Contamination and Translocation of Deoxynivalenol and Its Derivatives Associated with Fusarium Crown Rot of Wheat in Northern China.

Fusarium crown rot (FCR) is one of the most important wheat diseases in northern China. The main causal agent of FCR, Fusarium pseudograminearum, can produce mycotoxins such as type B trichothecenes. Therefore, FCR could be an additional source of mycotoxin contamination during wheat production. Field inoculation experiments demonstrated that FCR disease severity strongly impacts the distribution pattern of trichothecenes in different wheat tissues. Mycotoxins were mainly observed in lower internodes, and a low amount was detected in the upper parts above the fourth internode. However, high levels of trichothecene accumulation were detected in the upper segments of wheat plants under field conditions, which would threaten the feed production. The variation of mycotoxin content among sampling sites indicated that besides disease severity, other factors like climate, irrigation, and fungicide application may influence the mycotoxin accumulation in wheat. A comprehensive survey of deoxynivalenol (DON) and its derivatives in wheat heads with FCR symptoms in natural fields was conducted at 80 sites in seven provinces in northern China. Much higher levels of mycotoxin were observed compared with inoculation experiments. The mycotoxin content varied greatly among sampling sites, but no significant differences were observed if compared at province level, which indicated the variation is mainly caused by local conditions. Trace amounts of mycotoxin appeared to be translocated to grains, which revealed that FCR infection in natural fields poses a relatively small threat to contamination of grains but a larger one to plant parts that may be used as animal feed. To our knowledge, this is the first report of trichothecene accumulation in wheat stems and heads, as well as grains after FCR infection in natural field conditions. These investigations provide novel insights into food and feed safety risk caused by FCR in northern China.

A Novel ZRS Mutation in a Chinese Patient with Preaxial Polydactyly and Triphalangeal Thumb.

Preaxial polydactyly (PPD; OMIM 603596), which is characterized as having supernumerary fingers, is an unusual congenital hand abnormality. Triphalangeal thumb (TPT; OMIM 190600) is identified by an extra phalangeal bone and is often found in association with PPD. When in combination, the disease is referred to as PPD type II (PPD II; OMIM 174500). Previous studies have demonstrated that variations in the zone of polarizing activity regulatory sequence (ZRS; chr7:156,583,796-156,584,569; hg19) region are associated with PPD II. In this study, our patient was diagnosed with PPD II, having bilateral thumb duplication and unilateral TPT (on the right hand). Further investigation of possible causative genes identified a de novo heterozygous ZRS mutation (ZRS 428T>A). This novel mutation was neither found in 200 normal controls nor reported in online databases. Moreover, the bioinformatics program Genomic Evolutionary Rate Profiling (GERP) revealed this site (ZRS428) to be evolutionarily highly conserved, and the 428T>A point mutation was predicted to be deleterious by MutationTaster. In conclusion, the affected individual shows bilateral thumb duplication, but unilateral TPT making this case special. Thus, our findings not only further support the important role of ZRS in limb morphogenesis and expand the spectrum of ZRS mutations, but also emphasize the significance of genetic diagnosis and counseling of families with digit number and identity alterations as well.

[Advances in haustoria function of plants obligate parasite-A review].

Haustoria, one of the fundamental characteristics of obligate parasite, is a micro-branch produced by biotrophic fungi and oomycetes, which is composed of haustorial body, extrahaustorial matrix and extrahaustorial membrane. It is an abnormal structure that can invade the host cell interaction with the plant. Haustoria is not only the key factor of biotrophic fungi carrying on the living specimen nutrition way but also represents significant roles in the nutrition biosynthesis and inhibiting the defense reaction of host. The deeper understanding of haustoria will favor us acquaint obligate parasite enormously, so that we can control the corresponding diseases better. This paper summarized the function on nutrition and pathogenicity of haustoria, and the problems and the research trend in this area were discussed.

Silver-catalyzed ring-opening strategy for the synthesis of ß- and γ-fluorinated ketones.

A regioselective synthesis of ß- and γ-fluorinated ketones via silver-catalyzed ring opening is described. A variety of ß- and γ-fluorinated ketones are efficiently prepared, respectively, from tertiary cyclopropanol and cyclobutanol precursors, providing a straightforward approach for the introduction of a fluorine atom into complex molecules. Preliminary mechanistic studies suggest that a radical-mediated sequential C-C bond cleavage and C-F bond formation pathway is involved.

Reliable Fusion of Stereo Matching and Depth Sensor for High Quality Dense Depth Maps.

