The effectiveness of an ultra-brief intervention in 1 min for hazardous drinking in a general hospital setting: A quasi-randomized pilot trial.

Objective: We investigated the effectiveness of an ultra-brief intervention (Ultra-BI) for patients with hazardous drinking behaviors admitted to a general hospital. Method: In a quasi-randomized controlled trial at a general hospital in Japan, we assigned participants to intervention or control groups based on the last digit of their patient ID (odd for intervention, even for control). The study included inpatients with Alcohol Use Disorder Identification Test-Consumption (AUDIT-C) scores of ≥5 for men and ≥4 for women. The intervention involved providing advice and feedback within 1 min, accompanied by a leaflet on alcohol-related issues (Ultra-BI). The control group did not receive any intervention. The primary outcome was average weekly alcohol consumption at 3 months postintervention. Results: The study included 68 participants. The intervention group showed a reduction in average weekly alcohol consumption by -69.7 g/week compared to the control group (95% confidence interval [CI] -145.7 to 6.3 g/week, p = 0.07). Post-hoc analysis, adjusting for baseline values, indicated a between-group difference of -78.7 g/week (95% CI -135.2 to -22.2 g/week, p = 0.007). Conclusion: This pilot trial suggests the potential effectiveness of the Ultra-BI in general hospital wards. Further large-scale studies are required to confirm these findings.

Prevalence of hazardous drinking and suspected alcohol dependence in Japanese primary care settings.

OBJECTIVE: We aimed to assess the prevalence of hazardous drinking and potential alcohol dependence among Japanese primary care patients, and their readiness to change and awareness of others' concerns. METHODS: From July to August 2023, we conducted a multi-site cross-sectional study as a screening survey for participants in a cluster randomized controlled trial. The trial included outpatients aged 20-74 from primary care clinics. Using the Alcohol Use Disorders Identification Test (AUDIT) alongside a self-administered questionnaire, we evaluated the prevalence of hazardous drinking and suspected alcohol dependence, patients' readiness to change, and their awareness of others' concerns. RESULTS: Among the 1388 participants from 18 clinics, 22% (95% confidence interval (CI): 20% to 24%) were identified as engaging in hazardous drinking or suspected of being alcohol dependent. As the AUDIT scores increased, so did their readiness to change. However, only 22% (95%CI: 16% to 28%) of those with scores ranging from 8 to 14 reported that others, including physicians, had expressed concerns about their drinking during the past year. For those with scores of 15 or higher, the figure was 74%. CONCLUSIONS: This study underscores the need for universal or high-risk alcohol screening and brief intervention in Japanese primary care settings. Trial registry UMIN-CTR (https://www.umin.ac.jp/ctr/) (UMIN000051388).

Pineal malignant B-cell lymphoma with lower cranial nerve involvement.

A 62-year-old man was admitted to our hospital complaining of dysphagia and hoarseness that had persisted for five days. A neurological examination indicated bulbar palsy. Brain magnetic resonance imaging showed thickening of cranial nerves IX, X and XI, in addition to pineal body enlargement with diffuse contrast enhancement. A tumor biopsy overriding the spinal root of the right XIth cranial nerve was performed. The histologic analysis confirmed a diagnosis of diffuse large B-cell lymphoma. Malignant lymphoma should be considered in the differential diagnosis of pineal region tumors. Furthermore, obtaining histological confirmation is crucial for making proper management decisions.

Experimental transmission of bovine spongiform encephalopathy (BSE) to cynomolgus macaques, a non-human primate.

Bovine spongiform encephalopathy (BSE) was transmitted to three macaques by intracerebral inoculation of a brain homogenate from affected cattle detected in Japan. All monkeys developed abnormal behavioral signs, such as intermittent anorexia and hyperekplexia, around 24 months after inoculation. Neuronal symptoms, such as tremor, myoclonic jerking, and paralysis, appeared 27-44 months after inoculation. These symptoms worsened and total paralysis ensued within a year after onset. The disease duration was approximately 8-12 months. Both the incubation period and the duration of disease were shortened in the secondary transmission experiment to macaques. Heavy accumulation of disease-causing conformer(s) of prion protein (PrP(Sc)), with a similar glycoform profile to the PrP(Sc) contained in the inoculum, and severe spongiform changes in the histology of the brain, confirmed the successful transmission of BSE to monkeys. Florid plaques, a characteristic histological hallmark of variant Creutzfeldt-Jakob disease, were prominent in the cerebral cortex, in which a prion antigen was detected by immunohistochemistry (IHC). PrP(Sc) was mostly confined to the central nervous system, although small amounts of PrP(Sc) accumulated in the peripheral nerves of monkeys, as detected by Western blotting (WB). Neither IHC nor WB detected PrP(Sc) in the lymphatic organs/tissues, such as the tonsils, spleen, and appendix.

Atypical L-type bovine spongiform encephalopathy (L-BSE) transmission to cynomolgus macaques, a non-human primate.

A low molecular weight type of atypical bovine spongiform encephalopathy (L-BSE) was transmitted to two cynomolgus macaques by intracerebral inoculation of a brain homogenate of cattle with atypical BSE detected in Japan. They developed neurological signs and symptoms at 19 or 20 months post-inoculation and were euthanized 6 months after the onset of total paralysis. Both the incubation period and duration of the disease were shorter than those for experimental transmission of classical BSE (C-BSE) into macaques. Although the clinical manifestations, such as tremor, myoclonic jerking, and paralysis, were similar to those induced upon C-BSE transmission, no premonitory symptoms, such as hyperekplexia and depression, were evident. Most of the abnormal prion protein (PrP(Sc)) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrP(Sc) glycoform that accumulated in the monkey brain showed a similar profile to that of L-BSE and consistent with that in the cattle brain used as the inoculant. PrP(Sc) staining in the cerebral cortex showed a diffuse synaptic pattern by immunohistochemistry, whereas it accumulated as fine and coarse granules and/or small plaques in the cerebellar cortex and brain stem. Severe spongiosis spread widely in the cerebral cortex, whereas florid plaques, a hallmark of variant Creutzfeldt-Jakob disease in humans, were observed in macaques inoculated with C-BSE but not in those inoculated with L-BSE.