependent p38 MAPK activation was confirmed by the ability of the PKA inhibitors H89 (20 µm) and (Rp)-cAMP-S (1 mm) to block phosphorylation of p38 MAPK. Treatment of primary brown adipocytes with CL or forskolin induced the expression of UCP1 mRNA levels (6.8- ± 0.8-fold), and this response was eliminated by PKA inhibitors and SB202190. A similar stimulation of a 3.7-kilobase UCP1 promoter by CL and forskolin was also completely inhibited by PKA inhibitors and SB202190, indicating that these effects on UCP1 expression are transcriptional. Moreover, the PKA-dependent transactivation of the UCP1 promoter, as well as its sensitivity to SB202190, was fully reproduced by a 220-nucleotide enhancer element from the UCP1 gene. We similarly observed that increased phosphorylation of ATF-2 by CL was sensitive to both H89 and SB202190, while phosphorylation of cAMP-response element-binding protein was inhibited only by H89. Together, these studies illustrate that p38 MAPK is an important downstream target of the β-adrenergic/cAMP/PKA signaling pathway in adipocytes, and one of the functional consequences of this cascade is stimulation of UCP1 gene expression in brown adipocytes.

Critical protein-protein interactions among pre-mRNA splicing factors determine splicing efficiency and specificity. The serine/arginine proteins, a family of factors characterized by the presence of an RNA recognition motif and an arginine/serine domain, are essential for constitutive splicing and required for some alternative splicing decisions. ASF/SF2, SC35, and other members of the serine/arginine family, interact with the 70k protein of the U1 small nuclear ribonucleoprotein. The binding of this protein with ASF/SF2 is thought to enhance recognition of the 5′ splice site of pre-mRNAs by the U1 small nuclear ribonucleoprotein. It has been clearly documented that the arginine/serine domain of ASF/SF2 is responsible for binding to the U1 70k protein. In this manuscript we characterize the segment in the human U1 70k protein that is both necessary and sufficient for ASF/SF2 binding. A domain within this segment, which begins with Arg240and ends with Asp270, was shown to bind specifically to the arginine/serine domain of ASF/SF2 using a yeast two-hybrid system and a far Western assay. Mutational analysis of this segment suggested that several arginines are critical for the interaction with ASF/SF2 and for phosphorylation by SRPK1. Inspection of the sequence of the Arg248to Asp270region suggested this as an arginine/serine-like domain in U1 70k protein, and the data presented in this manuscript strongly support this view. Inspection of the human U1 70k protein sequence, comparison with homologues in other animal species, and mutational analysis indicated the importance of the sequence Arg-Arg-Arg-Ser-Arg-Ser-Arg-Asp, which is found repeated twice in the region from Arg248to Asp270in the human protein.

The purpose of this study was to evaluate the functional and cosmetic outcomes of a new modified Fox pentagon technique performed using polytetrafluoroethylene in frontalis suspension surgery for blepharophimosis syndrome. This retrospective study enrolled 40 patients diagnosed with blepharophimosis syndrome from March 2016 to October 2018. All patients underwent frontalis suspension using a new modified Fox pentagon technique. The functional and cosmetic outcomes were evaluated. After the operation, the mean palpebral fissure height increased from 2.68 to 6.93 in right eyes and from 2.73 to 6.98 in left eyes. The mean MRD1 increased from 0.53 to 3.76 in right eyes and from 0.50 to 3.78 in left eyes. While preoperative to postoperative differences were statistically significant (p< 0.01), there were no significant differences between right and left eyes either before or after the surgery (p> 0.01). All patients achieved good cosmetic results with an average score of 0.6. We have experimentally created a modified Fox pentagon technique performed using a polytetrafluoroethylene sling in a frontalis suspension to treat BPES; this approach yielded favorable cosmetic and functional outcomes.

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