Depth estimation is a classical problem in computer vision, which typically relies on either a depth sensor or stereo matching alone. The depth sensor provides real-time estimates in repetitive and textureless regions where stereo matching is not effective. However, stereo matching can obtain more accurate results in rich texture regions and object boundaries where the depth sensor often fails. We fuse stereo matching and the depth sensor using their complementary characteristics to improve the depth estimation. Here, texture information is incorporated as a constraint to restrict the pixel's scope of potential disparities and to reduce noise in repetitive and textureless regions. Furthermore, a novel pseudo-two-layer model is used to represent the relationship between disparities in different pixels and segments. It is more robust to luminance variation by treating information obtained from a depth sensor as prior knowledge. Segmentation is viewed as a soft constraint to reduce ambiguities caused by under- or over-segmentation. Compared to the average error rate 3.27% of the previous state-of-the-art methods, our method provides an average error rate of 2.61% on the Middlebury datasets, which shows that our method performs almost 20% better than other "fused" algorithms in the aspect of precision.

Analysis of the risk factors for central lymph-node metastasis of cN0 papillary thyroid microcarcinoma: A retrospective study.

OBJECTIVE: Cervical lymph node (CLN) metastasis (CLNM) can be found in some patients with CLN-negative (cN0) papillary thyroid microcarcinoma (PTMC), while the risk factors are still unknown. This study aimed to examine the risk factors of CLNM in patients with cN0 PTMC, contributing to screening cN0 PTMC patients with high risk in CLNM for preventive CLN dissection (CLND). METHODS: This retrospective study included consecutive patients pathologically diagnosed with cN0 PTMC and who underwent surgery at the General Surgery Department of China-Japan Friendship Hospital between 07/2016 and 01/2020. The patients were grouped according to whether CLNM was present. Factors associated with CLNM were analyzed, and a risk prediction model was established in logistic regression analysis, and their predictive power was evaluated by receiver operating characteristic curves (ROC). RESULTS: Finally, 171 patients were included; among them, 71 (41.5%) had CLNM. There were 32 males and 139 females. The multivariable analysis showed that males (OR = 5.619, 95%CI: 2.186-14.446; P < 0.001), age ≤45 years (OR = 2.982, 95%CI: 1.446-6.151; P = 0.003), adjacent to dorsal membrane (OR = 3.022, 95%CI: 1.430-6.387; P = 0.004), and irregular borders (OR = 4.332, 95%CI: 1.104-17.000; P = 0.036) were independent risk factors of CLNM. The risk prediction model composed of the four risk factors showed a relatively high AUC, at 0.760. When the cut-off was 0.38, the sensitivity was 67.6%, and the specificity was 73.0%. CONCLUSION: Male sex, age ≤45 years, adjacent to dorsal membranes, and irregular borders are independent risk factors for CLNM in patients with cN0 PTMC. This might help identify cN0 PTMC patients needing preventive CLND.

Effect of calcium supplementation on severe hypocalcemia in patients with secondary hyperparathyroidism after total parathyroidectomy.

BACKGROUND: Severe hypocalcemia (SH) is a dreaded complication of total parathyroidectomy (TPTX) without auto-transplantation. AIM: To compare conventional and preventive calcium supplementation (CS) regimens in terms of SH occurrence after TPTX. METHODS: This retrospective study included patients who underwent TPTX between January 2015 and May 2018 at the China-Japan Friendship Hospital. From January 2015 to May 2016, conventional CS was performed in patients who underwent TPTX, with calcium amounts adjusted according to postoperative serum calcium levels. From October 2016 to May 2018, preventive CS was performed according to preoperative alkaline phosphatase (ALP) levels. The patients were defined as low-risk (ALP < 500 U/L) and high-risk (ALP > 500 U/L) for SH. All preoperative blood samples were collected in the fasting state on the day before surgery. Postoperative blood samples were obtained at 6-7 AM from the first postoperative day. RESULTS: A total of 271 patients were included. These patients were 47.7 ± 11.1 years old, and 57.6% were male. Their mean body mass index (BMI) was 22.9 ± 3.8 kg/m2. There were no significant differences in sex, age, BMI, preoperative ALP, serum calcium, serum phosphorus, calcium-phosphorus ratio, and intact parathyroid hormone (iPTH) between the two CS groups. Compared with conventional CS, preventive CS led to lower occurrence rates of hypocalcemia within 48 h (46.0% vs 74.5%, P < 0.001) and SH (31.7% vs 64.1%, P < 0.001). Multivariable analysis showed that preoperative iPTH levels [odds ratio (OR) = 1.001, 95% confidence interval (CI): 1.000-1.001, P = 0.009), preoperative ALP amounts (OR = 1.002, 95%CI: 1.001-1.003, P = 0.002), preoperative serum phosphorus levels (OR = 8.729, 95%CI: 1.518-50.216, P = 0.015) and preventive CS (OR = 0.132, 95%CI: 0.067-0.261, P < 0.001) were independently associated with SH. In patients with preoperative ALP ≥ 500 U/L, only preventive CS (OR = 0.147, 95%CI: 0.038-0.562. P = 0.005) was independently associated with SH. CONCLUSION: This study suggests that preventive CS could reduce the occurrence of SH, indicating its critical value for hypocalcemia after TPTX.

