Diverse invertebrate species have been used for studies of learning and comparative cognition. Although we have gained invaluable information from this, in this study we argue that our approach to comparative learning research is rather deficient. Generally invertebrate learning research has focused mainly on arthropods, and most of that within the Hymenoptera and Diptera. Any true comparative analysis of the distribution of comparative cognitive abilities across phyla is hampered by this bias, and more fundamentally by a reporting bias toward positive results. To understand the limits of learning and cognition for a species, knowing what animals cannot do is at least as important as reporting what they can. Finally, much more effort needs to be focused on the neurobiological analysis of different types of learning to truly understand the differences and similarities of learning types. In this review, we first give a brief overview of the various forms of learning in invertebrates. We also suggest areas where further study is needed for a more comparative understanding of learning. Finally, using what is known of learning in honeybees and the well-studied honeybee brain, we present a model of how various complex forms of learning may be accounted for with the same neural circuitry required for so-called simple learning types. At the neurobiological level, different learning phenomena are unlikely to be independent, and without considering this it is very difficult to correctly interpret the phylogenetic distribution of learning and cognitive abilities. WIREs Cogn Sci 2013, 4:561-582. doi: 10.1002/wcs.1248 For further resources related to this article, please visit the WIREs website.

There is a controversy regarding most effective operative method for treatment of pyogenic spondylitis and whether to use metallic implants on the site of infection. This retrospective study reports on the outcome of 17 patients with persistent cervical and lumbar pyogenic spondylitis who had one-stage combined surgery and fusion with use of a titanium mesh cage for intractable pain, kyphosis, and neurologic impairment. All patients tolerated the combined operation and were followed up on for 45 months. Incomplete neurologic lesions improved postoperatively an average 1.4 Frankel grades. Visual analog pain score (mean) improved from 7 preoperatively to 2 postoperatively. Average correction of local kyphotic deformity was 6 degrees without loss of correction at final observation. There was no expulsion or migration of any titanium mesh cage or loosening of the posterior instrumentation. There was an approach-related abdominal hernia after wound infection. At the final followup, the combined operation in combination with the use of the mesh cage improved sagittal alignment and resulted in eradication of the infection and attainment of solid fusion. The presence of the titanium mesh cage anteriorly at the site of infection had no adverse effect on the course of infection. Patients with cervical and lumbar osteomyelitis can successfully have instrumented-combined, one-stage surgery.

METHODS

Prognostic study, Level II (retrospective study). Please see the Guidelines for Authors for a complete description of levels of evidence.

The internet has become a popular resource to learn about health and to investigate one's own health condition. However, given the large amount of inaccurate information online, people can easily become misinformed. Individuals have always obtained information from outside the formal health care system, so how has the internet changed people's engagement with health information? This review explores how individuals interact with health misinformation online, whether it be through search, user-generated content, or mobile apps. We discuss whether personal access to information is helping or hindering health outcomes and how the perceived trustworthiness of the institutions communicating health has changed over time. To conclude, we propose several constructive strategies for improving the online information ecosystem. Misinformation concerning health has particularly severe consequences with regard to people's quality of life and even their risk of mortality; therefore, understanding it within today's modern context is an extremely important task. Expected final online publication date for the Annual Review of Public Health, Volume 41 is April 1, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

Deubiquitylating (or deubiquitinating) enzymes (DUBs) are proteases that reverse protein ubiquitylation and therefore modulate the outcome of this post-translational modification. DUBs regulate a variety of intracellular processes, including protein turnover, signalling pathways and the DNA damage response. They have also been linked to a number of human diseases, such as cancer, and inflammatory and neurodegenerative disorders. Although we are beginning to better appreciate the role of DUBs in basic cell biology and their importance for human health, there are still many unknowns. Central among these is the conundrum of how the small number of ∼100 DUBs encoded in the human genome is capable of regulating the thousands of ubiquitin modification sites detected in human cells. This Commentary addresses the biological mechanisms employed to modulate and expand the functions of DUBs, and sets directions for future research aimed at elucidating the details of these fascinating processes.This article is part of a Minifocus on Ubiquitin Regulation and Function. For further reading, please see related articles: 'Exploitation of the host cell ubiquitin machinery by microbial effector proteins' by Yi-Han Lin and Matthias P. Machner (J. Cell Sci.130, 1985-1996). 'Cell scientist to watch - Mads Gyrd-Hansen' (J. Cell Sci.130, 1981-1983).

