We investigated whether an implicit association test (IAT) can be used to assess dysfunctional beliefs in the realm of psychopathology. As a first exploration we therefore constructed a IAT that was designed to differentiate between high and low social anxious individuals. Social situation and neutral words were the targets (e.g. date vs hall), and positive and negative outcomes (e.g. compliment vs rejection) the associated attributes. High social anxious women (N=32) showed the predicted deterioration of task performance if the required responses switched from compatible to incompatible with the idea that social situations are related to negative outcomes and vice versa, whereas the opposite was true for low anxious women (N=32). Thus a modified IAT seems a useful and highly flexible tool to implicitly assess complaint-specific dysfunctional associations and may be a valuable addition to the usual (explicit) self-report measures of patients' beliefs.

Problems with current strategies for assessing suicide risk are discussed and a two-tier method for evaluating imminent danger among adolescents is proposed. First, statistically-based data on suicide risk factors are collected; second, coping ability is assessed by having youths promise in writing not to try suicide, compliment themselves and others, assess their feelings; and develop a plan for dealing with suicidal circumstances.

OBJECTIVE

The purpose of this study was to determine the ability of pregnant women to incorporate sophisticated screening information about risk assessment into their decisions about invasive testing in an appropriate way.

METHODS

Assessment of risk for trisomy 21 was carried out by a combination of maternal age, fetal nuchal translucency (NT) thickness, and maternal serum free beta-human chorionic gonadotrophin (hCG) and pregnancy-associated plasma protein-A (PAPP-A) at 11 to 13+6 weeks. The patients were counseled with regards to their estimated risk, and were informed that the only way to know for sure whether or not the fetus has a chromosomal abnormality is by having an invasive test, but these tests carry a risk of miscarriage of about 1%. They were also informed that although a risk of 1 in 300 or more was generally considered to be high, it was up to them to decide in favor or against invasive testing.

RESULTS

Assessment of risk was carried out in 30,564 singleton pregnancies with live fetuses at 11 to 13+6. The median maternal age was 34 (range 15-49) years and, in 14,816 (48.5%), the age was 35 years or greater. The rate of invasive testing increased exponentially with increasing estimated risk (r = 0.917, P < .0001). The estimated risk for trisomy 21 was 1 in 300 or more in 2565 (8.4%) women, and 1991 (77.6%) of these had invasive testing. The risk was less than 1 in 300 in 27,999 (91.6%) women, and 1286 (4.6%) of these had invasive testing.

CONCLUSIONS

Pregnant women are able to use sophisticated screening information to make scientifically and ethically rational decisions about invasive testing for trisomy 21. These empiric data compliment the arguments of normative ethics to create evidence-based ethical standards for informed consent regarding invasive testing.

BACKGROUND

Disinvestment from inefficient or ineffective health services is a growing priority for health care systems. Provision of allied health services over the weekend is now commonplace despite a relative paucity of evidence supporting their provision. The relatively high cost of providing this service combined with the paucity of evidence supporting its provision makes this a potential candidate for disinvestment so that resources consumed can be used in other areas. This study aims to determine the effectiveness, cost-effectiveness and safety of the current model of weekend allied health service and a new stakeholder-driven model of weekend allied health service delivery on acute medical and surgical wards compared to having no weekend allied health service.

METHODS

Two stepped wedge, cluster randomised trials of weekend allied health services will be conducted in six acute medical/surgical wards across two public metropolitan hospitals in Melbourne (Australia). Wards have been chosen to participate by management teams at each hospital. The allied health services to be investigated will include physiotherapy, occupational therapy, speech therapy, dietetics, social work and allied health assistants. At baseline, all wards will be receiving weekend allied health services. Study 1 intervention will be the sequential disinvestment (roll-in) of the current weekend allied health service model from each participating ward in monthly intervals and study 2 will be the roll-out of a new stakeholder-driven model of weekend allied health service delivery. The order in which weekend allied health services will be rolled in and out amongst participating wards will be determined randomly. This trial will be conducted in each of the two participating hospitals at a different time interval. Primary outcomes will be length of stay, rate of unplanned hospital readmission within 28 days and rate of adverse events. Secondary outcomes will be number of complaints and compliments, staff absenteeism, and patient discharge destination, satisfaction, and functional independence at discharge.