Antihypertensive effects of selective prostaglandin E2 receptor subtype 1 targeting.

Clinical use of prostaglandin synthase-inhibiting NSAIDs is associated with the development of hypertension; however, the cardiovascular effects of antagonists for individual prostaglandin receptors remain uncharacterized. The present studies were aimed at elucidating the role of prostaglandin E2 (PGE2) E-prostanoid receptor subtype 1 (EP1) in regulating blood pressure. Oral administration of the EP1 receptor antagonist SC51322 reduced blood pressure in spontaneously hypertensive rats. To define whether this antihypertensive effect was caused by EP1 receptor inhibition, an EP1-null mouse was generated using a "hit-and-run" strategy that disrupted the gene encoding EP1 but spared expression of protein kinase N (PKN) encoded at the EP1 locus on the antiparallel DNA strand. Selective genetic disruption of the EP1 receptor blunted the acute pressor response to Ang II and reduced chronic Ang II-driven hypertension. SC51322 blunted the constricting effect of Ang II on in vitro-perfused preglomerular renal arterioles and mesenteric arteriolar rings. Similarly, the pressor response to EP1-selective agonists sulprostone and 17-phenyltrinor PGE2 were blunted by SC51322 and in EP1-null mice. These data support the possibility of targeting the EP1 receptor for antihypertensive therapy.

Stimuli-Responsive Polysaccharide Enveloped Liposome for Targeting and Penetrating Delivery of survivin-shRNA into Breast Tumor.

Silencing the inhibitor of apoptosis (IAP) by RNAi is a promising method for tumor therapy. One of the major challenges lies in how to sequentially overcome the system barriers in the course of the tumor targeting delivery, especially in the tumor accumulation and penetration. Herein we developed a novel stimuli-responsive polysaccharide enveloped liposome carrier, which was constructed by layer-by-layer depositing redox-sensitive amphiphilic chitosan (CS) and hyaluronic acid (HA) onto the liposome and then loading IAP inhibitor survivin-shRNA gene and permeation promoter hyaluronidase (HAase) sequentially. The as-prepared HA/HAase/CS/liposome/shRNA (HCLR) nanocarrier was verified to be stable in blood circulation due to the negative charged HA shield. The tumor targeting recognition and the enhanced tumor accumulation of HCLR were visualized by fluorescence resonance energy transfer (FRET) and in vivo fluorescence biodistribution. The deshielding of HA and the protonizing of CS in slightly acidic tumor extracellular pH environment (pHe, 6.8-6.5) were demonstrated by ζ potential change from -23.1 to 29.9 mV. The pHe-responsive HAase release was confirmed in the tumor extracellular mimicking environments, and the intratumoral biodistribution showed that the tumor penetration of HCLR was improved. The cell uptake of HCLR in pHe environment was significantly enhanced compared with that in physiological pH environment. The increased shRNA release of HCLR was approved in 10 mM glutathione (GSH) and tumor cells. Surprisingly, HCLR suppressed the tumor growth markedly through survivin silencing and meanwhile maintained low toxicity to mice. This study indicates that the novel polysaccharide enveloped HCLR is promising in clinical translation, thanks to the stimuli-triggered tumor accumulation, tumor penetration, cell uptake, and intracellular gene release.

Enhancing Reverse Intersystem Crossing via Secondary Acceptors: toward Sky-Blue Fluorescent Diodes with 10-Fold Improved External Quantum Efficiency.

