Underlying Mechanism Of Vulnerability Research Articles

Vulnerability of Chinese rural-to-urban migrants to social exclusion: Spatial pattern and mechanism

In response to China's new “people-oriented urbanization” strategy, investigating the current integration situation of rural-to-urban migrants (RUMs) in cities is essential. However, existing studies have not focused on their subjective willingness and adaptive capacity. Moreover, the mechanism of RUMs' urban integration has not been fully explored.The conceptual framework of vulnerability, which originated from the discipline of natural hazards, is perfectly constructive to address these drawbacks. It consists of three main components, including exposure, sensitivity, and adaptive capacity. Vulnerability index has been constructed and calculated by combining the analytic hierarchy process (AHP) and Delphi method. The spatial pattern of vulnerability level is also analyzed with geographic information system (GIS). Furthermore, the underlying mechanism of vulnerability and its associated factors are investigated with the principle component regression.Three major conclusions are reached. First, the vulnerability level of the RUMs to social exclusion presents a heterogeneous pattern between inland and coastal cities in Shandong Province. Second, while the exposure and sensitivity level of each city correlate spatially with the vulnerability level, RUMs’ adaptive capacity further moderates it. Lastly, the level of urban development is revealed to be a key factor influencing vulnerability. This study offers meaningful references to promote inclusive urbanization and sustainable urban development.

The role of altered brain structural connectivity in resilience, vulnerability, and disease expression to schizophrenia

BackgroundSchizophrenia (SCZ) is a highly heritable disorder associated with brain connectivity changes. Although the mechanism of disease expression and vulnerability of SCZ have been reported by previous studies, the mechanism of resilience to SCZ based on the brain structural connectivity is poorly understood. The goal of the present study was to identify the structural brain connectivity related with the resilience to SCZ, which is defined here as the capacity to avoid or delay the onset of SCZ in unaffected siblings of SCZ probands. MethodWe collected diffusion tensor imaging (DTI) data of 49 medication-naive, first-episode SCZ (FE-SCZ) patients, 56 unaffected siblings of SCZ probands (SIB-SCZ), and 90 healthy controls. Then we used graph theoretical approach to calculate the topological properties of the brain structural network, including global, subnetwork, and regional parameters. Finally, we compared the parameters between the three groups, and identified the brain structural network related to the resilience, vulnerability and disease expression to SCZ. ResultsWith respect to resilience, only the SIB-SCZ showed significantly increased connectivity in the subnetworks of the left cuneus-precuneus and left posterior cingulate gyrus–precuneus, and in brain areas of right supramarginal gyrus and right inferior temporal gyrus. With respect to vulnerability, both the FE-SCZ and SIB-SCZ had decreased cluster coefficients and local efficiency, and decreased nodal efficiency in the right medial superior frontal gyrus and right medial orbital superior frontal gyrus compared with the healthy controls. With respect to disease expression, only the FE-SCZ group showed decreased or increased global, subnetwork, and nodal connectivity in broader brain regions compared with the healthy controls. ConclusionDifference in the topological properties of brain structural connectivity not only reflect the underlying mechanism of vulnerability but also that of resilience to schizophrenia. Alteration in the brain structural connectivity associating with resilience and disease expression may contribute to the onset of SCZ.

Habenular TCF7L2 links nicotine addiction to diabetes.

Diabetes is far more prevalent in smokers than non-smokers, but the underlying mechanisms of vulnerability are unknown. Here we show that the diabetes-associated gene Tcf7l2 is densely expressed in the medial habenula (mHb) region of the rodent brain, where it regulates the function of nicotinic acetylcholine receptors. Inhibition of TCF7L2 signalling in the mHb increases nicotine intake in mice and rats. Nicotine increases levels of blood glucose by TCF7L2-dependent stimulation of the mHb. Virus-tracing experiments identify a polysynaptic connection from the mHb to the pancreas, and wild-type rats with a history of nicotine consumption show increased circulating levels of glucagon and insulin, and diabetes-like dysregulation of blood glucose homeostasis. By contrast, mutant Tcf7l2 rats are resistant to these actions of nicotine. Our findings suggest that TCF7L2 regulates the stimulatory actions of nicotine on a habenula-pancreas axis that links the addictive properties of nicotine to its diabetes-promoting actions.