CONCLUSIONS

This is the world's first application of the recently described non-inferiority (roll-in) stepped wedge trial design, and the largest investigation of the effectiveness of weekend allied health services on acute medical surgical wards to date.

BACKGROUND

Australian New Zealand Clinical Trials Registry.

BACKGROUND

ACTRN12613001231730 (first study) and ACTRN12613001361796 (second study). Was this trial prospectively registered?: Yes. Date registered: 8 November 2013 (first study), 12 December 2013 (second study). Anticipated completion: June 2015. Protocol version: 1. Role of trial sponsor: KP and DL are directly employed by one of the trial sponsors, their roles were: KP assisted with overall development of research design and assisted with overall project management; DL contributed to project management, administration and communications strategy.

BACKGROUND

Recent clinical data suggest statins have transient but significant effects in patients with pulmonary arterial hypertension. In this study we explored the molecular effects of statins on distal human pulmonary artery smooth muscle cells (PASMCs) and their relevance to proliferation and apoptosis in pulmonary arterial hypertension.

METHODS

Primary distal human PASMCs from patients and controls were treated with lipophilic (simvastatin, atorvastatin, mevastatin and fluvastatin), lipophobic (pravastatin) and nitric-oxide releasing statins and studied in terms of their DNA synthesis, proliferation, apoptosis, matrix metalloproteinase-9 and endothelin-1 release.

RESULTS

Treatment of human PASMCs with selected statins inhibited DNA synthesis, proliferation and matrix metalloproteinase-9 production in a concentration-dependent manner. Statins differed in their effectiveness, the rank order of anti-mitogenic potency being simvastatin>> atorvastatin>>>> pravastatin. Nevertheless, a novel nitric oxide-releasing derivative of pravastatin (NCX 6550) was effective. Lipophilic statins, such as simvastatin, also enhanced the anti-proliferative effects of iloprost and sildenafil, promoted apoptosis and inhibited the release of the mitogen and survival factor endothelin-1. These effects were reversed by mevalonate and the isoprenoid intermediate geranylgeranylpyrophosphate and were mimicked by inhibitors of the Rho and Rho-kinase.

CONCLUSIONS

Lipophilic statins exert direct effects on distal human PASMCs and are likely to involve inhibition of Rho GTPase signalling. These findings compliment some of the recently documented effects in patients with pulmonary arterial hypertension.

A 21-year-old female with trisomy 21 Down's syndrome delivered a normal male child with 46, XY chromosome compliment. The case is described as a first report from India.

The bases of using blood enzyme activity measurements [e.g. AChE, non-specific cholinesterase (BChE), carboxylesterase] as markers of organophosphate ester (OP) exposure are inhibition of activity by the binding of OPs to serine active sites in the enzymes, and the accessibility of the enzymes in RBCs and serum. The methods used to determine esterases in the blood of humans, experimental animals, and wildlife are outlined with emphasis on the acetylcholinesterase (AChE) of the red blood cell. Adaptations of an acetylthiocholine ester assay of Ellman et al. (1961) are common, but other colorimetric procedures, radiometric assays, and pH methods are also in use. Optimized, standardized methods are needed to assess exposures and provide a solid basis for risk assessment analyses. Useful adjuncts to ChE measurements are oxime reactivation tests and assay of neuropathy target esterase, an enzyme associated with organophosphate-induced delayed neuropathy. Determination of urinary metabolites compliments, but does not substitute for, the information obtained from blood ChE studies. Future assays are likely to involve antibodies to OP-protein complexes. Improvements in techniques permit the detection of small decreases in ChE activities. Whether or not such small decreases in ChE activities can, by themselves, constitute an adverse effect for input into risk assessment analyses is a controversial matter.