How to simply but effectively facilitate reverse intersystem crossing (RISC) transition is always the key issue for developing high-performance thermally activated delayed fluorescence dyes. In this work, as a proof of concept, a feasible strategy named "acceptor enhancement" is demonstrated with a series of ternary blue emitters ( xCz mPO nTPTZ) using diphenylphosphine oxide (PO) as secondary acceptors. Compared with its PO-free binary analogue, such a simple introduction of PO groups in pCzPO2TPTZ dramatically enhances its RISC rate constant ( kRISC) by 10 times the level of ∼105 s-1, accompanied by RISC efficiency (ηRISC) of 92%, which further improves the triplet-to-singlet upconversion for effective triplet harvesting in its devices. As a result, on the basis of a trilayer device structure, pCzPO2TPTZ realized a state-of-the-art external quantum efficiency beyond 20% with a 10-fold improvement.

A novel proximal 3q29 chromosome microdeletion in a Chinese patient with Chiari malformation type II and Sprengel's deformity.

BACKGROUND: Chiari malformation type II (CM-II) is mainly characterized by elongation and descent of the cerebellum through the foramen magnum into the spinal canal. Moreover, CM-II is uniquely associated with myelomeningocele. Sprengel's deformity refers to the malposition of the scapula, i.e. scapular elevation which is sometimes accompanied with scapula dysplasia. Although few familial cases of CM-II and Sprengel's deformity have been previously reported, both of these defects are considered to be sporadic, thus the exact etiology and causative genes have largely remained unknown. CASE PRESENTATION: The patient was diagnosed with CM-II accompanied with Sprengel's deformity. Further genetic investigation revealed a novel 666 kb microdeletion located in 3q29 (chr3:194,532,035-195,198,585; Hg19). Subsequently, genes within the affected region were summarized, and XXYLT1 and ACAP2 were identified as the candidate genes. CONCLUSION: We reported a case of a patient with CM-II and Sprengel's deformity harboring a microdeletion in 3q29. This case highlights the importance of 3q29 in early neural and skeletal development, as well as expands the phenotype spectrum of this rare disorder.

Peroxisome proliferator-activated receptor-alpha deficiency protects aged mice from insulin resistance induced by high-fat diet.

BACKGROUND/AIMS: Insulin resistance is a central feature of the metabolic syndrome and progressively increases with age, resulting in excessively high incidence of type II diabetes in the elderly population. Peroxisome proliferator-activated receptor-alpha (PPARalpha) is widely expressed in insulin target tissues, including those of the liver, kidney, and muscle, where it mediates expression of genes promoting fatty acid beta-oxidation. The aim of this study was to evaluate the potential role of PPARalpha in insulin resistance in aging mice induced by a high-fat diet. METHODS: We used male PPARalpha knockout (KO) mice and wild-type (WT) littermates that were 18 months old. Animals were fed with a high-fat diet (HFD) for 4 weeks, and metabolic parameters associated with insulin sensitivity were assessed. RESULTS: Following HFD treatment, WT mice showed more severe insulin resistance than did mice lacking the PPARalpha gene, as assessed by both the glucose tolerance test (GTT) and insulin tolerance test (ITT). In addition, WT mice exhibited significantly higher HOMA-IR, plasma total cholesterol levels and urinary albumin-creatinine ratio but less liver weight than did PPARalpha KO mice. CONCLUSION: These data suggest that PPARalpha gene deficiency may protect aged mice from developing insulin resistance and albuminuria induced by a HFD.

Whole­exome sequencing identifies a novel mutation (R367G) in SCN5A to be associated with familial cardiac conduction disease.

Cardiac conduction disease is a primary cause of sudden cardiac death. Sodium voltage­gated channel­α subunit 5 (SCN5A) mutations have been reported to underlie a variety of inherited arrhythmias. Numerous disease­causing mutations of SCN5A have been identified in patients with ≥10 different conditions, including type 3 long­QT syndrome and Brugada syndrome. The present study investigated a family with a history of arrhythmia, with the proband having a history of arrhythmia and syncope. Whole­exome sequencing was applied in order to detect the disease­causing mutation in this family, and Sanger sequencing was used to confirm the co­segregation among the family members. A missense mutation (c.1099C>G/p.R367G) of SCN5A was identified in the family and was observed to be co­segregated in all affected members of the family. The missense mutation results in a substitution of glycine for arginine, which may affect sodium transmembrane transport. The present study provides an accurate genetic test which may be used in individuals who exhibit no clinical symptoms.

A mutation of beta-tropomyosin gene in a Chinese family with distal arthrogryposis type I.

