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Photosensitivity can be due to numerous causes. The photosensitivity associated with deficiency of xeroderma pigmentosum type A (XPA) has been previously shown to be associated with excess levels of the lipid mediator platelet‐activating factor (PAF) generated by the keratinocyte. As PAF has been reported to trigger the production of subcellular microvesicle particles (MVP) due to the enzyme acid sphingomyelinase (aSMase), the goal of these studies was to discern if PAF and aSMase could serve as therapeutic targets for the XPA deficiency photosensitivity. HaCaT keratinocytes lacking XPA generated greater levels of MVP in comparison to control cells. Mice deficient in XPA also generated enhanced MVP levels in skin and in plasma in response to UV radiation. Use of a genetic strategy with mice deficient in both XPA and PAF receptors revealed that these mice generated less MVP release as well as decreased skin erythema and cytokine release compared to XPA knockout mice alone. Finally, the aSMase inhibitor imipramine blocked UV‐induced MVP release in HaCaT keratinocytes, as well as XPA knockout mice. These studies support the concept that the photosensitivity associated with XPA involves PAF‐ and aSMase‐mediated MVP release and provides a potential pharmacologic target in treating this form of photosensitivity. [ABSTRACT FROM AUTHOR]

HECTD3 (HECT domain E3 ubiquitin protein ligase 3) exerts biological activities in neuroinflammation of distinct diseases, such as autoimmune encephalomyelitis and donations after heart death. However, the effect of HECTD3 on diabetes-associated cognitive decline (DACD) remains unclear. Wild-type or HECTD3-knockout rats were administered with streptozotocin to establish diabetic model. Pathological changes in the hippocampus were assessed by NISSL and haematoxylin and eosin staining. Morris water maze test was used to assess cognitive function. Neuronal survival and inflammation were investigated by immunofluorescence staining and ELISA assay. NLRP3 inflammasome and pyroptosis were assessed by western blot, immunofluorescence and flow cytometry assays. HECTD3 was up-regulated in hippocampus of streptozotocin-induced diabetic rats and high glucose-induced PC12 cells. Knockout of HECTD3 increased the number of neurons and improved the learning and memory function. Moreover, knockout of HECTD3 promoted in vivo neuronal survival, and reduced levels of IL-1β, TNF-α, and IL-6 in the hippocampus. Silencing of HECTD3 increased cell viability, and reduced IL-1β, TNF-α, and IL-6 in high glucose-induced PC12 cells. Fluorescence intensities of NLRP3, GSDMD-N and caspase-1 were reduced in HECTD3-knockout diabetic rats, and knockdown of HECTD3 down-regulated protein expression of NLRP3, GSDMD-N, caspase-1, IL-1β, and IL-18 in high glucose-induced PC12 cells to suppress the pyroptosis. HECTD3 promoted the stability of mucosa-associated lymphoid tissue 1 (MALT1) through up-regulation of c-JUN and phospho (p)-JNK in high glucose-induced PC12 cells. Over-expression of MALT1 attenuated neuroprotective effects of HECTD3 silencing on high glucose-induced PC12 cells. HECTD3 silencing exerted neuroprotective effect against DACD through MALT1-mediated JNK signalling. HECTD3 was up-regulated in hippocampus of streptozotocin-induced diabetic rats and high glucose-induced PC12. Knockout of HECTD3 promoted in vivo neuronal survival, reduced inflammation and pyroptosis, and improved the learning and memory function in diabetic rats. Knockout of HECTD3 suppressed the activation of NLRP3 inflammasome in diabetic rats. Silencing of HECTD3 exerted neuroprotective effects through MALT1-mediated JNK signalling. [ABSTRACT FROM AUTHOR]

Catatonia is a state of high-degree psychomotor inhibition in which patients often maintain a constant fixed posture, and generally have unconscious obstacles and various reflex preservation. Patients suffering from severe catatonia will become stiff. Catatonia generally manifests unconsciousness while various reflexes are preserved. Patients show reticence, no food or drink intake, and immobility as signs of complete suppression of speech and movement, and even incontinence. Patients are often first diagnosed in non-psychiatric departments and are more likely to be misdiagnosed as having ‘coma’ or ‘epilepsy’, thus delaying treatment. This article reports a case of a 19-year-old female patient who was misdiagnosed with ‘catatonia’. A month ago, she was admitted to a general hospital of our city because of “intermittent attacks of nausea, vomiting, stupor for 15 years, with one week of exacerbation”. During her hospitalisation, she suddenly appeared was mute, had no food or drink intake, and showed immobility and incontinence, presenting a ‘coma state’. She was transferred to a general hospital in Wuhan to further investigate the cause of her “coma”. After 7 days in the hospital, no abnormal examination results were found and the symptoms were not alleviated. Later, she was transferred to the mental health centre for hospitalisation in this city. The patient was diagnosed as having (1) ‘epileptic psychosis’ and (2) ‘catatonic stupor’. After 3 days of treatment, the patient's recovered consciousness. She was clinically cured and discharged half a month later. We hereby report this case.