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In this work, a system consisting of two resistive sensors working in tandem to detect and quantify the acetic acid released during the degradation of cellulose acetate-based ancient cinematographic and photographic films is presented. Acetic acid must be constantly monitored to prevent reaching concentrations at which autocatalytic degradation processes begin. The sensors are constituted by a thin layer of metal oxide (tungsten oxide and tin oxide) deposited over an interdigitated electrode capable of being heated, chosen to maximize the array response towards acetic acid vapors. The signals obtained from the sensor array are mathematically processed to reduce the background signal due to interferent gases produced during degradation of ancient cinematographic films. The sensor array reported a LOD of 30 ppb for acetic acid, with a linearity range up to 30 ppm. Finally, the sensor array was tested with different cinematographic and photographic film samples made of cellulose acetate, whose degradation state and acetic acid production was validated using the conventional technique (A-D strips). The presented array is suitable for remote monitoring large number of films in collections since, compared to the official technique, it has a lower detection limit (30 ppb vs. 500 ppb) and is much quicker in providing accurate acetic acid concentration in the film boxes (15 min vs. 24 h).

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Pathologische Krankheitsängste wurden bislang nach ICD und DSM primär als somatoforme Störung bzw. als somatische Belastungsstörung klassifiziert. Theoretische Erwägungen und empirische Befunde legen jedoch nahe, dass es sich bei pathologischen Krankheitsängsten eigentlich um eine Angststörung handelt. Innerhalb des vorliegenden Beitrags wird dafür argumentiert, dass Defizite in der aktuellen Behandlungspraxis und in der Wahrnehmung von Patienten mit Hypochondrie als „schwierige Patienten“ teilweise auf Unklarheit in der Nosologie sowie bezüglich der entscheidenden Mechanismen der Entstehung und Aufrechterhaltung zurückzuführen sind. Ausgehend von innovativen theoretischen Ansätzen zur Erklärung pathologischer Krankheitsängste werden Vorschläge für eine verbesserte therapeutische Praxis skizziert. Der Fokus liegt hierbei auf einem verstärken Einsatz expositionsbasierter Behandlungselemente, die sich am „Inhibitory-learning“-Ansatz orientieren und sich bei anderen Angststörungen bereits bewährt haben. Up to now pathological health anxiety has been classified primarily as a somatoform disorder or a somatic symptom disorder in ICD and DSM. Theoretical and empirical evidence, however, suggest that pathological health anxiety basically represents an anxiety disorder. In this paper, it is argued that deficits in the treatment and perception of patients with pathological health anxiety as "difficult patients" are partly attributable to a lack of clarity in terms of nosology and with respect to central mechanisms of etiology and pathogenesis. Based on novel theoretical approaches for the explanation of pathological health anxiety, suggestions for an improved therapeutic practice are outlined. This approach focuses on a more intensive use of exposure-based treatment elements that are oriented to the inhibitory learning approach, which has already proven its effectiveness for other anxiety disorders.

The negative interpretation of body sensations (e.g., as sign of a severe illness) is a crucial cognitive process in pathological health anxiety (HA). However, little is known about the nature and the degree of automaticity of this interpretation bias. We applied an implicit association test (IAT) in 20 subjects during functional magnetic resonance imaging (fMRI) to investigate behavioral and neural correlates of implicit attitudes towards symptom words. On the behavioral level, body symptom words elicited strong negative implicit association effects, as indexed by slowed reaction times when symptom words were paired with the attribute harmless (incongruent condition) relative to a control condition. fMRI revealed increased activation in the dorsolateral prefrontal cortex and posterior parietal cortex for the comparison of incongruent words with control words, as well as with a lower significance threshold also in comparison to congruent words. Moreover, activation in the dorsolateral prefrontal cortex, posterior parietal cortex, nucleus accumbens, and cerebellum varied with individual levels of HA (again, in comparison to control words, as well as with a lower significance threshold also in comparison to congruent words). Slowed reaction times as well as increased activation in dorsolateral prefrontal and posterior parietal cortex point to increased inhibitory demands during the incongruent IAT condition. The positive association between HA severity and neural activity in nucleus accumbens, dorsolateral prefrontal, and posterior parietal cortex suggests that HA is characterized by both intensified negative implicit attitudes and hampered cognitive control mechanisms when confronted with body symptoms.