Abnormal cell wall structure caused by boron nutrient imbalance in orchards could affect psyllid feeding behaviour, resulting in epidemic variation of Asian citrus psyllid.

The control of Huanglongbing (HLB), one of the most destructive pests of citrus, relies heavily on the reduction of Asian citrus psyllid (ACP), Diaphorina citri Kuwayama. An in-depth understanding of ACP feeding behaviours among citrus plants is urgent for comprehensive management of orchards. An investigation was conducted in 37 citrus orchards in HLB epidemic areas, sampling shoots in the area with aggregation feeding of ACP (ACPf) and shoots in a neighbouring area without ACP feeding (CK), to study the interaction between leaf chemical composition and ACP psyllid feeding behaviours. Results of FTIR showed a strong absorption peak intensity, mainly representing functional groups originating from cell wall components in the leaf with ACP feeding. As compared with the control, cell wall components, such as alkali-soluble pectin, water-soluble pectin, total soluble pectin, cellulose, and hemicellulose, of the cell wall of ACPf increased by 134.0%, 14.0%, 18.0%, 12.5%, and 20.35%, respectively. These results suggest that cell wall mechanical properties significantly decreased in the term of decreases in pectin performance and cellulose mechanical properties. In addition, there was a remarkably lower boron (B) content in leaves and cell wall components with ACP feeding. Further analysis indicated that leaf B content significantly affected leaf cell wall components. Taken together, we provide evidence to demonstrate that the regional distribution of nutrient imbalance in orchards could affect psyllid feeding behaviour by weakening the cell wall structure, resulting in epidemic variation in ACP. This could help us to understand the management of psyllid infections in orchards with unbalanced nutrition.

Impact of drinking water supplemented 2-hydroxy-4-methylthiobutyric acid in combination with acidifier on performance, intestinal development, and microflora in broilers.

In addition to offering methionine, 2-hydroxy-4-methylthiobutyric acid (HMTBa) is also an organic acid and shows excellent bacteriostasis. Therefore, 3 experiments were conducted to determine the influence of drinking water supplemented HMTBa in combination with acidifier on performance, intestinal development, and microflora in broilers. The addition of different concentration (0.02-0.20%) of the blend of HMTBa and other acids significantly reduced the pH of water and exerted antimicrobial activity in dose-dependent manner in vitro. The outcomes from animal trial consisting of the drinking water with blended acidifier at 0.00, 0.05, 0.10, 0.15, and 0.20% indicated that the water with 0.15 or 0.20% acidifier resulted in linear and quadratic higher body weight at 42 d, gain and water consumption during 1 to 42 d (P < 0.05). In experiment 3, responding to graded blended acidifier in drinking water, birds receiving 0.10, 0.15, and 0.20% acidifier decreased the internal pH of gastrointestinal tract and muscle, and exhibited increased duodenal weight, length, villus high, and the ratio of villus high to crypt depth. Drinking water with 0.2% blended acidifier increased the abundance of probiotics (Bacteroidaceae, Ruminococcaceae, and Lachnospiraceae) and decreased the account of pathogenic bacteria such as Desulfovibrionaceae. Alternations in gut microflora were closely related to the metabolism of carbohydrate, amino acid, and vitamins. These findings, therefore, suggest that drinking water with 0.10 to 0.13% the combination HMTBa with acidifier might benefit to intestinal development and gut microbiota, and the subsequent produce a positive effect on the performance of broilers.

[To further improve the understanding of traditional treatment methods for chronic wounds].

With the rapid development of modern treatment methods for chronic wounds, it plays a positive role in the clinical treatment of this kind such disease. However, the traditional treatment methods for chronic wounds also have potential advantages. We should conduct in-depth research on these methods to improve the relevant understanding and actively apply these methods in clinic to exert their therapeutic role. This article discusses the application of wound cleaning, conservative debridement, traditional Chinese medicine, maggot treatment, and enzymatic debridement in the treatment of chronic wounds.