Polyunsaturated fatty acids (PUFAs) can influence tumor growth and migration, both in vitro and in vivo. The PUFA gamma-linolenic acid (GLA) has been reported to improve the poor prognosis associated with human gliomas, although its effects at sublethal concentrations on residual cells postsurgery are poorly understood. The study investigated the effects sublethal PUFA doses (90 or 150 microM) may have on rat C6 glioma cell energy metabolism, since an adequate energy supply is essential for cell proliferation, migration, and apoptosis. Of note was the identification of mitochondrial heterogeneity in relation to the mitochondrial membrane potential (MMP), which has been suggested but unproven in previous studies. GLA and eicosapentaenoic acid (EPA) caused significant changes in cellular fatty acid composition and increased the percentage of cells with a low MMP after a 96-h exposure period. The presence of PUFAs inhibited C6 cell proliferation and migration, although apoptosis was not induced. The protein expression and activity of glucose-6-phosphate dehydrogenase was increased after 96-h incubation with 90 microM GLA and EPA and would allow redox regulation through increased NADPH production, permitting the maintenance of adequate intracellular reduced glutathione concentrations and limiting rates of lipid peroxidation and reactive oxygen species generation. Neither NADP(+)-isocitrate dehydrogenase nor NADP(+)-malate dehydrogenase activity responded to PUFAs, suggesting it is glucose-6-phosphate dehydrogenase that is the principal source of NADPH in C6 cells. These data compliment studies showing that higher concentrations of GLA induced glioma cell death and tumor regression and suggest that GLA treatment could be useful for the inhibition of residual cell proliferation and migration after surgical removal of the tumor mass.

Despite numerous clinical and animal studies, the initial injury and pathogenesis of aminoglycoside nephrotoxicity remains unclear. To compliment and extend existing research avenues, a cell culture model system representative of the human proximal tubule (HPT) was tested to determine its applicability for use in studies assessing aminoglycoside-induced cellular toxicity. For this determination, the proximal tubule cell cultures were exposed to increasing concentrations of streptomycin and monitored for cell death and light and electron microscopic changes under both confluent (resting) and subconfluent (actively-dividing) culture conditions. Confluent cultures exposed to streptomycin were also assessed for possible alterations in transport activities by monitoring the electrical properties of the cells through Ussing chamber analysis. Both the confluent and subconfluent cultures demonstrated concentration-dependent toxicity to streptomycin. Ultrastructural analysis disclosed that both actively-dividing and stationary cultures contained "myeloid bodies" within the cytoplasm, consistent with those known to occur in vivo. In studies relating cell numbers to the dosage and time of exposure to streptomycin, the confluent cultures demonstrated and "insult-recovery" period at toxic, but sub-lethal, concentration, again correlating to the known in vivo experience with this class of antibiotics. The subconfluent cultures demonstrated increased resistance to the toxic effects of streptomycin, again mimicking the clinical experience with aminoglycoside toxicity. Chamber analysis, at a streptomycin dose well below the toxic level, indicated changes in the transport activities of these cultured cells. It is proposed that the use of cultured proximal tubule cells could be a useful model system to extend current research avenues assessing the mechanism of aminoglycoside nephrotoxicity.

The last decade has witnessed a resurgence of interest in the surgical treatment of metastatic spinal disease to compliment radiotherapy. A recent randomized controlled trial looking directly at this issue concluded strongly in favour of a combination of surgical decompression and radiotherapy, and there is now growing enthusiasm for surgery to play a role in the management of these patients. We present a prospective cohort study of 62 patients who presented with metastatic cord or cauda equina compression, and were treated with surgical decompression and fixation where necessary. Patients were treated by one surgeon working in a single unit. They were followed-up long term and were assessed objectively, by clinical assessment and prospective questionnaires that included SF36, visual analogue pain scores and Roland Morris back pain scores. Sixty-two patients with a median age of 62 (22-79 years, 27 male) were included in the study. The commonest primary tumours were breast (26%) and lymphoma (13%). The majority of patients had involvement of thoracic vertebrae (58%). 56% of patients were alive at 1 year and 28% at 3 years, with significant improvements observed in both walking and continence. Similarly, significant improvements were seen in SF36 quality of life scores as well as pain. With careful patient selection, long-term survival and good quality of life can be achieved. However, not every patient is suitable or appropriate for surgery, and the discussion focuses on where the surgical threshold should be set.

