Association between a malnutrition screening tool and mealtime observation checklist items in older people receiving oral intake support: A cross-sectional study of four long-term care facilities.

Background: Multiple nutritional screening tools are available for older people; however, few screening tools include specific eating behaviours as risk factors that could lead to poor food intake. The 24-item mealtime observation checklist (MOCL), developed by the Japanese Ministry of Health, Labour and Welfare in 2015, comprises signs, symptoms and conditions during mealtime that reflect eating and swallowing functions and oral conditions.

Objectives: To examine factors associated with malnutrition among the MOCL items in older people.

Validation of the applicability of the mealtime observation checklist in predicting the risk of aspiration pneumonia in older adults receiving oral intake support: A retrospective cohort study of four long-term care facilities.

Aim: In Japan, a 24-item mealtime observation checklist (MOCL) was developed in 2015 to support oral intake and prevent aspiration in older adults. The MOCL consists of signs/symptoms/conditions that reflect eating and swallowing functions and oral conditions. This study aimed to examine the association between each MOCL item and the onset of aspiration pneumonia (AP).

Temporal expression of growth factors triggered by epiregulin regulates inflammation development.

In this study, we investigated the relationship between several growth factors and inflammation development. Serum concentrations of epiregulin, amphiregulin, betacellulin, TGF-α, fibroblast growth factor 2, placental growth factor (PLGF), and tenascin C were increased in rheumatoid arthritis patients. Furthermore, local blockades of these growth factors suppressed the development of cytokine-induced arthritis in mice by inhibiting chemokine and IL-6 expressions.

The Gateway Reflex, which is mediated by the inflammation amplifier, directs pathogenic immune cells into the CNS.

The brain-blood barrier (BBB) tightly limits immune cell migration into the central nervous system (CNS), avoiding unwanted inflammation under the normal state. However, immune cells can traverse the BBB when inflammation occurs within the CNS, suggesting a certain signal that creates a gateway that bypasses the BBB might exist. We revealed the inflammation amplifier as a mechanism of this signal, and identified dorsal vessels of the fifth lumber (L5) spinal cord as the gateway.

Disease-association analysis of an inflammation-related feedback loop.

The IL-6-triggered positive feedback loop for NFκB signaling (or the IL-6 amplifier/Inflammation amplifier) was originally discovered as a synergistic-activation signal that follows IL-17/IL-6 stimulation in nonimmune cells. Subsequent results from animal models have shown that the amplifier is activated by stimulation of NFκB and STAT3 and induces chemokines and inflammation via an NFκB loop. However, its role in human diseases is unclear.