Parkinson's Disease (PD) is characterized by a loss of nigral dopamine (DA) neurons, followed by a striatal DA deficit. Inhibition of the subthalamic nucleus (STN) reverses L-DOPA sensitive motor symptoms and improves efficacy of pharmacotherapy in PD-patients. The underlying mechanism of these effects, however, remains largely unknown. Previously, we could show in the rat's 6-hydroxyDA (6-OHDA) model of PD that ablative STN-lesioning exerts functionally neuroprotective effects on the DAergic nigrostriatal pathway against 6-OHDA toxicity, in terms of elevating the number of tyrosine hydroxylase (TH)-expressing neurons rather than enhancing the total number of cells surviving 2 and 6 weeks post lesioning, as assessed via fluorogold staining. These data were correlated with increased functional recovery of 6-OHDA-lesioned rats with preceding STN-lesioning. Here, we extend the previous study design to observation periods of up to 12 weeks to assess long-term effects. Furthermore, to elucidate cellular mechanisms underlying potential neuroprotective effects, we explore the regulation of cellular markers involved in neurodegenerative cascades via immunocytochemistry. We show that preceding STN-lesioning significantly inhibits 6-OHDA induced expression/phosphorylation of the transcription factor c-Jun in surviving nigral neurons in comparison with controls. However, we also demonstrate that functionally neuroprotective effects of preceding STN-lesioning subside after 12 weeks, as assessed with TH immunostaining. We therefore conclude that c-Jun induction/phosphorylation is involved in 6-OHDA toxicity and that STN-lesioning transiently preserves of dopaminergic phenotype of nigral neurons partially via delaying the induction and attenuating the expression and phosphorylation of c-Jun.
Introduction
Between May 2022 and January 2023, a global mpox outbreak affected more than 84,000 patients across all continents. Transmission of mpox occurs through large respiratory droplets and direct contact with skin lesions.
Case presentation
We present the case of a 31-year-old previously healthy male with mpox-Infection following occupational exposure to mpox from a needle stick injury with a sterile needle through a contaminated glove. The patient presented with a three-day history of fever, malaise, and an increasing erythema and swelling of one fingertip. The patient works as a medical doctor with regular exposure to patients infected with mpox. Mpox-PCR from a swab of the lesion and an oro-pharyngeal swab were positive. The lesion on his finger evolved into a necrotic skin lesion finally healing, leaving a scar. He did not develop any secondary pox on his skin and recovered fully.
Discussion
Only a minority of patients with mpox infection develop illness with pronounced local complications as in this case.
Conclusion
Mpox can potentially be transmitted in an occupational context. Medical personnel should be informed about this possible route of transmission.
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