Comparative analysis of Escherichia coli Nissle 1917 ghosts quality: a study of two chemical methods.

The gram-negative bacterium Escherichia coli Nissle 1917 (EcN) has long been recognized for its therapeutic potential in treating various intestinal diseases. Bacterial ghosts (BGs) are empty shells of non-living bacterial cells that demonstrate enormous potential for medicinal applications. Genetic and chemical techniques can create these BGs. In the current study, we produced Escherichia coli Nissle 1917 ghosts (EcNGs) for the first time using benzoic acid (BA) and sodium hydroxide (SH). BA is a feeble acidic chemical that enhances gram-negative bacteria's external membrane permeability, reduces energy production, and decreases internal pH. SH has shown success in producing BGs from some gram-negative and gram-positive organisms. This research aims to produce EcNGs using the minimum inhibitory concentration (MIC) of SH and BA, specifically 3.125 mg/mL. We assessed the bacterial quality of the BGs produced using quantitative PCR (qPCR) and Bradford protein assays. Field emission scanning electron microscopy (FE-SEM) showed the three-dimensional structure of EcNGs. The study confirmed the presence of tunnel-like pores on the outer surface, indicating the preservation of cell membrane integrity. Importantly, this investigation introduces BA as a novel chemical inducer of EcNGs, suggesting its potential alongside SH for efficient EcNG formation.

Effects of Botulinum Toxin Injection on Reducing Myogenic Artifacts during Video-EEG Monitoring: A Longitudinal Study.

Medically refractory seizures affect one-third of patients with epilepsy (PwE), for whom epilepsy surgery is considered. Video electroencephalography (vEEG) monitoring is a fundamental tool for pre-operative seizure localization. Facial and cranial myogenic artifacts can obscure vEEG findings, thus interfering with seizure localization. Studies have shown the beneficial effects of botulinum toxin type A (BTX-A) injection into cranial muscles for reducing myogenic artifacts. This longitudinal study aimed to assess the effects of BTX-A injection on these artifacts. Twenty-two patients with medically refractory hypermotor seizures with daily seizure frequency and undetermined epilepsy localization were included in this study and underwent Dysport® injection (200 units) into the frontotemporal region. vEEG recordings were performed at baseline (one week before the injection), and at three days and six days post-injection. Before and after the injection, the amplitudes of myogenic artifacts were compared during various states (ictal, blinking, chewing, bruxism, head lateralization, scowling, talking, and yawning). BTX-A injection significantly reduced the amplitudes of EEG myogenic artifacts, except during blinking (day three) and talking (days three and six). On day six, significant reduction in EEG myogenic artifacts were noted during blinking, chewing, and bruxism for the greatest number of patients (95.5%, 90.9%, 81.8%), while significant reductions in EEG myogenic artifacts during talking, head lateralization, and ictal phase were associated with the least number of patients (22.7%, 36.3%, and 40.9%). Therefore, BTX-A injection could be a convenient method for filtering myogenic contamination, improving EEG interpretation, and facilitating seizure localization in patients with medically refractory seizures.

GnRH protective effects against amyloid ß-induced cognitive decline: A potential role of the 17ß-estradiol.

INTRODUCTION: The 17ß-estradiol (E2) enhances hippocampal dendritic spine synapses, facilitates learning processes, and exerts neuroprotection. Brain estrogen decline has been reported in Alzheimer's disease. The role of GnRH in modulating steroid biosynthesis convinced us to examine whether hippocampal GnRH administration could enhance the local E2 levels and overcome the development of cognition decline in amyloid ß (Aß) neurotoxicity. To explore if GnRH acts through regulating E2 synthesis, letrozole, an aromatase inhibitor, has been applied in combination with GnRH. METHODS: Female rats received an intracerebroventricular injection of Aß. The GnRH and, or letrozole were injected into the CA1 for 14 consecutive days. Working memory, novel object recognition memory, and anxiety-like behavior were evaluated. Serum and hippocampal E2 levels were measured. Hippocampal mRNA expression of GnRH (GnRH-R) and E2 (ERα and ERß) receptors was assessed. GnRH effect on the excitability of pyramidal cells was studied by in vivo single-unit recording. RESULTS: GnRH increased hippocampal E2 levels, evoked an increase in the spontaneous firing of pyramidal neurons, and caused mRNA overexpression of hippocampal GnRH receptors. GnRH prevented the adverse effects of Aß on working memory, NOR index, and anxiogenic behavior. Letrozole did not reverse GnRH modulatory effects on hippocampal E2 levels and neuroprotection. CONCLUSION: GnRH prevented the Aß-induced memory deficit, which may be mediated through hippocampal E2 levels enhancement. The electrophysiological analysis revealed the enhanced neuronal excitability in the CA1 region. All these data suggest that GnRH might be a promising candidate that reduces anxiety and improves memory indices in the context of Aß neurotoxicity.