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While beneficial health properties of tea leaves have been extensively studied, less attention is paid to the flowers of tea. In this study, the anti-inflammatory effects of hot water extract of tea (Camellia sinensis) flowers were investigated. Pharmacological studies found that administration of tea flowers extract (TFE) could effectively inhibit croton oil-induced ear edema and carrageenin-induced paw edema. Furthermore, administration of TFE also protected against Propionibacterium acnes (P. ances) plus lipopolysaccharide-(LPS-) induced liver inflammation by reversing the histologic damage and plasma alanine aminotransferase (ALT) increase. Moreover, the levels of nitric oxide (NO), tumor necrosis factor-(TNF)-α and interleukin-(IL-) 1β mRNA in mouse liver were markedly suppressed after treatment with TFE in mice with immunological liver inflammation. These results indicated that tea flowers had potent anti-inflammatory effects on acute and immunological inflammation in vivo, and may be used as a functional natural food.

The discovery of a novel five-component 1,2,3-triazole-containing pharmacophore that exhibits potent and selective inhibition of aromatase (CYP 450 19A1) is described. All compounds are derived from an initial aldol reaction of a phenylacetate derivative with an aromatic aldehyde. Structure-activity data generated from both syn- and anti-aldol adducts provides initial insights into the requirements for both potency and selectivity., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Carnosine is a natural dipeptide that has shown multiple benefits in the treatment of various diseases. This study investigated the ameliorative effects of carnosine on glucose metabolism in restraint-stressed mice. Our results showed that restraint stress could significantly influence glucose metabolism, as reflected by lowered glucose tolerance, hepatic and muscle glycogen content, and increased plasma corticosterone concentration in mice. Oral administration of carnosine (150 and 300 mg/kg) not only reverted stress-induced decline in glucose tolerance and glycogen content in liver and muscle, but also reduced plasma corticosterone level. Carnosine has also significantly suppressed mRNA expression of glucose-6-phosphatase, while elevating glycogen synthase 2, glucokinase and glucose transporter 2 expressions in the liver. The obtained results demonstrated the harmful effects induced by restraint stress, while proving that carnosine could ameliorate stress-induced glucose metabolism disturbance. It is presumable that carnosine exerts its anti-stress effects by indirectly affecting the histaminergic neuron system, modulating the stress-activated hypothalamic-pituitary-adrenal axis and improving glucose metabolism through regulation of the enzymes in the glucose metabolic pathways.

Shigellosis is the third most common enteric bacterial infection in the United States. Although infection is typically self-limiting, empiric treatment is often prescribed. Because of increasing antimicrobial resistance to Shigella, empiric treatment options are decreasing. Identifying resistance patterns can inform empiric treatment recommendations. The goals of our study were to examine risk factors associated with antimicrobial resistance of Shigella and examine issues related to empiric treatment and antimicrobial resistance of Shigella. During June 2006-February 2009, we attempted to interview all New York City patients reported to have shigellosis. Their Shigella isolates were tested for antimicrobial susceptibility to examine the level of resistance and identify risk factors for resistance. Analysis was conducted on two groups distinguished by a large outbreak that was documented during the data collection period. Of the 477 nonoutbreak patients, 333 (70%) patients reported taking an antibiotic for shigellosis and 36 (11%) were treated with an antibiotic to which their Shigella infection was resistant. Among this group, high levels of antimicrobial resistance were detected to amoxicillin-clavulanate (66%), ampicillin (68%), and trimethoprim-sulfamethoxazole (66%). Non-travel-associated ciprofloxacin-resistant Shigella (five patients) and ciprofloxacin-resistant Shigella sonnei (four patients) were reported for the first time to our knowledge. Antimicrobial resistance is significantly higher in New York City residents compared with national data. Some patients were treated with therapies that were not effective and to which the patient's Shigella infection was resistant. Shigella infections should not be treated with antibiotics unless the patient presents with severe or underlying illness and is at risk for systemic illness. When treatment is indicated, local monitoring of Shigella for antimicrobial resistance will provide local clinicians with the best guidance for effective empiric treatments.

Locomotor sensitization induced by the dopamine agonist quinpirole can be potentiated by co-treatment with the synthetic kappa opioid agonist U69593. The identification of salvinorin A, an active component of the psychotropic sage Salvia divinorum, as a structurally different agonist of kappa-opioid receptors raised the question of whether this compound would similarly potentiate sensitization to quinpirole. Rats were co-treated with 0.5 mg/kg quinpirole and either salvinorin A (0.04, 0.4 or 2.0 mg/kg) or U69593 (0.3 mg/kg). Control groups were co-treated with vehicle and saline, vehicle and quinpirole (0.5 mg/kg), or saline and salvinorin A (0.4 mg/kg). Rats were injected biweekly for a total of 10 injections and locomotor activity measured after each treatment. Results showed that the highest dose of salvinorin A potentiated sensitization to quinpirole as did U69593, the middle salvinorin A dose had no effect on quinpirole sensitization, and the lowest dose of salvinorin A attenuated sensitization to quinpirole. These findings indicate that structural differences between salvinorin A and U69593 do not affect the potentiation of quinpirole sensitization. Moreover, the opposite effects of high and low salvinorin A doses suggest that salvinorin A can produce bidirectional modulation of sensitization to dopamine agonists.