[The role of the traditional surgical procedures for gastroesophageal reflux disease cannot be ignored].

Gastroesophageal reflux disease (GERD) is a common digestive disease with characteristics of a multitude of pathogenesis, a variety of clinical manifestations and a strong negative impact on physical and mental health of the patients. GERD is classified into non-erosive reflux disease and reflux esophagitis in terms of absence or presence of mucosal damage at endoscopic findings. Proton pump inhibitors (PPI) are widely used in the treatment of GERD, especially for patients with non-erosive reflux disease or mild reflux esophagitis. However, PPI do not affect pathophysiologic mechanisms of GERD or reduce the number of reflux events. When PPI fails to adequately control the symptoms of GERD as a result of gastroesophagel junction structural defects, the antireflux surgical procedures are indicated to create a mechanical barrier to reflux. The laparoscopic fundoplication remains the most commonly performed and is the current "gold-standard" anti-reflux procedure. The outcomes of the antireflux surgical procedures are superior to medical therapy for GERD in light of subjective symptoms, objective examinations, quality of life and patient satisfaction. As of now, enough attention has not been paid to the traditional surgical procedures of GERD in China. It is controversial about which is optimal among the three major types of procedures, selection should be tailored to classification, mechanism, age, mental status and esophageal motility. GERD is a chronic disease and either medical or surgical therapy may put the patient at different risk, therefore the patient's preferences should be considered adequately before choosing the treatment protocols.

A novel FGFR1-binding peptide attenuates the degeneration of articular cartilage in adult mice.

OBJECTIVE: We previously reported that genetic ablation of (Fibroblast Growth Factors Receptors) FGFR1 in knee cartilage attenuates the degeneration of articular cartilage in adult mice, which suggests that FGFR1 is a potential targeting molecule for osteoarthritis (OA). Here, we identified R1-P1, an inhibitory peptide for FGFR1 and investigated its effect on the pathogenesis of OA in mice induced by destabilization of medial meniscus (DMM). DESIGN: Binding ability between R1-P1 and FGFR1 protein was evaluated by enzyme-linked immuno sorbent assay (ELISA) and molecular docking. Alterations in cartilage were evaluated histologically. The expression levels of molecules associated with articular cartilage homeostasis and FGFR1 signaling were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting and immunohistochemistry (IHC). The chondrocyte apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay. RESULTS: R1-P1 had highly binding affinities to human FGFR1 protein, and efficiently inhibited extracellular signal-regulated kinase (ERK)1/2 pathway in mouse primary chondrocytes. In addition, R1-P1 attenuated the IL-1ß induced significant loss of proteoglycan in full-thickness cartilage tissue from human femur head. Moreover, this peptide can significantly restore the IL-1ß mediated loss of proteoglycan and type II collagen (Col II) and attenuate the expression of matrix metalloproteinase-13 (MMP13) in mouse primary chondrocytes. Finally, intra-articular injection of R1-P1 remarkably attenuated the loss of proteoglycan and the destruction of articular cartilage and decreased the expressions of extracellular matrix (ECM) degrading enzymes and apoptosis in articular chondrocytes of mice underwent DMM surgery. CONCLUSIONS: R1-P1, a novel inhibitory peptide for FGFR1, attenuates the degeneration of articular cartilage in adult mice, which is a potential leading molecule for the treatment of OA.

Therapeutic efficacy of atypical antipsychotic drugs by targeting multiple stress-related metabolic pathways.

