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Oral diseases such as tooth caries, periodontal diseases, endodontic infections, etc., are prevalent worldwide. The heavy burden of oral infectious diseases and their consequences on the patients' quality of life indicates a strong need for developing effective therapies. Advanced understandings of such oral diseases, e.g., inflammatory periodontal lesions, have raised the demand for antibacterial therapeutic strategies, because these diseases are caused by viruses and bacteria. The application of antimicrobial photodynamic therapy (aPDT) on oral infectious diseases has attracted tremendous interest in the past decade. However, aPDT had a minimal effect on the viability of organized biofilms due to the hydrophobic nature of the majority of the photosensitizers (PSs). Therefore, novel nanotechnologies were rapidly developed to target the delivery of hydrophobic PSs into microorganisms for the antimicrobial performance improvement of aPDT. This review focuses on the state-of-the-art of nanomaterials applications in aPDT against oral infectious diseases. The first part of this article focuses on the cutting-edge research on the synthesis, toxicity, and therapeutic effects of various forms of nanomaterials serving as PS carriers for aPDT applications. The second part discusses nanomaterials applications for aPDT in treatments of oral diseases. These novel bioactive nanomaterials have demonstrated great potential to serve as carriers for PSs to substantially enhance the PDT therapeutic effects. Furthermore, the novel aPDT applications not only have exciting therapeutic potential to inhibit bacterial plaque-initiated oral diseases, but also have a wide applicability to other biomedical and tissue engineering applications.

Motion sickness is a complex syndrome that includes many features besides nausea and vomiting. This review describes some of these factors and points out that under normal circumstances, many cases of motion sickness go unrecognized. Motion sickness can occur during exposure to physical motion, visual motion, and virtual motion, and only those without a functioning vestibular system are fully immune. The range of vulnerability in the normal population varies about 10,000 to 1. Sleep deprivation can also enhance susceptibility. Systematic studies conducted in parabolic flight have identified velocity storage of semicircular canal signals—velocity integration—as being a key factor in both space motion sickness and terrestrial motion sickness. Adaptation procedures that have been developed to increase resistance to motion sickness reduce this time constant. A fully adequate theory of motion sickness is not presently available. Limitations of two popular theories, the evolutionary and the ecological, are described. A sensory conflict theory can explain many but not all aspects of motion sickness elicitation. However, extending the theory to include conflicts related to visceral afferent feedback elicited by voluntary and passive body motion greatly expands its explanatory range. Future goals should include determining why some conflicts are provocative and others are not but instead lead to perceptual reinterpretations of ongoing body motion. The contribution of visceral afferents in relation to vestibular and cerebellar signals in evoking sickness also deserves further exploration. Substantial progress is being made in identifying the physiological mechanisms underlying the evocation of nausea, vomiting, and anxiety, and a comprehensive understanding of motion sickness may soon be attainable. Adequate anti-motion sickness drugs without adverse side effects are not yet available.

Tinnitus is a common medical symptom that can be debilitating. Risk factors include hearing loss, ototoxic medication, head injury, and depression. At presentation, the possibilities of otological disease, anxiety, and depression should be considered. No effective drug treatments are available, although much research is underway into mechanisms and possible treatments. Surgical intervention for any otological pathology associated with tinnitus might be effective for that condition, but the tinnitus can persist. Available treatments include hearing aids when hearing loss is identified (even mild or unilateral), wide-band sound therapy, and counselling. Cognitive behavioural therapy (CBT) is indicated for some patients, but availability of tinnitus-specific CBT in the UK is poor. The evidence base is strongest for a combination of sound therapy and CBT-based counselling, although clinical trials are constrained by the heterogeneity of patients with tinnitus.

Benign paroxysmal positional vertigo is characterized by brief spinning sensations, which are generally induced by a change in head position with respect to gravity. Treatment involves canalith-repositioning maneuvers, which are reviewed in detail. Foreword This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors' clinical recommendations. Stage A 58-year-old woman seeks care from her primary physician after the occurrence of sudden vertigo and imbalance with nausea and vomiting, which began that morning when she got out of bed. The vertigo lasted less than a minute but recurred when she lay back down in bed, rolled over in bed, or got up again. She reports no tinnitus or hearing loss. How should this patient be evaluated and treated? The Clinical Problem Benign paroxysmal positional vertigo (BPPV) is by far the most common type of vertigo, with a reported prevalence between 10.7 and 64.0 cases per 100,000 population . . .

