Aetiology of melanized inclusions in the body cavity of Neodiprion sertifer (Geoffroy) (Hym., Diprionidae) adults

Abstract: The aetiology of large melanized inclusions occurring in the haemocoel of adults of some diprionid sawflies is not fully understood. Their occurrence has been associated with nuclear polyhedrosis virus (NPV), but also with extreme temperatures, parasitism, and prolonged diapause. High frequencies of inclusions are found most often during NPV epizootics. In laboratory experiments with Neodiprion sertifer larvae, ingestion of large doses of a common bacterium, Enterobacter cloacae , was shown to induce inclusions indistinguishable from those associated with NPV infection. It is argued that a bacterial aetiology is not contradicted by the other conditions reported to be associated with inclusions. The bacterial aetiology provides an explanation for the low frequencies of inclusions in N. sertifer populations with no NPV infection. It is proposed that the ability to form inclusions may have evolved as a defence against bacterial infection.     

Shifting white pox aetiologies affecting Acropora palmata in the Florida Keys, 1994–2014

We propose ‘the moving target hypothesis’ to describe the aetiology of a contemporary coral disease that differs from that of its historical disease state. Hitting the target with coral disease aetiology is a complex pursuit that requires understanding of host and environment, and may lack a single pathogen solution. White pox disease (WPX) affects the Caribbean coral Acropora palmata. Acroporid serratiosis is a form of WPX for which the bacterial pathogen (Serratia marcescens) has been established. We used long-term (1994–2014) photographic monitoring to evaluate historical and contemporary epizootiology and aetiology of WPX affecting A. palmata at eight reefs in the Florida Keys. Ranges of WPX prevalence over time (0–71.4%) were comparable for the duration of the 20-year study. Whole colony mortality and disease severity were high in historical (1994–2004), and low in contemporary (2008–2014), outbreaks of WPX. Acroporid serratiosis was diagnosed for some historical (1999, 2003) and contemporary (2012, 2013) outbreaks, but this form of WPX was not confirmed for all WPX cases. Our results serve as a context for considering aetiology as a moving target for WPX and other coral diseases for which pathogens are established and/or candidate pathogens are identified. Coral aetiology investigations completed to date suggest that changes in pathogen, host and/or environment alter the disease state and complicate diagnosis.     

An NZB virus or NZB mice with viral infections?

Evidence for and against the possibility that the autoimmune disease of NZB mice has a viral aetiology is presented. It is considered that the case for a viral aetiology is unproven, although the possibility exists that virus may be present in incomplete form. Widely varying experimental results can be expected in experiments involving NZB mice until acceptable standards of mouse strain definition are laid down. Thus the comparison of results obtained from studies of NZB mice of diverse origin may invite misleading conclusions.     

原因不明子宫内膜薄雌激素受体β基因RsaⅠ、AluⅠ多态性

旨在探讨重庆地区雌激素受体β基因RsaⅠ、AluⅠ多态性与原因不明子宫内膜薄的关系.选择重庆地区120名原因不明子宫内膜薄患者为试验组,120名正常子宫内膜作为对照组.应用聚合酶链反应-限制性片段长度多态性的方法分析ERβ基因RsaⅠ、AluⅠ多态性.观察ER β基因多态性在试验组与对照组中的分布,分析各基因型、等位基因型及单倍体型特征.结果显示,两组ER β基因RsaⅠ基因型比较差异有显著性,R等位基因型频率试验组为37.1%,对照组为48.3%,OR值为0.630(95%CI=0.438～0.907),P=0.013;两组ER β基因AluⅠ基因型比较差异没有显著性.试验组和对照组ER β基因RsaI和AluI单倍体型D′分别=0.1138、0.0680,其连锁不平衡性不强.ER β基因多态性与原因不明子宫内膜薄有关,R等位基因可能是其保护因素.     

A critical review of the use of Clara cell secretory protein (CC16) as a biomarker of acute or chronic pulmonary effects

Biomarkers associated with asthma aetiology and exacerbation have been sought to shed light on this multifactorial disease. One candidate is the serum concentration of the Clara cell secretory protein (CC16, sometimes referred to as CC10 or uteroglobin). In this review, we examine serum CC16's relation to asthma aetiology and exacerbation. There is evidence that acute exposures to certain pulmonary irritants can cause a transient increase in serum CC16 levels, and limited evidence also suggests that a transient increase in serum CC16 levels can be caused by a localized pulmonary inflammation. Research also indicates that a transient increase in serum CC16 is not associated with measurable pulmonary damage or impairment of pulmonary function. The biological interpretation of chronic changes in serum CC16 is less clear. Changes in serum CC16 concentrations (either transient or chronic) are not specific to any one agent, disease state, or aetiology. This lack of specificity limits the use of serum CC16 as a biomarker of specific exposures. To date, many of the critical issues that must be understood before serum CC16 levels can have an application as a biomarker of effect or exposure have not been adequately addressed.     