The hypothesis that growth hormone (GH) up-regulates the expression of enzymes, matrix proteins, and differentiation markers involved in mineralization of tooth and bone matrices was tested by the treatment of Lewis dwarf rats with GH over 5 days. The molar teeth and associated alveolar bone were processed for immunohistochemical demonstration of bone morphogenetic proteins 2 and 4 (BMP-2 and -4), bone morphogenetic protein type IA receptor (BMPR-IA), bone alkaline phosphatase (ALP), osteocalcin (OC), osteopontin (OPN), bone sialoprotein (BSP), and E11 protein (E11). The cementoblasts, osteoblasts, and periodontal ligament (PDL) cells responded to GH by expressing BMP-2 and -4, BMPR-IA, ALP, OC, and OPN and increasing the numbers of these cells. No changes were found in patterns of expression of the late differentiation markers BSP and E11 in response to GH. Thus, GH evokes expression of bone markers of early differentiation in cementoblasts, PDL cells, and osteoblasts of the periodontium. We propose that the induction of BMP-2 and -4 and their receptor by GH compliments the role of GH-induced insulin-like growth factor 1 (IGF-1) in promoting bone and tooth root formation.

Ring chromosome 18 is a rare condition which has predominantly been described by case reports and small case series. We assessed a cohort of 30 individuals with ring 18 using both microarray comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH). We determined that each participant had a unique combination of hemizygosity for the p and q arms. Four ring chromosomes had no detectable deletion of one of the chromosome arms using aCGH. However, two of these ring chromosomes had telomeric sequences detected using FISH. These data confirm the importance of molecular and cytogenetic analysis to determine both chromosome content and morphology. We failed to find dramatic changes in mosaicism percentage between cytogenetic measurements made at the time of diagnosis and those made years later at the time of this study, demonstrating that dynamic ring mosaicism is unlikely to be a major cause of phenotypic variability in the ring 18 population. Lastly, we present data on the clinical features present in our cohort, though the extreme genotypic variability makes it impossible to draw direct genotype-phenotype correlations. Future work will focus on determining the role of specific hemizygous genes in order to create individualized projections of the effect of each person's specific ring 18 compliment.

The ability of cloned Rous sarcoma virus (RSV) DNA encoding the v-src oncogene to neoplastically transform normal, diploid Syrian hamster embryo (SHE) cells was examined. Transfection of RSV DNA into early passage SHE cells resulted in a low but significant number of tumors when treated cells were injected into nude mice. Tumors formed with a low frequency (two tumors out of ten sites injected) and only after a long latency period (14 weeks). In contrast to the normal SHE cells, several different carcinogen-induced preneoplastic immortal SHE cell lines were highly susceptible to transformation by the v-src oncogene to the neoplastic phenotype. Tumors formed with high efficiency and a short latency period (less than 3 weeks). Further studies were performed to determine the basis for the inefficient transformation of the normal SHE cells. NeoR clones isolated after cotransfection of SHE cells with pSV2-neo and RSV DNAs were neither morphologically altered nor immortal and did not contain detectable levels of the v-src gene product. These results suggest that neoplastic transformation by v-src DNA in the normal cells is initially suppressed. However, cells from a v-src-induced tumor expressed v-src RNA, and antibody to v-src protein precipitated from the tumor cells a 60,000-molecular-weight protein which displayed protein kinase activity. Karyotypic analyses confirmed that the tumor was derived from Syrian hamster cells and suggested that it was clonal in nature. These results indicate that the v-src oncogene was primarily responsible for neoplastic transformation of SHE cells. In contrast to the results with the v-src oncogene, our previous studies showed that v-Ha-ras oncogene alone is unable to induce neoplastic transformation of SHE cells. Furthermore, the v-myc oncogene was able to compliment v-Ha-ras to neoplastically transform SHE cells, while cotransfection with v-src plus v-myc did not increase the incidence of tumors.