Recent molecular genetic findings on endometriosis and normal endometrium suggest a modified model in which circulating epithelial progenitor or stem cells intended to regenerate uterine endometrium after menstruation may become overreactive and trapped outside the uterus. These trapped epithelium-committed progenitor cells form nascent glands through clonal expansion and recruit polyclonal stromal cells, leading to the establishment of deep infiltrating endometriosis. Once formed, the ectopic tissue becomes subject to immune surveillance, resulting in chronic inflammation. The inflammatory response orchestrated by nuclear factor-κB signaling is exacerbated by aberrations in the estrogen receptor-β and progesterone receptor pathways, which are also affected by local inflammation, forming a dysregulated inflammation-hormonal loop. Glandular epithelium within endometriotic tissue harbors cancer-associated mutations that are frequently detected in endometriosis-related ovarian cancers. In this review, we summarize recent advances that have illuminated the origin and pathogenesis of endometriosis and have provided new avenues for research that promise to improve the early diagnosis and management of endometriosis. Expected final online publication date for the Annual Review of Pathology: Mechanisms of Disease, Volume 15 is January 24, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Current osteoporosis medications reduce fractures significantly but have rare and serious adverse effects (osteonecrosis of the jaw, atypical femoral fractures) that may limit their safety for long-term use. Insights from basic bone biology and genetic disorders have led to recent advances in therapeutics for osteoporosis. New approaches now in clinical use include the antisclerostin monoclonal antibody romosozumab, as well as the parathyroid hormone-related peptide analog abaloparatide. Clinical trial data show significant antifracture benefits with recently approved romosozumab. Studies using abaloparatide build on our longstanding experience with teriparatide and the importance of consolidating the bone mineral density gains achieved from an anabolic agent by following it with an antiresorptive. Combination and sequential treatments using osteoporosis medications with different mechanisms of action have also been tested with promising results. On the horizon is the potential for cell-based therapies (e.g., mesenchymal stem cells) and drugs that target the elimination of senescent cells in the bone microenvironment. Expected final online publication date for the Annual Review of Medicine, Volume 71 is January 27, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Dengue is an emerging viral disease principally transmitted by the Aedes (Stegomyia) aegypti mosquito. It is one of the fastest-growing global infectious diseases, with 100-400 million new infections a year, and is now entrenched in a growing number of tropical megacities. Behind this rapid rise is the simple adaptation of Ae. aegypti to a new entomological niche carved out by human habitation. This review describes the expansion of dengue and explores how key changes in the ecology of Ae. aegypti allowed it to become a successful invasive species and highly efficient disease vector. We argue that characterizing geographic heterogeneity in mosquito bionomics will be a key research priority that will enable us to better understand future dengue risk and design control strategies to reverse its global spread. Expected final online publication date for the Annual Review of Entomology, Volume 65 is January 7, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Depression remains one of the most prevalent psychiatric disorders, with many patients not responding adequately to available treatments. Chronic or early-life stress is one of the key risk factors for depression. In addition, a growing body of data implicates chronic inflammation as a major player in depression pathogenesis. More recently, the gut microbiota has emerged as an important regulator of brain and behavior and also has been linked to depression. However, how this holy trinity of risk factors interact to maintain physiological homeostasis in the brain and body is not fully understood. In this review, we integrate the available data from animal and human studies on these three factors in the etiology and progression of depression. We also focus on the processes by which this microbiota-immune-stress matrix may influence centrally mediated events and on possible therapeutic interventions to correct imbalances in this triune. Expected final online publication date for the Annual Review of Psychology, Volume 71 is January 4, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee (https://doi.org/10.2337/dc21-SPPC), are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction (https://doi.org/10.2337/dc21-SINT). Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

BACKGROUND

The Gene Ontology Project provides structured controlled vocabularies for molecular biology that can be used for the functional annotation of genes and gene products. In a collaboration between the Gene Ontology (GO) Consortium and the muscle biology community, we have made large-scale additions to the GO biological process and cellular component ontologies. The main focus of this ontology development work concerns skeletal muscle, with specific consideration given to the processes of muscle contraction, plasticity, development, and regeneration, and to the sarcomere and membrane-delimited compartments. Our aims were to update the existing structure to reflect current knowledge, and to resolve, in an accommodating manner, the ambiguity in the language used by the community.

RESULTS

The updated muscle terminologies have been incorporated into the GO. There are now 159 new terms covering critical research areas, and 57 existing terms have been improved and reorganized to follow their usage in muscle literature.