The origin of the internal “sensory conflict” stimulus causing motion sickness has been debated for more than four decades. Recent studies show a subclass of neurons in the vestibular nuclei and deep cerebellar nuclei that respond preferentially to passive head movements. During active movement, the semicircular canal and otolith input (“reafference”) to these neurons are canceled by a mechanism comparing the expected consequences of self-generated movement (estimated with an internal model—presumably located in the cerebellum) with the actual sensory feedback. The un-canceled component (“exafference”) resulting from passive movement normally helps compensate for unexpected postural disturbances. Notably, the existence of such vestibular “sensory conflict” neurons had been postulated as early as 1982, but their existence and putative role in posture control and motion sickness have been long debated. Here, we review the development of “sensory conflict” theories in relation to recent evidence for brainstem and cerebellar reafference cancelation, and identify some open research questions. We propose that conditions producing persistent activity of these neurons, or their targets, stimulate nearby brainstem emetic centers—via an as yet unidentified mechanism. We discuss how such a mechanism is consistent with the notable difference in motion sickness susceptibility of drivers as opposed to passengers, human immunity to normal self-generated movement and why head restraint or lying horizontal confers relative immunity. Finally, we propose that fuller characterization of these mechanisms and their potential role in motion sickness could lead to more effective, scientifically based prevention and treatment for motion sickness.

Zirconia-based restorations are widely used in prosthetic dentistry; however, their susceptibility to hydrothermal degradation remains elusive. We hypothesized that CAD/CAM machining and subsequent surface treatments, i.e., grinding and/or grit-blasting, have marked effects on the hydrothermal degradation behavior of Y-TZP. CAD/CAM-machined Y-TZP plates (0.5 mm thick), both with and without subsequent grinding with various grit sizes or grit-blasting with airborne alumina particles, were subjected to accelerated aging tests in a steam autoclave. Results showed that the CAD/CAM-machined surfaces initially exhibited superior hydrothermal degradation resistance, but deteriorated at a faster rate upon prolonged autoclave treatment compared with ground and grit-blasted surfaces. The accelerated hydrothermal degradation of CAD/CAM surfaces is attributed to the CAD/CAM machining damage and the absence of surface compressive stresses in the fully sintered material. Clinical relevance for surface treatments of zirconia frameworks in terms of hydrothermal and structural stabilities is addressed.

Vomiting and nausea can be elicited by a variety of stimuli, although there is considerable evidence that the same brainstem areas mediate these responses despite the triggering mechanism. A variety of experimental approaches showed that nucleus tractus solitarius, the dorsolateral reticular formation of the caudal medulla (lateral tegmental field), and the parabrachial nucleus play key roles in integrating signals that trigger nausea and vomiting. These brainstem areas presumably coordinate the contractions of the diaphragm and abdominal muscles that result in vomiting. However, it is unclear whether these regions also mediate the autonomic responses that precede and accompany vomiting, including alterations in gastrointestinal activity, sweating, and changes in blood flow to the skin. Recent studies showed that delivery of an emetic compound to the gastrointestinal system affects the processing of vestibular inputs in the lateral tegmental field and parabrachial nucleus, potentially altering susceptibility for vestibular-elicited vomiting. Findings from these studies suggested that multiple emetic inputs converge on the same brainstem neurons, such that delivery of one emetic stimulus affects the processing of another emetic signal. Despite the advances in understanding the neurobiology of nausea and vomiting, much is left to be learned. Additional neurophysiologic studies, particularly those conducted in conscious animals, will be crucial to discern the integrative processes in the brain stem that result in emesis.