A recent review on facial mimicry concludes that emotional mimicry is less ubiquitous than has been suggested, and only occurs in interactions that are potentially affiliative (see Hess and Fischer, in revision). We hypothesize that individuals do not mimic facial expressions that can be perceived as offensive, such as disgust, and mimic positive emotion displays, but only when the context is affiliative (i.e., with intimates). Second, we expect that in spontaneous interactions not mimicry, but empathic feelings with the other predict the accurateness of emotion recognition. Data were collected in a pseudo-experimental setting, during an event organized for subscribers of a large Dutch women's magazine. One woman (expresser) was exposed to two emotional stimuli (i.e., a vile smell, a compliment) in order to evoke disgust and pride respectively. Another woman (observer: intimate or stranger) was sitting opposite of her. We collected self-report measures on emotions and empathy, and coded facial expressions of disgust and smiling on the basis of FACS. The results show that participants do not mimic disgust. In contrast, smiles displayed after the vile smell and the compliment were mimicked, but only among intimates. We also found that self-reported empathy and not mimicry is related to the recognition of disgust. These findings are discussed in the light of a Social Contextual view on emotional mimicry.

The United Nations General Assembly has convened a Summit on non-communicable diseases (NCDs), an historic moment in the global combat of these disorders. Lifestyles in increasingly urban and globalised environments have led to a steep surge in NCD incidence in low and middle income countries, where two thirds of all NCD deaths occur (most importantly from cancer, cardiovascular and respiratory disease as well as diabetes). Treatment of NCDs is usually long term and expensive, thus threatening patients' and nations' budgets and putting them at high risk for poverty. The NCD Summit offers an opportunity for strengthening and shaping primary prevention, the most cost-effective instrument to fight major risk factors such as tobacco smoking, alcohol abuse, physical inactivity and unhealthy diet. From a Swiss perspective, we also emphasised the efforts for new laws on prevention and diagnosis registration, in accordance with the recommendations of the NCD summit in order to strengthen primary prevention and disease monitoring. In addition, the need for structural prevention across all policy sectors with leadership in environmental policy making to prevent NCDs as well as the need to adapt and strengthen primary health care are equally relevant for Switzerland. To compliment efforts in primary prevention, the field of NCDs requires special R&D platforms for affordable NCD drugs and diagnostics for neglected population segments in both Switzerland and low and middle income countries. Switzerland has a track record in research and development against diseases of poverty on a global scale that now needs to be applied to NCDs.

The nucleosome core particle (NCP), comprised of histone proteins wrapped with ∼146 base pairs of DNA, provides both protection and controlled access to DNA so as to regulate vital cellular processes. High-resolution structures of nucleosomes and nucleosome complexes have afforded a clear understanding of the structural role of NCPs, but a detailed description of the dynamical properties that facilitate DNA-templated processes is only beginning to emerge. Using methyl-TROSY NMR approaches we evaluate the effect of point mutations designed to perturb key histone interfaces that become destabilized during nucleosome remodeling in an effort to probe NCP plasticity. Notably the NCP retains its overall structural integrity, yet relaxation experiments of mutant nucleosomes reveal significant dynamics within a central histone interface associated with alternative NCP conformations populated to as much as 15% under low salt conditions. This work highlights the inherent plasticity of NCPs and establishes methyl-TROSY NMR as a valuable compliment to current single molecule methods in quantifying NCP dynamic properties.