El potencial de la percepción social aplicada al análisis de la vulnerabilidad en planificación urbana

Today, the role of the social perception of urban space is scarce in the documents that guide the adequate integration of the urban development of cities. A better understanding of the influence of social relationships within the city allows new knowledge to be brought to the underlying mechanisms of vulnerability and social exclusion in the urban space. This work focuses on studying the relationship between the quantitative approach of current urban vulnerability reports and a qualitative approach based on social perception, developed within the framework of the Social Risk Map of Zaragoza (Spain) research project between 2014-2017. The cartographical analysis shows that the risk of social isolation is not greater unequivocally in the areas currently characterized as vulnerable and reveals the importance of this type of research for city and urban planning activities.

What Lies Beneath Trait-Anxiety? Testing the Self-Regulatory Executive Function Model of Vulnerability.

Vulnerability to psychological disorder can be assessed with constructs such as trait anxiety and neuroticism which among others are transdiagnostic risk factors. However, trait-anxiety and related concepts have been criticised because they don’t illuminate the etiological mechanisms of psychopathology. In contrast, the metacognitive (S-REF) model offers a framework in which metacognitive knowledge conceptualised in trait terms is part of a core mechanism underlying trait-anxiety and related constructs. The present study therefore set out to explore metacognitions as potential underlying factors in trait-anxiety (the propensity to depression and anxiety). Nine hundred and eighty two participants completed self-report measures of metacognitions and trait-anxiety at time 1, and 425 individuals completed the same measures 8 weeks later. At the cross-sectional level, metacognitions accounted for 83% of the variance in anxiety- and 64% of depression propensity. Furthermore, despite both domains of trait-anxiety showing high stability over time, negative- and positive metacognitive beliefs were significant prospective predictors of both domains of vulnerability. These findings suggests that metacognitive beliefs may be an underlying mechanism of vulnerability attributed to trait-anxiety with the implication that the metacognitive (S-REF) model informs conceptualization of psychological vulnerability, and that metacognitive therapy applications might be employed to enhance psychological resilience.

Pubertal development and anxiety risk independently relate to startle habituation during fear conditioning in 8-14 year-old females.

Reduced habituation to aversive stimuli has been observed during adolescence and may reflect an underlying mechanism of vulnerability for anxiety disorders. This study examined the startle reflex during a fear-learning task in 54 8-14-year-old girls. We examined the relationship between mean startle, startle habituation, pubertal development, and two measures linked to risk for anxiety: behavioral inhibition system (BIS) and the error-related negativity (ERN). Puberty, BIS, and the ERN were unrelated to mean startle; however, each measure modulated startle habituation. Greater pubertal development was associated with reduced startle habituation across the CS+ and CS-. Higher BIS related to a larger ERN, and both were associated with reduced startle habituation specifically to the CS+. All effects were independent of each other. Findings suggest that puberty alters habituation of defense system activation to both threat and safety cues, and this is independent of risk for anxiety, which uniquely impacts habituation to threat cues.

Connexin43 and Angiotensin II Alterations in Hearts of Rats Having Undergone an Acute Exposure to Alcohol

Alcohol-induced heart damage is associated with enzyme and protein alterations. The purpose of this study was to investigate alcohol-induced alterations in cardiac connexin 43 (Cx43) and angiotensin II (Ang II) after acute alcohol administration. Male Wistar rats were randomly divided into 2 groups: a control group and an ethanol group. The ethanol group intraperitoneally received 3.8 g/kg ethanol; the controls were given the same amount of saline via the same route. After the righting reflex disappeared, midsternotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of Cx43 and Ang II. Sections were analyzed by digital image analysis. The expression of Cx43 was significantly reduced after acute ethanol treatment, with the integrated optical density lower when compared with control (P < 0.05). The expression of Ang II was significantly increased after acute ethanol treatment, supported by integrated optical density when compared with control (P < 0.05). In summary, cardiac protein expression of Cx43 and Ang II were found to be significantly altered after acute ethanol treatment, suggesting that these 2 proteins may be important underlying mechanisms of vulnerability to oxidative injury in the heart during acute ethanol. The present study indicated that acute ethanol toxicity caused different alterations in heart proteins that would be related to oxidative stress.