【Objective】 We will clarify minor problems caused by physical activity during pregnancy, along with the associated effects thereof on an individual’s state of mind.【Method】 The subjects were healthy expecting mothers who are our outpatients. We surveyed objective physical activity using an accelerometer, subjective physical activity using a self-recorded questionnaire, the state of symptoms of minor problems, and the state of mind, then considered the correlation thereof with minor problems using a logistic regression analysis.【Results】A significant odds ratio was confirmed for the constipation-related symptom group in maternity sports (OR＝0.51) and the sleep-related symptom group in indoor cleaning (such as vacuuming) (OR＝1.38) .【Discussion】 Although we are unable to indicate the effects on constipation as we have not narrowed down the types of maternity sports, it was valuable to expecting mothers that we were able to increase the options for methods of dealing with constipation, in addition to methods such as diet and laxatives. Furthermore, the number of individuals in the sleep-related symptom group increased despite an increase in the frequency of indoor cleaning, which is a housework activity. This result was contrary to a report indicating that daily physical activity affects sleep and that sleep duration during pregnancy increases with housework.

We report a 6-year-old girl with atopic dermatitis who developed eczema coxsackium caused by coxsackievirus A6 (CVA6) . At the time of her initial diagnosis, based on her medical history and clinical symptoms, we considered her to have Kaposi's varicella-like rash (eczema herpeticum) caused by herpes simplex virus (HSV) and started her on acyclovir, but later found that her serum HSV antibody titer was negative and CVA6 antibody titer was positive on admission. Although eczema herpeticum often presents with corneal and periocular symptoms, no periocular skin rash was seen in this case. If the periocular rash is not severe, a viral infection other than HSV may be suspected, and searching for the causative virus, including CVA6, may help in the diagnosis.

The brain is known to actively interact with the immune system under inflammatory conditions. However, acute immune reactions by intracranial tissues to endotoxemia-induced inflammation have not been clarified well. In the Pathology Research Team at the Faculty of Health Sciences of Kyorin University, we wanted to elucidate what intracranial tissues contribute to the initial responses, what cytokines are produced to spread inflammation to brain parenchyma, and how brain cells are activated to interact with systemic inflammation. The present article reviewed our previously published papers to go over our findings obtained with adult mouse experimental models. Two-month-old C57BL/6N mice were treated with single intraperitoneal injection of lipopolysaccharide (LPS) . Brains were removed at 4, 24, 48 and 72 h after LPS injection, and tissue concentrations of multiple cytokines were determined by immunoassays. The choroid plexuses were collected at 4 h after LPS. The brains were dissociated and CD11b (＋) cells were isolated at 48 h after LPS. RNA was extracted from these tissues and cells, and real-time RT-PCR was performed. For histology, mice were perfused with 4% paraformaldehyde at 1，4，24 and 48 h after LPS. The choroid plexus and leptomeninges responded at 1 h after LPS, evidenced by IL-1β production by macrophages. The choroid plexus epithelial and stromal cells then produced CCL2, CXCL1, CXCL2 and IL-6 at 4 h, which were transported into the brain parenchyma. Astrocytes responded most quickly among brain parenchymal cells using the cytokine receptors on the endfeet. Astrocytes thereafter produced CCL11, CXCL10 and G-CSF at 24 h after LPS. The cytokines derived from astrocytes activated microglia via receptors. Activated microglia changed gene expression pattern toward the M2 phenotype. The concentrations of brain cytokines returned to control levels by 72 h after LPS. Therefore, the choroid plexus and leptomeningeal macrophages responded most quickly to systemic inflammation and stimulated choroid plexus epithelial and stromal cells to produce CCL2, CXCL1, CXCL2 and IL-6. These cytokines stimulated astrocytes to produce CCL11, CXCL10 and G-CSF, which activated microglia to contribute to the resolution of neuroinflammation. This review was written as a report for the Intramural Grants Program “Health Sciences Collaborative Research Promotion Project”, in which the authors were awarded a grant in FY 2020.

It has been established that patients with diabetes have movement disorders, such as lower muscle force in lower extremities and balance disturbance. Although diabetic peripheral neuropathy and disorders of muscle fibers are widely known to cause such disorders, recently, it was revealed that diabetes also targets the component of the central nervous system that controls body movement, such as the cerebral motor cortex and corticospinal tract (motor system) . Disorders of the motor system may have caused movement disorders in patients with diabetes. In this review, we focused on disorders in the motor system in patients with diabetes and the diabetic model, as well as their rehabilitation. Studies on patients with diabetes revealed micro-structural changes and reduced volume in the motor cortex and corticospinal tract, along with reduced electrical excitability and plasticity of the motor cortex and reduced conduction velocities of corticospinal tract. On the other hand, studies using the diabetic model revealed predominant atrophy of the corticospinal tract fibers and a projecting lumbosacral segment, causing disorder of excitatory conduction from motor cortex to the lumbar spinal cord. How rehabilitation via exercise training will affect disorders of the motor system caused by diabetes mellitus is still unclear. However, we recently investigated the rehabilitative effects of two weeks of aerobics training and motor skills training (ST) on motor disorders in streptozotocin-induced type 1 diabetic rats. We found ST induced plastic changes in the rubrospinal tract to strengthen synaptic connections between the red nucleus and spinal cord, which can compensate for injured corticospinal tract system components that control the hindlimb. There is a need for more investigations on the cause of motor system disfunction caused by diabetes to determine a novel rehabilitation strategy to improve motor dysfunctions in diabetic patients.