Metabolic syndrome in polycystic ovary syndrome

Both metabolic syndrome (MS) and polycystic ovary syndrome (PCOS) are common among women. The exact prevalence of MS in women with PCOS is dependent upon the diagnostic criteria used for each. However, the frequent co-occurrence of both MS and PCOS in women is suggestive of a common aetiology. In this short review article we argue that insulin resistance, as a consequence of abdominal obesity, may represent such a common aetiology. We also review the literature on the prevalence of MS in women with PCOS and consider the impact that the particular criteria used to diagnose both MS and PCOS may have had on these estimates of prevalence.     

A critical review of the use of Clara cell secretory protein (CC16) as a biomarker of acute or chronic pulmonary effects

Biomarkers associated with asthma aetiology and exacerbation have been sought to shed light on this multifactorial disease. One candidate is the serum concentration of the Clara cell secretory protein (CC16, sometimes referred to as CC10 or uteroglobin). In this review, we examine serum CC16's relation to asthma aetiology and exacerbation. There is evidence that acute exposures to certain pulmonary irritants can cause a transient increase in serum CC16 levels, and limited evidence also suggests that a transient increase in serum CC16 levels can be caused by a localized pulmonary inflammation. Research also indicates that a transient increase in serum CC16 is not associated with measurable pulmonary damage or impairment of pulmonary function. The biological interpretation of chronic changes in serum CC16 is less clear. Changes in serum CC16 concentrations (either transient or chronic) are not specific to any one agent, disease state, or aetiology. This lack of specificity limits the use of serum CC16 as a biomarker of specific exposures. To date, many of the critical issues that must be understood before serum CC16 levels can have an application as a biomarker of effect or exposure have not been adequately addressed.     

Mitochondrial dysfunction and Down's syndrome

Neither the pathogenesis nor the aetiology of Down's syndrome (DS) are clearly understood. Numerous studies have examined whether clinical features of DS are a consequence of specific chromosome 21 segments being triplicated. There is no evidence, however, that individual loci are responsible, or that the oxidative damage in DS could be solely explained by a gene dosage effect. Using astrocytes and neuronal cultures from DS fetuses, a recent paper shows that altered metabolism of the amyloid precursor protein and oxidative stress result from mitochondrial dysfunction.1 These findings are consistent with considerable data implicating the role of the mitochondrial genome in DS pathogenesis and aetiology.     

High frequency hearing loss correlated with mutations in the GJB2 gene

Genetic hearing impairment affects approximately 1/2000 live births. Mutations in one gene, GJB2, coding for connexin 26 cause 10%-20% of all genetic sensorineural hearing loss. Mutation analysis in the GJB2 gene and audiology were performed on 106 families presenting with at least one child with congenital hearing loss. The families were recruited from a hospital-based multidisciplinary clinic, which functions to investigate the aetiology of sensorineural hearing loss in children and which serves an ethnically diverse population. In 74 families (80 children), the aetiology was consistent with non-syndromic recessive hearing loss. Six different connexin 26 mutations, including one novel mutation, were identified. We show that GJB2 mutations cause a range of phenotypes from mild to profound hearing impairment and that loss of hearing in the high frequency range (4000-8000 Hz) is a characteristic feature in children with molecularly diagnosed connexin 26 hearing impairment. We also demonstrate that this type of audiology and high frequency hearing loss is found in a similar-sized group of deaf children in whom a mutation could only be found in one of the connexin 26 alleles, suggesting connexin 26 involvement in the aetiology of hearing loss in these cases. In our study of the M34T mutation, only compound heterozygotes exhibited hearing loss, suggesting autosomal recessive inheritance.     

Aetiology and therapeutics of burning mouth syndrome: an update

doi: 10.1111/j.1741‐2358.2010.00384.x Aetiology and therapeutics of burning mouth syndrome: an update Objective: To provide a review on the aetiology and therapeutic options for the management of patients with burning mouth syndrome (BMS). Background: BMS is a chronic disorder that frequently affects women and is characterised by burning symptoms of the oral mucosa without clinical signs. This syndrome has a complex and multifactorial characteristics, but its aetiology remains unknown and this makes it difficult with regard to the treatment and management of such patients. Despite not being accompanied by evident organic changes and not presenting risks to health, BMS can significantly reduce the quality of life for patients. Methods and materials: The article reviews the literature regarding aetiologic factors, clinical implications and treatment of BMS. Conclusion: The involvement of neurological, emotional and hormonal alterations is proposed in BMS aetiology. However the mechanisms of its development are complex and not completely understood. Tricyclic antidepressants, benzodiazepines and antipsychotic drugs are the most accepted options in treatment and show variable results. The correct diagnosis of BMS and the exclusion of possible local or systemic factors that can be associated with the symptoms are fundamental. It is also important to evaluate the quality of life for these patients to recognise the potential impact of this condition on their lives.     