CONCLUSIONS

The revised GO structure should improve the interpretation of data from high-throughput (e.g. microarray and proteomic) experiments in the area of muscle science and muscle disease. We actively encourage community feedback on, and gene product annotation with these new terms. Please visit the Muscle Community Annotation Wiki http://wiki.geneontology.org/index.php/Muscle_Biology.

In most clinical trials of antiretroviral therapy for patients infected with HIV, the major outcome variable has been the combined clinical endpoint of any new or recurrent AIDS defining event. We review features of combined endpoints and use data from the Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA) to evaluate this outcome measure in terms of relevance, diagnostic certainty and sensitivity. We conclude that this endpoint is not relevant because: (i) the 19 different events constituting the combined endpoint are equally weighted in analyses even though they vary considerably in terms of risk of death; and (ii) events after the first are ignored, thus the event profile of patients is not taken into account in making treatment comparisons. We also conclude that power may be low with use of this endpoint if treatments under study do not have an immediate impact on disease progression, if some events which occur soon after randomization represent a disease process that has already begun to incubate, or if treatment differences for the various events constituting the combined endpoint are differentially effected by treatment. Since the ease and certainty of diagnosis of each of the 19 events also vary, we recommend that survival be the primary endpoint of antiretroviral trials, and that all opportunistic events experienced by patients, not just the first, be collected and summarized. Trial reports should include comparisons of incidence of each event by treatment group so that readers can rank events as they please. A single summary measure which considers severity and the entire event profile, as described here, would also be useful for assessing the impact of treatments on quality of life. Further research on approaches for weighting and combining multiple outcome measures is needed.

The purpose of this phenomenological study was to describe the experience of quality of life of women, taking care of husbands with chronic obstructive pulmonary disease (COPD). Unstructured, in-depth, tape-recorded personal interviews were used to collect data from six women living with husbands with COPD. The women ranged from 47 to 69 years in age and their husbands had given up work because of the illness. The wives in the study were dissatisfied with their lack of recreation, as well as support from friends, families and health care providers. Factors that increased the wife's quality of life were children and grandchildren and being able to please the husband and care for him until the very end.

Rozin & Rozin (1981) have suggested that the addition of flavour principles (the distinctive combinations of seasonings which characterize many cuisines) may facilitate the introduction of a new staple food into a culture. That is, the reluctance of omnivores to approach novel foods can be reduced by adding the familiar flavor principle to the unfamiliar food. To test this hypothesis, we "created" flavor principles in the laboratory by exposing children repeatedly to one of two initially novel chip dips. After the exposure phase, they were offered familiar and unfamiliar chips and asked about their willingness to taste each, alone, with the exposed dip, the unexposed dip, and several other dips. The main prediction was that addition of the exposed dip to the unfamiliar chip would increase children's willingness to taste it. Since individuals are not reluctant to taste familiar foods, addition of the exposed dip to the familiar chip was not expected to increase willingness to taste it. The results confirmed this prediction. Practical and theoretical implications of this finding were discussed.

BACKGROUND

Bacteriorhodopsin (bR) is the simplest known light driven proton pump and has been heavily studied using structural methods: eighty four X-ray diffraction, six electron diffraction and three NMR structures of bR are deposited within the protein data bank. Twenty one X-ray structures report light induced structural changes and changes induced by mutation, changes in pH, thermal annealing or X-ray induced photo-reduction have also been examined.

METHODS

We argue that light-induced structural changes that are replicated across several studies by independent research groups are those most likely to represent what is happening in reality. We present both internal distance matrix analyses that sort deposited bR structures into hierarchal trees, and difference Fourier analysis of deposited X-ray diffraction data.

CONCLUSIONS

An internal distance matrix analysis separates most wild-type bR structures according to their different crystal forms, indicating how the protein's structure is influenced by crystallization conditions. A similar analysis clusters eleven studies of illuminated bR crystals as one branch of a hierarchal tree with reproducible movements of the extracellular portion of helix C towards helix G, and of the cytoplasmic portion of helix F away from helices A, B and G. All crystallographic data deposited for illuminated crystals show negative difference density on a water molecule (Wat402) that forms H-bonds to the retinal Schiff Base and two aspartate residues (Asp85, Asp212) in the bR resting state. Other recurring difference density features indicated reproducible side-chain, backbone and water molecule displacements. X-ray induced radiation damage also disorders Wat402 but acts via cleaving the head-groups of Asp85 and Asp212.

CONCLUSIONS

A remarkable level of agreement exists when deposited structures and crystallographic observations are viewed as a whole. From this agreement a unified picture of the structural mechanism of light-induced proton pumping by bR emerges. This article is part of a Special Issue entitled Structural biochemistry and biophysics of membrane proteins.