BACKGROUND: Distal arthrogryposis (DA) is the most common congenital limb malformation secondary to the functional defects of joints and muscles. DA1 is one of the most commonly described forms of DA. The characteristics of DA1 include bilateral and symmetric clenched fist, overlapping fingers, camptodactyly, ulnar deviation of fingers, and positional foot deformities such as talipes equinovarus. Previous studies demonstrate that mutations of TPM2, TNNI2, TNNT3, MYH3 and MYBPC1 may contribute to DA1. MATERIALS AND METHODS: The present study investigated 8 DA1 families/patients and 1 DA2B patient, determined sequences of TPM2, TNNI2, TNNT3, MYH3 and MYBPC1 and detected the mutation by multiple sequence alignments and bioinformatic prediction of mutation. RESULTS: We identified a novel missense mutation of TPM2 (c.463G>A; p.A155T) in a DA1 family without genetic mutant of TNNI2, TNNT3, MYH3 and MYBPC1. CONCLUSION: The mutation of TPM2 (c.463G>A; p.A155T) led to DA1 of the family. The identification of the mutation expands the spectrum of known TPM2 mutations, and it may contribute to novel approaches to genetic diagnosis and counseling of families with DA1.

Genomic structure and genitourinary expression of mouse cytosolic prostaglandin E(2) synthase gene.

Prostaglandin E(2) (PGE(2)) plays an important role in genitourinary function. Multiple enzymes are involved in its biosynthesis. Here we report the genomic structure and tissue-selective expression of cytosolic PGE(2) synthase (cPGES) in genitourinary tissues. Full-length mouse cPGES cDNA was cloned by reverse transcript-polymerase chain reaction (RT-PCR) and 5'- and 3'-rapid amplification of cDNA ends (RACE). Analysis of a cPGES cDNA with partially sequenced cPGES genomic clones and bioinformatic databases demonstrates that the murine cPGES gene spans approximately 22 kb and consists of eight exons. The cPGES gene promoter is GC-rich and contains many SP1 sites but lacks an obvious TATA box motif. RNase protection assay revealed constitutive expression of cPGES was greatest in the testis with lower levels in the ovary, kidney, bladder and uterus. In situ hybridization studies demonstrated that cPGES mRNA was most highly expressed in the epithelial cells of seminiferous tubules in the testis. In the female reproductive tissues, cPGES was mainly localized in ovarian primary and secondary follicles and oviductal epithelial cells with less expression in uterine endometrium. In the kidney cPGES expression was diffusely expressed. In urinary bladder, cPGES expression was restricted to the transitional epithelial cells. This expression pattern is consistent with an important role for cPGES-mediated PGE(2) in urogenital tissue function.

Membrane-associated PGE synthase-1 (mPGES-1) is coexpressed with both COX-1 and COX-2 in the kidney.

BACKGROUND: Prostaglandin E2 (PGE2) plays an important role in many physiologic and pathophysiologic processes in the kidney. Multiple enzymes are involved in PGE2 biosynthesis, including phospholipases, cyclooxygenases (COX), and the PGE2 synthases (PGES). The present studies were aimed at determining the intrarenal localization of mPGES-1 and whether it is coexpressed with COX-1 or COX-2. METHODS: Rabbit mPGES-1 and COX-1 cDNAs were cloned using reverse transcription-polymerase chain reaction (RT-PCR) and screening a cDNA library. RNase protection assay and immunoblotting were used to examine mPGES-1 expression levels. In situ hybridization and immunostaining were used to determine the intrarenal localization of mPGES-1 and cyclooxygenases. RESULTS: Rabbit mPGES-1 shares high sequence similarity to the human homolog. Nuclease protection studies showed that the kidney expresses among the highest level of mPGES-1 of any rabbit tissue. In situ hybridization showed COX-1 and mPGES-1 mRNA was highly expressed in renal medullary collecting ducts (MCD), and to a lesser extent in cortical collecting ducts (CCD). Fainter mPGES-1 expression was also observed in macula densa (MD) and medullary interstitial cells (RMICs), where COX-2 is highly expressed. Double-labeling studies (immunostaining plus in situ hybridization) and immunohistochemistry of mouse tissues confirmed that mPGES-1 predominantly colocalizes with COX-1 in distal convoluted tubule (DCT), CCD, and MCD, and is coexpressed with COX-2 at lower levels in MD and RMICs. CONCLUSION: Together, these studies suggest mPGES-1 colocalizes with both COX-1 and COX-2 to mediate the biosynthesis of PGE2 in the kidney.