Protective effect of hydrangenol on lipopolysaccharide-induced endotoxemia by suppressing intestinal inflammation.

Hydrangenol, a dihydroisocoumarin, isolated from the leaves of Hydrangea serrata, possesses anti-inflammatory, anti-obesity, and anti-photoaging activities. In this study, we investigated the protective effects of hydrangenol (HG) against lipopolysaccharide (LPS)-induced endotoxemia and elucidated the underlying molecular mechanisms of action in C57BL/6 mice. Oral administration of HG (20 or 40 mg/kg) significantly restored the survival rate and population of macrophages, T helper cells (CD3+/CD4+), and Th17 cells (CD3+/CD4+/CCR6+) in the spleens of mice with LPS-induced endotoxemia. HG suppressed the expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1ß, and Interferon (IFN)-γ and the mRNA and protein expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in the intestine and lung of LPS-treated mice. Molecular data showed that HG ameliorated the activation of nuclear factor kappa B (NF-κB) p65, signal transducers and activators of transcription 3 (STAT3), and c-Fos and c-Jun (AP-1 subunits) via the myeloid differentiation primary response 88 (MyD88) dependent toll-like receptor 4 (TLR4) signaling pathway in the LPS-treated mouse intestines. HG treatment caused the recovery of LPS-induced impaired tight junction (occludin and claudin-2) protein and mRNA expressions. Furthermore, HG improved LPS-induced gut dysbiosis in mice. Taken together, our results suggest that HG protects against LPS-induced endotoxemia by restoring immune cells and the capacity of the intestinal barrier, reducing intestinal inflammation, and improving the composition of the gut microbiota.

A case of leucine-rich glioma-inactivated 1 antibody encephalitis with schizophrenia-like symptoms as an initial clinical manifestation.

Leucine-rich glioma-inactivated 1 (LGI-1) antibody encephalitis is a type of limbic encephalitis characterized by faciobrachial dystonic seizure and short-term memory loss as initial clinical symptoms. We present a case initially misdiagnosed as schizophrenia and finally diagnosed as LGI-1 antibody encephalitis. A 41-year-old female presented to the neurology clinic with a 4-month history of anxiety and disoriented speech and a new onset headache. Her explanation of symptoms was unclear, and she was unable to answer questions properly. Her brain magnetic resonance imaging (MRI) showed no specific lesions. After 6 months, depersonalization, place disorientation and memory impairment were noted. Her symptoms continue to progress, experiencing visual/auditory hallucinations. She was diagnosed with schizophrenia and admitted to a closed psychiatric ward. In the hospital, she showed mild fever, and her memory loss worsened faster than her psychiatric symptoms, unlike in schizophrenia. Follow-up MRI scans showed a diffusely enlarged right hippocampus with a 2.5 × 1.3-cm mass lesion. Electroencephalogram showed rhythmic theta activities/interictal spikes in the right frontal lobe, for which she was treated with an antiepileptic drug. Cerebrospinal fluid analysis results showed pleocytosis. Based on this, autoimmune encephalitis was diagnosed, and steroid pulse treatment and immunoglobulin treatment were performed. Positivity for LGI-1 antibody was reported and finally led to diagnosis of LGI-1 antibody encephalitis. Clinical symptoms gradually improved, and the lesion had shrunk considerably on MRI performed 6 months after immunoglobulin treatment. She reports persistent amnesia for 6 months but has returned to her daily life under follow-up observation.

An Exploratory Study on the Effects of Forest Therapy on Sleep Quality in Patients with Gastrointestinal Tract Cancers.

The improvement of sleep quality in patients with cancer has a positive therapeutic effect on them. However, there are no specific treatment guidelines for treating sleep disturbance in cancer patients. We investigated the effect of forest therapy on the quality of sleep in patients with cancer. This study was conducted on nine patients (one male, eight female; mean age, 53.6 ± 5.8 years) with gastrointestinal tract cancer. All patients participated in forest therapy for six days. They underwent polysomnography (PSG) and answered questionnaires on sleep apnea (STOP BANG), subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI), sleepiness (Stanford and Epworth Sleepiness Scales), and anxiety and depression (Hospital Anxiety and Depression Scale) to evaluate the quality of sleep before and after forest therapy. Sleep efficiency from the PSG results was shown to have increased from 79.6 ± 6.8% before forest therapy to 88.8 ± 4.9% after forest therapy (p = 0.027) in those patients, and total sleep time was also increased, from 367.2 ± 33.4 min to 398 ± 33.8 min (p = 0.020). There was no significant difference in the STOP BANG score, PSQI scores, daytime sleepiness based on the results of the Stanford and Epworth Sleepiness Scales, and depression and anxiety scores. Based on the results of this study, we suggest that forest therapy may be helpful in improving sleep quality in patients with gastrointestinal cancers.