Everolimus (RAD001, Afinitor®) is an oral protein kinase inhibitor of the mammalian target of rapamycin (mTOR) serine/threonine kinase signal transduction pathway. The mTOR pathway regulates cell growth, proliferation, and survival and is frequently deregulated in cancer. Everolimus has been approved by the FDA and the EMA for the treatment of advanced renal cell carcinoma (RCC), subependymal giant cell astrocytoma (SEGA) associated with tuberous sclerosis (TSC), pancreatic neuroendocrine tumors (PNET), in combination with exemestane in advanced hormone-receptor (HR)-positive, HER2-negative breast cancer. Everolimus shows promising clinical activity in additional indications. Multiple phase 2 and phase 3 trials of everolimus alone or in combination are ongoing and will help to further elucidate the role of mTOR in oncology. For a review on everolimus as immunosuppressant, please consult other sources.

The Quebec Task Force (QTF) on Whiplash Associated Disorders (WAD)--1995--sent a clear message that we need to re-evaluate the basis for our treatment strategies, and in particular place more emphasis on research to better define these strategies. Judging by many of the clinical strategies currently in use, the Task Force recommendations seem to have been largely ignored three years later. A further compelling reason to re-evaluate our current practices at this time is the finding of much more rapid recovery rates in some cultures, even with little or no therapy. This commentary is a frank consideration of the therapeutic community's responsibility to not only help solve the dilemma of whiplash, but also avoid contributing to the problem. We thus explore a new biopsychosocial model of whiplash, considering the effects of symptom expectation, amplification, and attribution in chronic pain reporting. Based on that model we propose a treatment strategy, and conclude that such strategies provide the only viable approach to this medicolegal and social dilemma.

Heredoataxias are a group of genetic disorders with a cerebellar syndrome as the leading clinical manifestation. The current classification distinguishes heredoataxias according to the trait of inheritance into autosomal dominant, autosomal recessive, X-linked, and maternally inherited heredoataxias. The autosomal dominant heredoataxias are separated into spinocerebellar ataxias (SCA1-8, 10-15, 17-23, 25-30, and dentato-rubro-pallido-luysian atrophy), episodic ataxias (EA1-7), and autosomal dominant mitochondrial heredoataxias (Leigh syndrome, MIRAS, ADOAD, and AD-CPEO). The autosomal recessive ataxias are separated into Friedreich ataxia, ataxia due to vitamin E deficiency, ataxia due to Abeta-lipoproteinemia, Refsum disease, late-onset Tay-Sachs disease, cerebrotendineous xanthomatosis, spinocerebellar ataxia with axonal neuropathy, ataxia telangiectasia, ataxia telangiectasia-like disorder, ataxia with oculomotor apraxia 1 and 2, spastic ataxia of Charlevoix-Saguenay, Cayman ataxia, Marinesco-Sjögren syndrome, and autosomal recessive mitochondrial ataxias (AR-CPEO, SANDO, SCAE, AHS, IOSCA, MEMSA, LBSL CoQ-deficiency, PDC-deficiency). Only two of the heredoataxias, fragile X/tremor/ataxia syndrome, and XLSA/A are transmitted via an X-linked trait. Maternally inherited heredoataxias are due to point mutations in genes encoding for tRNAs, rRNAs, respiratory chain subunits or single large scale deletions/duplications of the mitochondrial DNA and include MELAS, MERRF, KSS, PS, MILS, NARP, and non-syndromic mitochondrial disorders. Treatment of heredoataxias is symptomatic and supportive and may have a beneficial effect in single patients. **Please see page 424 for abbreviation list.

A classic puzzle in understanding visual scene perception is how to reconcile the physiological constraints of vision with the phenomenology of seeing. Vision captures information via discrete eye fixations, interrupted by saccadic suppression, and limited by retinal inhomogeneity. Yet scenes are effortlessly perceived as coherent, continuous, and meaningful. Two conceptualizations of scene representation will be contrasted. The traditional visual-cognitive model casts visual scene representation as an imperfect reflection of the visual sensory input alone. By contrast, a new multisource model casts visual scene representation in terms of an egocentric spatial framework that is 'filled-in' by visual sensory input, but also by amodal perception, and by expectations and by constraints derived from rapid-scene classification and object-to-context associations. Together, these nonvisual sources serve to 'simulate' a likely surrounding scene that the visual input only partially reveals. Pros and cons of these alternative views will be discussed. WIREs Cogn Sci 2012, 3:117-127. doi: 10.1002/wcs.149 For further resources related to this article, please visit the WIREs website.