Introduction: Few state or local health agencies have accurate local-level information on the prevalence of the leading causes of morbidity and mortality. The New York City Health and Nutrition Examination Survey (NYC HANES) was designed as a new local surveillance initiative to determine the prevalence of health conditions among adult residents of New York City., Methods: Modeled after the National Health and Nutrition Examination Survey, the survey was initiated in June 2004 as a population-based cross-sectional study of New York City adults aged 20 and older. The survey was designed using a three-stage cluster sampling plan; 4026 households were randomly selected. Selected households were visited, and residents were given an initial eligibility screening questionnaire. Eligible participants were asked to schedule an appointment at an NYC-HANES-dedicated health center to complete the NYC HANES. A completed survey was defined as completion of a demographic interview and at least one examination component. Health conditions examined included cholesterol levels, diabetes status, blood pressure, environmental biomarkers, depression, anxiety, and antibodies to infectious diseases., Results: Of the 4026 households approached, eligibility screening questionnaires were completed for 3388 (84%) households, and 3047 survey participants were identified. Of the 3047 participants, 76% made an appointment, and 66% completed the survey. The overall response rate was 55% (n = 1999)., Conclusion: NYC HANES is the first successful local-level examination survey modeled on NHANES. With periodic repetition, NYC HANES will provide surveillance information on leading causes of morbidity and mortality.

The family of interferon-induced transmembrane protein (Ifitm/mil/fragilis) genes encodes cell surface proteins that may modulate cell adhesion and influence cell differentiation. Mouse Ifitm1 and -3, which are expressed in primordial germ cells (PGCs), are implicated to have roles in germ cell development, but the specific functions have been unclear. Our results show that Ifitm1 activity is required for PGC transit from the mesoderm into the endoderm, and that it appears to act via a repulsive mechanism, such that PGCs avoid Ifitm1-expressing tissues. In contrast, Ifitm3, which is expressed in migratory PGCs, is sufficient to confer autonomous PGC-like homing properties to somatic cells. These guidance activities are mediated by the N-terminal extracellular domain of the specific IFITM, which cannot be substituted by that of another family member. Complex homo- and/or heterotypic intercellular interactions among various IFITMs in PGCs and neighboring cells may underpin coordinated germ cell guidance in mice.

A 6-kb antisense transcript (Dnm3os) contained within an intron of the mouse Dnm3 gene has been identified in a screen for genes that may be regulated by the basic helix-loop-helix transcription factor Twist during mouse development. The antisense transcript is highly conserved between vertebrate species, but does not appear to encode a protein. We show that expression of the Dnm3 and Dnm3os transcripts overlaps during embryogenesis and in adult tissues, except that Dnm3 is most highly expressed in adult brain and testis and expressed at lower levels in embryos, whereas the antisense transcript is most strongly expressed in embryos and gravid uterus. Both Dnm3 and Dnm3os are downregulated in branchial arch tissue of Twist-null embryos. The conservation and restricted expression pattern of this noncoding transcript suggest that it may perform an important function during embryonic development and further suggest a connection between the regulation of Dnm3 and this novel intronic, antisense transcript.

PDGF-C is a member of the platelet-derived growth factor (PDGF) family, which signals through PDGF receptor (PDGFR) alphaalpha and alphabeta dimers. Here we show that Pdgfc(-/-) mice die in the perinatal period owing to feeding and respiratory difficulties associated with a complete cleft of the secondary palate. This phenotype was less severe than that of Pdgfra(-/-) embryos. Pdgfc(-/-) Pdgfa(-/-) embryos developed a cleft face, subepidermal blistering, deficiency of renal cortex mesenchyme, spina bifida and skeletal and vascular defects. Complete loss of function of both ligands, therefore, phenocopied the loss of PDGFR-alpha function, suggesting that both PDGF-A and PDGF-C signal through PDGFR-alpha to regulate the development of craniofacial structures, the neural tube and mesodermal organs. Our results also show that PDGF-C signaling is a new pathway in palatogenesis, different from, and independent of, those previously implicated.

In a screen for potential targets of regulation by TWIST in mouse embryos we isolated a fragment with homology to type II early transposon (ETn) and type D endogenous provirus (MusD) elements. Whole-mount in situ hybridization to E7.5-E13.5 mouse embryos reveals a tissue- and stage-specific expression pattern that contrasts with the previously reported lack of expression of ETn elements in mouse embryos beyond late gastrulation. Transcripts were detected in the epiblast at E7.5 and in the neural tube from E8.5 to E10.5. Later expression is predominantly confined to the mesodermal tissues of craniofacial structures, limb buds and somites. The tissue specificity of expression suggests tight regulation of the activity of this early transposon element during embryogenesis.

Twist encodes a basic helix-loop-helix transcription factor that is required for normal craniofacial morphogenesis in the mouse. Loss of Twist activity in the cranial mesenchyme leads to aberrant migratory behaviour of the neural crest cells, whereas Twist-deficient neural crest cells are located in an inappropriate location in the first branchial arch and display defective osteogenic and odontogenic differentiation (Soo et al. [2002] Dev. Biol. 247:251-270). Results of the present study further show that loss of Twist impacts on the patterning of the cranial ganglia and nerves but not that of the peripheral ganglia and nerves in the trunk region of the body axis. Analyses of the expression of molecular markers of early differentiation of the paraxial mesoderm and the histogenetic potency of somites of Twist(-/-) embryos reveal that Twist-deficient somites can differentiate into muscles, cartilage, and bones, albeit less prolifically. Twist function, therefore, is not essential for mesoderm differentiation. The poor growth of the Twist-deficient somites after transplantation to the ectopic site may be attributed to reduced proliferative capacity and extensive apoptosis of the paraxial mesoderm, suggesting that Twist is required for maintaining cell proliferation and viability in the mesodermal progenitors., (Copyright 2004 Wiley-Liss, Inc.)