Schizophrenia (SZ) is considered to be a multifactorial brain disorder with defects involving many biochemical pathways. Patients with SZ show variable responses to current pharmacological treatments of SZ because of the heterogeneity of this disorder. Stress has a significant role in the pathophysiological pathways and therapeutic responses of SZ. Atypical antipsychotic drugs (AAPDs) can modulate the stress response of the hypothalamic-pituitary-adrenal (HPA) axis and exert therapeutic effects on stress by targeting the prefrontal cortex (PFC) and hippocampus. To evaluate the effects of AAPDs (such as clozapine, risperidone and aripiprazole) on stress, we compared neurochemical profile variations in the PFC and hippocampus between rat models of chronic unpredictable mild stress (CUMS) for HPA axis activation and of long-term dexamethasone exposure (LTDE) for HPA axis inhibition, using an ultraperformance liquid chromatography-mass spectrometry (UPLC-MS/MS)-based metabolomic approach and a multicriteria assessment. We identified a number of stress-induced biomarkers comprising creatine, choline, inosine, hypoxanthine, uric acid, allantoic acid, lysophosphatidylcholines (LysoPCs), phosphatidylethanolamines (PEs), corticosterone and progesterone. Specifically, pathway enrichment and correlation analyses suggested that stress induces oxidative damage by disturbing the creatine-phosphocreatine circuit and purine pathway, leading to excessive membrane breakdown. Moreover, our data suggested that the AAPDs tested partially restore stress-induced deficits by increasing the levels of creatine, progesterone and PEs. Thus, the present findings provide a theoretical basis for the hypothesis that a combined therapy using adenosine triphosphate fuel, antioxidants and omega-3 fatty acids as supplements may have synergistic effects on the therapeutic outcome following AAPD treatment.

Identifying Corticothalamic Network Epicenters in Patients with Idiopathic Generalized Epilepsy.

BACKGROUND AND PURPOSE: Corticothalamic networks are considered core pathologic substrates for idiopathic generalized epilepsy; however, the predominant epileptogenic epicenters within these networks are still largely unknown. The current study aims to identify these epicenters by resting-state functional connectivity. MATERIALS AND METHODS: To identify epicenters within the corticothalamic networks in idiopathic generalized epilepsy, we retrospectively studied a large cohort of patients with this condition (n = 97) along with healthy controls (n = 123) by resting-state functional MR imaging. The thalamus was functionally divided into subregions corresponding to distinct cortical lobes for 5 parallel corticothalamic networks. The functional connectivity between each voxel in the cortical lobe and the corresponding thalamic subregion was calculated, and functional connectivity strength was used to evaluate the interconnectivity of voxels in the cortex and thalamus. RESULTS: The projection of 5 cortical lobes to the thalamus is consistent with previous histologic findings in humans. Compared with controls, patients with idiopathic generalized epilepsy showed increased functional connectivity strength in 4 corticothalamic networks: 1) the supplementary motor area, pulvinar, and ventral anterior nucleus in the prefrontal-thalamic network; 2) the premotor cortex and ventrolateral nucleus in motor/premotor-thalamic networks; 3) the visual cortex, posterior default mode regions, and pulvinar in parietal/occipital-thalamic networks; and 4) the middle temporal gyrus in the temporal-thalamic network. CONCLUSIONS: Several key nodes were distinguished in 4 corticothalamic networks. The identification of these epicenters refines the corticothalamic network theory and provides insight into the pathophysiology of idiopathic generalized epilepsy.

Gastrodin ameliorates anxiety-like behaviors and inhibits IL-1beta level and p38 MAPK phosphorylation of hippocampus in the rat model of posttraumatic stress disorder.

Gastrodin, a main constituent of a Chinese herbal medicine, has been shown to be effective in treating various mood disorders. The purpose of the present study was to determine whether gastrodin could ameliorate stress-associated behavior in a rat model of enhanced single prolonged stress (ESPS)-induced posttraumatic stress disorder (PTSD). Following ESPS, rats were administered orally with gastrodin (50, 100, or 200 mg/kg daily) or vehicle for 2 weeks. Animals were then tested in the open field and elevated plus-maze, and the levels of IL-6 and IL-1beta, the expression of iNOS, p38 and phospho-p38 (p-p38) in hippocampus were also tested. ESPS exposure resulted in pronounced anxiety-like behavior, elevated IL-6 and IL-1beta levels, and the higher expression of iNOS and p-p38 in hippocampus. However, repeated treatment with gastrodin, particularly at higher doses, reversed the aforementioned changes, including anxiety-like behavior, levels of IL-6 and IL-1beta, and the expression of iNOS and the p38 MAPK phosphorylation. These results indicate that gastrodin possesses anxiolytic effect and may be an effective herbal preparation for the treatment of PTSD.