Key Points Clefts of the lip and/or palate (CLP) are common birth defects of complex aetiology. CLP affects approximately 1 in 700 live births, with wide variability across geographic origin, racial and ethnic groups, as well as environmental exposures and socioeconomic status. CLP can occur in syndromic or non-syndromic forms. This Review focuses on the latter. Although twin studies and familial clustering studies have provided compelling evidence for a genetic component to non-syndromic CLP, few pedigrees show clear-cut Mendelian inheritance and many cases appear to be sporadic. Accurate phenotyping is crucial to understanding both the epidemiology and aetiology of any congenital malformation because the power to detect effects is weakened when heterogeneous groups are treated as a single entity. To date, genetic approaches to non-syndromic CLP have included: linkage analysis using large, multiplex families or smaller but inbred families, or analysis of affected relative pairs; association studies using case–parent trios or case–control samples; identification of chromosomal anomalies or micro-deletions in cases; and direct sequencing of affected individuals. Genome-wide association studies have provided recent major advances in our understanding of genes and pathways that have a role in the aetiology of CLP. There is remarkable heterogeneity by ancestry in the relative contributions by genes found with common variants contributing to CLP. There is evidence that environmental factors have a role in CLP risk and interactions of the environment with certain genetic variants have been identified. The next critical phase of statistical analyses will be to examine the heterogeneity underlying the aetiology of oral clefts and to investigate the gene–gene and gene–environment interactions that control risk. Integration of genetic and environmental risk using epigenetics, systems biology, gene expression and epidemiology will be required to generate a synthesis that will both better characterize aetiologies and eventually lead to improvements in prevention and clinical care. Clefts of the lip and/or palate are common and have a complex genetic and environmental basis. Recent work on these birth defects illustrates the value of combining genome-wide association studies, animal models and improved clinical phenotyping. Future work may also address gene–environment interactions. Clefts of the lip and/or palate (CLP) are common birth defects of complex aetiology. CLP can occur in isolation or as part of a broad range of chromosomal, Mendelian or teratogenic syndromes. Although there has been marked progress in identifying genetic and environmental triggers for syndromic CLP, the aetiology of the more common non-syndromic (isolated) forms remains poorly characterized. Recently, using a combination of epidemiology, careful phenotyping, genome-wide association studies and analysis of animal models, several distinct genetic and environmental risk factors have been identified and confirmed for non-syndromic CLP. These findings have advanced our understanding of developmental biology and created new opportunities for clinical translational research.

Head and neck squamous cell carcinoma (HNSCC) is a common, morbid, and frequently lethal malignancy. To uncover its mutational spectrum, we analyzed whole-exome sequencing data from 74 tumor-normal pairs. The majority exhibited a mutational profile consistent with tobacco exposure; human papillomavirus was detectable by sequencing DNA from infected tumors. In addition to identifying previously known HNSCC genes (TP53, CDKN2A, PTEN, PIK3CA, and HRAS), our analysis revealed many genes not previously implicated in this malignancy. At least 30% of cases harbored mutations in genes that regulate squamous differentiation (for example, NOTCH1, IRF6, and TP63), implicating its dysregulation as a major driver of HNSCC carcinogenesis. More generally, the results indicate the ability of large-scale sequencing to reveal fundamental tumorigenic mechanisms.

Allergic rhinitis is a very common disorder that affects people of all ages, peaking in the teenage years. It is frequently ignored, underdiagnosed, misdiagnosed, and mistreated, which not only is detrimental to health but also has societal costs. Although allergic rhinitis is not a serious illness, it is clinically relevant because it underlies many complications, is a major risk factor for poor asthma control, and affects quality of life and productivity at work or school. Management of allergic rhinitis is best when directed by guidelines. A diagnostic trial of a pharmacotherapeutic agent could be started in people with clinically identified allergic rhinitis; however, to confirm the diagnosis, specific IgE reactivity needs to be recorded. Documented IgE reactivity has the added benefit of guiding implementation of environmental controls, which could substantially ameliorate symptoms of allergic rhinitis and might prevent development of asthma, especially in an occupational setting. Many classes of drug are available, effective, and safe. In meta-analyses, intranasal corticosteroids are superior to other treatments, have a good safety profile, and treat all symptoms of allergic rhinitis effectively. First-generation antihistamines are associated with sedation, psychomotor retardation, and reduced academic performance. Only immunotherapy with individually targeted allergens has the potential to alter the natural history of allergic rhinitis. Patients' education is a vital component of treatment. Even with the best pharmacotherapy, one in five affected individuals remains highly symptomatic, and further research is needed in this area.