Shell disease syndromes of decapod crustaceans

The term shell disease subsumes a number of debilitating conditions affecting the outer integument (the carapace) of decapod crustaceans, such as lobsters and crabs. Herein, we seek to find commonality in the aetiology and pathology of such conditions, and those cases that result in the progressive erosion of the cuticle through to the visceral tissues by a cocktail of microbial-derived enzymes including lipases, proteases and chitinases. Aquimarina spp. are involved in shell disease in many different crustaceans across a wide geographical area, but the overall view is that the condition is polymicrobial in nature leading to dysbiosis within the microbial consortium of the damaged cuticle. The role of environment, decapod behaviour and physiology in triggering this disease is also reviewed. Finally, we provide a conceptual model for disease aetiology and suggest several avenues for future research that could improve our understanding of how such factors trigger, or exacerbate, this condition.     

Cell-free transmission of a haemic neoplasm in the cockle Cerastoderma edule

A haemic neoplasm occurs in populations of the common cockle Cerastoderma edule L. along the coast of Ireland. The morphology, epizootiology and distribution of the disease have previously been described. The aetiology of the neoplasm is unknown. In this study transmission of the neoplasm between cockles was accomplished using both whole neoplastic cells and neoplastic cell-free homogenates which were filtered through 0.45 microm Millipore filters. Successful transmission of the disease has been achieved by both methods. These results indicate that the neoplasm in cockles may have a viral aetiology. Whole neoplastic cell inoculation resulted in a higher level of disease development compared to that of cell-free inoculates. The survival rates of the inoculated groups were compared and a significant decrease in survival was found in those groups which developed the disease.     

Wilms' tumour and related syndromes. A unifying theory

The major role of somatic crossing-over in the aetiology of Wilms' tumour and other forms of cancer is emphasized. A model is proposed to show that tumour development is due to a cis-trans disruptive effect of somatic crossing-over on the maintenance of differential parental imprinting.     

Assigning cause for emerging diseases of aquatic organisms

Resolving the cause of disease (= aetiology) in aquatic organisms is a challenging but essential goal, heightened by increasing disease prevalence in a changing climate and an interconnected world of anthropogenic pathogen spread. Emerging diseases play important roles in evolutionary ecology, wildlife conservation, the seafood industry, recreation, cultural practices, and human health. As we emerge from a global pandemic of zoonotic origin, we must focus on timely diagnosis to confirm aetiology and enable response to diseases in aquatic ecosystems. Those systems’ resilience, and our own sustainable use of seafood, depend on it. Synchronising traditional and recent advances in microbiology that span ecological, veterinary, and medical fields will enable definitive assignment of risk factors and causal agents for better biosecurity management and healthier aquatic ecosystems.     

Synergy of molecular and serological methods in minimally invasive diagnosis of enteroviral cardiac infection

Treatment of myocarditis and pericarditis can differ on the basis of aetiology: systemic or auto-immune disease can be positively influenced by corticoid therapy, whereas this kind of treatment can worsen the course of virus-induced disease. Therefore, the aetiological diagnosis is extremely important. The synergistic use of minimally invasive serological, IgG, IgM, IgA, and neutralizing titres, and RNA detection was evaluated on representative patients out of 238 suffering from cardiopathies. The results obtained for each case can yield reliable guidelines that rapidly highlight the presence of a viral aetiology so that an endomyocardial biopsy can be performed thus eliminating incorrect therapies. Thus, not only is this technique rapid, minimally invasive providing the clinician with decisive data, but it is cost effective for the health system.     

Oligohydramnios syndrome and XYY karyotype.

A case of oligohydramnios syndrome was found to have an XYY karyotype and an inherited 9qh inversion. It is suggested that normal and extra Y chromosomes are a predisposing factor in the aetiology of severe congenital renal anomalies.     

La personalidad premórbida como factor de riesgo en la aparición de síntomas psicológicos y conductuales de la demencia: revisión sistemática

The aetiology of behavioural and psychological symptoms of dementia (BPSD) is defined by a diversity of factors, and recent studies suggest that premorbid personality could be a risk factor for BPSD. This study aimed to review studies on the relationship between premorbid personality and BPSD.Studies were identified using PsycInfo, MedLine, and PubMed. The searches combined terms for premorbid personality, dementia and BPSD. Ten studies have been included in this review.Eight out of ten studies show a relationship between premorbid personality and BPSD. Neuroticism is associated with behavioural disturbances and anxiety. Extraversion is associated with wandering. Low agreeableness is associated with affective disturbance and aggression-related behaviours and high agreeableness is associated with wandering. The studies found no congruent results for openness and conscientiousness.In conclusion, premorbid personality may increase the risk of developing BPSD during the course of the disease. Even so, the relationship between personality and BPSD is complex due to multifactorial aetiology.