| 1. |
- Klionsky, Daniel J., et al.
(author)
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Guidelines for the use and interpretation of assays for monitoring autophagy
- 2012
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In: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
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Research review (peer-reviewed)abstract
- In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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| 2. |
- Tettamanti, Giorgio, et al.
(author)
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Influence of Smoking, Coffee, and Tea Consumption on Bladder Pain Syndrome in Female Twins.
- 2011
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In: Urology. - : Elsevier BV. - 1527-9995 .- 0090-4295.
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Journal article (peer-reviewed)abstract
- OBJECTIVES: To assess the influence of smoking, coffee and tea consumption on the risk for bladder pain syndrome (BPS) using the O'Leary Interstitial Cystitis Symptom Index (ICSI). METHODS: In 2005, all twins born between 1959 and 1985 in Sweden (n = 42,852) were invited to participate in a web-based survey to screen for complex diseases, including BPS. Analyses were limited to female twins with information regarding bladder pain symptoms (n = 9349). Women with an ICSI score ≥6 with required nocturia and bladder pain were defined as having BPS symptoms. Logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Environmental and genetic influences were assessed in co-twin control analysis. RESULTS: Tea consumption was associated with an increased risk for BPS (OR 1.26, 95% CI 1.02-1.55 for low tea consumption; OR 1.74, 95% CI 1.24-2.44 for high tea consumption). Coffee consumption was not a risk factor for BPS (OR 1.1, 95% CI .84-1.45). Former and current smoking was associated with a higher risk of BPS (OR 1.5, 95% CI 1.18-1.89; and OR 1.49, 95% CI 1.16-1.92, respectively), but results from co-twin control analysis suggested that the association between smoking and BPS was confounded by familial factors. CONCLUSIONS: Tea and smoking are environmental risk factors for BPS, which are amenable to intervention. The effects of smoking on the risk for BPS may, however, be confounded by familial factors.
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| 3. |
- Tettamanti, Giorgio
(author)
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Studies on risk factors for urinary incontinence in Swedish female twins
- 2013
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Doctoral thesis (other academic/artistic)abstract
- Approximately half of all women in industrialized countries will experience urinary incontinence during their lifetime. Even though urinary incontinence is not a life threatening disease, it often has severe implications for daily function, social interactions, sexuality and psychological well-being. Moreover, urinary incontinence has a major impact on health economy and is increasingly recognized as a global health burden. Hence, identifying risk factors for urinary incontinence is of importance for individual women at risk, as well as for society’s health care costs. In the first study, the association between coffee and tea intake and urinary incontinence was evaluated. Women with a high coffee intake were at lower risk of overall incontinence, while no effect was observed between coffee intake and other urinary incontinence subtypes. A higher risk of nocturia and overactive bladder was found among women with a high tea intake. However, results from co-twin control analysis showed that these associations were likely confounded by familial factors. In the second study, the effect of gestational diabetes mellitus on overactive bladder was investigated. Women with gestational diabetes mellitus had an almost two times higher odds of overactive bladder compared to women without gestational diabetes. The effect of gestational diabetes mellitus on overactive bladder was not mediated by body mass index or diabetes later in life. In the third study, the association between depressive mood disorders (depressive symptoms and major depression) and neuroticism with urinary incontinence was investigated. In logistic regression analysis depressive mood disorders and neuroticism were positively associated with urinary incontinence. Results from quantitative genetic analysis showed that the association between depressive mood disorders, neuroticism and urinary incontinence was partly determined by genetic factors in common to the disorders. In the fourth study, the effect of birth weight and being born small for gestational age on urinary incontinence later in life was evaluated. Results showed that birth weight and being born small for gestational age had no effect on urinary incontinence. However, women who had a low birth weight and then became overweight had a borderline statistically significant higher odds of overall and stress incontinence compared to overweight women who had a normal birth weight. This finding suggests that low birth weight in combination with elevated adult body mass index may contribute to the risk of urinary incontinence later in life.
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