Growing evidence indicates that the melanocortin 1 receptor (MC1R) and its ligand α-melanocyte-stimulating hormone (α-MSH) have other functions in the skin in addition to pigment production. Activation of the MC1R/α-MSH signaling pathway has been implicated in the regulation of both inflammation and extracellular matrix homeostasis. However, little is known about the role of MC1R/α-MSH signaling in the regulation of inflammatory and fibroproliferative responses to cutaneous injury. Although MC1R and α-MSH localization has been described in uninjured skin, their spatial and temporal expression during cutaneous wound repair has not been investigated. In this study, the authors report the localization of MC1R and α-MSH in murine cutaneous wounds, human acute burns, and hypertrophic scars. During murine wound repair, MC1R and α-MSH were detected in inflammatory cells and suprabasal keratinocytes at the leading edge of the migrating epithelial tongue. MC1R and α-MSH protein levels were upregulated in human burn wounds and hypertrophic scars compared to uninjured human skin, where receptor and ligand were absent. In burn wounds and hypertrophic scars, MC1R and α-MSH localized to epidermal keratinocytes and dermal fibroblasts. This spatiotemporal localization of MC1R and α-MSH in cutaneous wounds warrants future investigation into the role of MC1R/α-MSH signaling in the inflammatory and fibroproliferative responses to cutaneous injury. This article contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Most, if not all, dorsal root ganglion (DRG) neurons use the neurotransmitter glutamate. There are, however, conflicting reports of the percentages of DRG neurons that express glutaminase (GLS), the enzyme that synthesizes glutamate, ranging from 30% to 100% of DRG neurons. Defining DRG neuron populations by the expression of proteins like GLS, which indicates function, is routinely accomplished with immunolabeling techniques. Proper characterization of DRG neuron populations relies on accurate detection of such antigens. It is known intuitively that fixation can alter immunoreactivity (IR). In this study, we compared the effects of five formaldehyde concentrations between 0.25% and 4.0% (w/v) and five picric acid concentrations between 0.0% and 0.8% (w/v) on the IR of GLS, the voltage-gated sodium channel 1.8 (Na(v)1.8), and the capsaicin receptor TRPV1. We also compared the effects of five incubation time lengths from 2 to 192 hr, in primary antiserum on IR. Lowering formaldehyde concentration elevated IR for all three antigens, while raising picric acid concentration increased Na(v)1.8 and TRPV1 IR. Increasing IR improved detection sensitivity, which led to higher percentages of labeled DRG neurons. By selecting fixation conditions that optimized IR, we found that all DRG neurons express GLS, 69% of neurons express Na(v)1.8, and 77% of neurons express TRPV1, indicating that some previous studies may have underestimated the percentages of DRG neurons expressing these proteins. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Since Panayiotis Gennadius first identified the whitefly, Aleyrodes tabaci in 1889, there have been numerous revisions of the taxonomy of what has since become one of the world's most damaging insect pests. Most of the taxonomic revisions have been based on synonymising different species under the name Bemisia tabaci. It is now considered that there is sufficient biological, behavioural and molecular genetic data to support its being a cryptic species complex composed of at least 34 morphologically indistinguishable species. The first step in revising the taxonomy of this complex involves matching the A. tabaci collected in 1889 to one of the members of the species complex using molecular genetic data. To do this we extracted and then amplified a 496 bp fragment from the 3' end of the mitochondrial DNA cytochrome oxidase one (mtCOI) gene belonging to a single whitefly taken from Gennadius' original 1889 collection. The sequence identity of this 123 year-old specimen enabled unambiguous assignment to a single haplotype known from 13 Mediterranean locations across Greece and Tunisia. This enabled us to unambiguously assign the Gennadius A. tabaci to the member of the B. tabaci cryptic species complex known as Mediterranean or as it is commonly, but erroneously referred to, as the 'Q-biotype'. Mediterranean is therefore the real B. tabaci. This study demonstrates the importance of matching museum syntypes with known species to assist in the delimitation of cryptic species based on the organism's biology and molecular genetic data. This study is the first step towards the reclassification of B. tabaci which is central to an improved understanding how best to manage this globally important agricultural and horticultural insect pest complex.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor in Chief. The term miR-143 has been used instead of the term miR-143* in the introduction and discussion which is misleading. With the misuse of this term subsequent errors and misleading statements appear throughout the paper. The authors apologize for this mistake.