In this study, measurement of Epstein-Barr virus (EBV) and cytomegalovirus (CMV) viral antibody titers and analysis of both viral genomic sequences using polymerase chain reaction (PCR) were performed to clarify the correlation of viral infection and Moyamoya disease. Serum samples were obtained from 64 patients with Moyamoya disease. The ages ranged from 5 to 66 years, with a mean age of 35.1 years. There were 23 males and 41 females. The serum antibody titers to CMV and EBV were measured by means of compliment fixation test and fluorescent antibody method respectively. Those titers of the patients were compared with those of 13 patients of atherosclerotic internal carotid occlusion and 34 normal volunteers. On the other hand, CMV and EBV genomic sequence using PCR, which was utilized with specific primer pairs, were performed in 22 patients of Moyamoya disease and ten normal volunteers. The following results were obtained; The antibody titer of EBV in Moyamoya disease was significantly higher than that in controls. However, no significant difference of antibody titer against CMV was detected. In EBV DNA analysis by use of PCR, EBV DNA was proved in 15 out of 20 patients with Moyamoya disease and four out of nine normal controls. Namely, EBV DNA was seen more frequently in patients with Moyamoya disease, compared with normal controls. In inverse, CMV DNA was not seen in patients with Moyamoya disease nor normal controls. In conclusion, the antibody titer of EBV revealed high levels in Moyamoya disease and EBV DNA was also detected more frequently in patients with Moyamoya disease. These results suggested a possibility that EBV infection might be involved in the pathogenesis of Moyamoya disease.

There have been a variety of approaches taken to try to characterize and identify the genetic basis of adaptation in nature, spanning theoretical models, experimental evolution studies and direct tests of natural populations. Theoretical models can provide formalized and detailed hypotheses regarding evolutionary processes and patterns, from which experimental evolution studies can then provide important proofs of concepts and characterize what is biologically reasonable. Genetic and genomic data from natural populations then allow for the identification of the particular factors that have and continue to play an important role in shaping adaptive evolution in the natural world. Further to this, experimental evolution studies allow for tests of theories that may be difficult or impossible to test in natural populations for logistical and methodological reasons and can even generate new insights, suggesting further refinement of existing theories. However, as experimental evolution studies often take place in a very particular set of controlled conditions--that is simple environments, a small range of usually asexual species, relatively short timescales--the question remains as to how applicable these experimental results are to natural populations. In this review, we discuss important insights coming from experimental evolution, focusing on four key topics tied to the evolutionary genetics of adaptation, and within those topics, we discuss the extent to which the experimental work compliments and informs natural population studies. We finish by making suggestions for future work in particular a need for natural population genomic time series data, as well as the necessity for studies that combine both experimental evolution and natural population approaches.

The brain-gut axis plays a critical role in the regulation of different diseases, many of which are characterized by sympathetic dysregulation. However, a direct link between sympathetic dysregulation and gut dysbiosis remains to be illustrated. Bone marrow (BM)-derived immune cells continuously interact with the gut microbiota to maintain homeostasis in the host. Their function is largely dependent upon the sympathetic nervous system acting via adrenergic receptors present on the BM immune cells. In this study, we utilized a novel chimera mouse that lacks the expression of BM beta1/2 adrenergic receptors (b1/2-ARs) to investigate the role of the sympathetic drive to the BM in gut and microbiota homeostasis. Fecal analyses demonstrated a shift from a dominance of Firmicutes to Bacteroidetes phylum in the b1/2-ARs KO chimera, resulting in a reduction in Firmicutes/Bacteroidetes ratio. Meanwhile, a significant reduction in Proteobacteria phylum was determined. No changes in the abundance of acetate-, butyrate-, and lactate-producing bacteria, and colon pathology were observed in the b1/2-ARs KO chimera. Transcriptomic profiling in colon identified Killer Cell Lectin-Like Receptor Subfamily D, Member 1 (Klrd1), Membrane-Spanning 4-Domains Subfamily A Member 4A (Ms4a4b), and Casein Kinase 2 Alpha Prime Polypeptide (Csnk2a2) as main transcripts associated with the microbiota shifts in the b1/2-ARs KO chimera. Suppression of leukocyte-related transcriptome networks (i.e., function, differentiation, migration), classical compliment pathway, and networks associated with intestinal function, barrier integrity, and excretion was also observed in the colon of the KO chimera. Moreover, reduced expression of transcriptional networks related to intestinal diseases (i.e., ileitis, enteritis, inflammatory lesions, and stress) was noted. The observed suppressed transcriptome networks were associated with a reduction in NK cells, macrophages, and CD4+ T cells in the b1/2-ARs KO chimera colon. Thus, sympathetic regulation of BM-derived immune cells plays a significant role in modifying inflammatory networks in the colon and the gut microbiota composition. To our knowledge, this study is the first to suggest a key role of BM b1/2-ARs signaling in host-microbiota interactions, and reveals specific molecular mechanisms that may lead to generation of novel anti-inflammatory treatments for many immune and autonomic diseases as well as gut dysbiosis across the board.