Gene expression in epithelial ovarian cancer: a study of intratumor heterogeneity.

The aim of this study was to investigate the intratumor heterogeneity of gene expression profiles in epithelial ovarian cancer (EOC). This was done to evaluate whether sampling of a single macrodissected tissue sample from each EOC case would bias the data and result in, eg, prognostic studies based on gene expression microarray experiments. From nine EOCs removed at Odense University Hospital, Denmark, three tumor samples of 200-300 mg each were taken with greatest possible mutual distance. The samples were immediately flash frozen. A parallel section was taken for histopathologic comparison. RNA was extracted from the tissue samples. Five micrograms of each RNA sample was used for labeling. The fragmented biotin-labeled complementary RNA was hybridized to Affymetrix GeneChip Human Genome U133 plus 2.0 arrays, and scanning was performed on the GeneArray scanner 3000 (Affymetrix, Santa Clara, CA). Data were evaluated using hierarchical clustering and intraclass correlation coefficient (ICC) from reliability analysis. All evaluation methods revealed low intratumor heterogeneity. Intratumor ICCs ranged from 0.888 to 0.978. In contrast, "between-tumor" ICC was 0.549 indicating much lower intra- than intertumor heterogeneity. Due to a low degree of intratumor variation, we conclude that it is sufficiently accurate in a clinical setup to use single, macrodissected tumor samples in the evaluation of gene expression in EOCs.

Selective distribution of selenium in colon parallels its antitumor activity.

Results of epidemiologic and experimental studies suggest that selenium can inhibit the development of tumors. In rats, the administration of selenium decreases the incidence of carcinogen-induced colon tumors; the inhibition is greater in the proximal colon that in the distal colon. We investigated the distribution of selenium in the different segments of rat colon and determined the uptake of selenium in the mucosa and in the muscle layers of each segment. The colon was perfused before removal of the segments to ensure complete removal of blood-borne selenium. We found that the concentration of selenium was greater in the proximal colon than in the distal colon and that within each segment the uptake was higher in mucosa than in muscle. In addition, we determined the level of selenium in blood, serum, and liver at different times after the administration of various doses of selenium. Though the mechanism by which selenium prevents tumor development is unknown, the data indicate a correlation between the uptake of selenium in different segments of colon and inhibition of tumorigenesis.

Selenium and the acute effects of the carcinogens, 2-acetylaminofluorene and methylazoxymethanol acetate.

Selenium inhibits the development of 2-acetylaminofluorene-induced hepatic tumors and methylazoxymethanol-induced colon tumors. It has been suggested that selenium exerts these protective effects by inhibiting metabolic activation of the carcinogen. We have studied the effects of selenium upon the acute inhibition of RNA and DNA synthesis induced by 2-acetylaminofluorene or methylazoxymethanol in intact liver, regenerating liver, and colon of weanling male Sprague-Dawley rats. Some animals received selenium in the drinking water (4 ppm) for 1 week, while others received a single injection of selenium (1 mg/kg i.p.) prior to being treated with the carcinogens. No protection against the effects of the carcinogens on RNA or DNA synthesis was noted with either treatment of selenium. Disulfiram did protect against the 2-acetylaminofluorene-induced inhibition of hepatic RNA synthesis, and pyrazole prevented the inhibition of RNA synthesis induced by methylazoxymethanol in both liver and colon. Serum selenium levels are reported. The data indicate that selenium does not influence the acute alterations induced by the carcinogens 2-acetylaminofluorene or methylazoxymethanol and suggest that the tumor-preventive effects of selenium are probably due to a mechanism other than interference with carcinogen activation and interaction with cellular macromolecules.