Familial hypercholesterolemia (FH) is a common genetic cause of premature cardiovascular disease (CVD). The reported prevalence rates for both heterozygous FH (HeFH) and homozygous FH (HoFH) vary significantly, and this can be attributed, at least in part, to the variable diagnostic criteria used across different populations. Due to lack of consistent data, new global registries and unified guidelines are being formed, which are expected to advance current knowledge and improve the care of FH patients. This review presents a comprehensive overview of the pathophysiology, epidemiology, manifestations, and pharmacological treatment of FH, whilst summarizing the up-to-date relevant recommendations and guidelines. Ongoing research in FH seems promising and novel therapies are expected to be introduced in clinical practice in order to compliment or even substitute current treatment options, aiming for better lipid-lowering effects, fewer side effects, and improved clinical outcomes.

Seaweeds are an underutilised nutritional resource that could not only compliment the current western diet but potentially bring additional health benefits over and above their nutritional value. There are four groups of seaweed algae; green algae (Chlorophyceae), red algae (Rhodophycae), blue-green algae (Cyanophyceae) and brown algae (Phaeophyceae). Seaweeds are rich in bioactive components including polysaccharides and polyphenols. Polysaccharides content, such as fucoidan, laminarin, as well as alginate is generally high in brown seaweeds which are also a source of polyphenols such as phenolic acids, flavonoids, phlorotannin, stilbenes and lignans. These components have been shown to reduce the activity of digestive enzymes, modulating enzymes such as α-amylase, α-glucosidase, pepsin and lipase. This review discusses the effect of several of these components on the digestive processes within the gastrointestinal tract; focusing on the effect of alginate on pancreatic lipase activity and its potential health benefits. Concluding that there is evidence to suggest alginate has the potential to be used as an obesity treatment, however, further in vivo research is required and an effective delivery method for alginate must be designed.

Urine cytology continues to play an important role in the diagnosis and management of urothelial carcinoma, a common cancer of adults with significant morbidity and mortality. Because of its high sensitivity for high-grade urothelial tumors, including lesions that may be cystoscopically occult, urine cytology nicely compliments cystoscopic examination, a method that detects most low-grade tumors. Over the decades, several reporting schemes for urine cytology have been published in the literature, each of which has relative strengths and weaknesses. Unlike cervical cytology, there has not been widespread acceptance and use of any particular reporting scheme for urine cytology studies. Thus, terminology and criteria for urine cytology reporting are not uniform among pathologists, which can frustrate clinicians and hinders interlaboratory comparisons.

Mammalian carnivores have suffered the biggest range contraction among all biodiversity and are particularly vulnerable to habitat loss and fragmentation. Therefore, we identified priority areas for the conservation of mammalian carnivores, while accounting for species-specific requirements for connectivity and expected agricultural and urban expansion. While prioritizing for carnivores only, we were also able to test their effectiveness as surrogates for 23,110 species of amphibians, birds, mammals and reptiles and 867 terrestrial ecoregions. We then assessed the risks to carnivore conservation within each country that makes a contribution to global carnivore conservation. We found that land use change will potentially lead to important range losses, particularly amongst already threatened carnivore species. In addition, the 17% of land targeted for protection under the Aichi Target 11 was found to be inadequate to conserve carnivores under expected land use change. Our results also highlight that land use change will decrease the effectiveness of carnivores to protect other threatened species, especially threatened amphibians. In addition, the risk of human-carnivore conflict is potentially high in countries where we identified spatial priorities for their conservation. As meeting the global biodiversity target will be inadequate for carnivore protection, innovative interventions are needed to conserve carnivores outside protected areas to compliment any proposed expansion of the protected area network.