Patients with heart failure (HF) have structural and functional changes of the gut as a result of microcirculatory disturbances. A disrupted gut epithelial barrier may lead to translocation of microbial products into systemic circulation, possibly aggravating HF by inducing inflammatory responses. Gut microbiota play an essential role in the maintenance of host homeostasis because large quantities of their gene products complement host physiological processes. Emerging evidence has suggested the potential clinical significance of gut microbiota in the pathophysiology of HF. Imbalances of gut microbe-derived metabolites can contribute to cardiac dysfunction and other morbidities in patients with HF. Therapeutic research for HF through targeting microbiota is under way. Thus, the novel concept of a heart-gut axis may lead to breakthroughs in the development of innovative diagnostics and therapeutic approaches for HF.
Complement System Proteins ; Dysbiosis ; Gastrointestinal Microbiome ; Heart Failure* ; Heart* ; Homeostasis ; Humans ; Microbiota ; Physiological Processes ; Therapeutic Human Experimentation

No abstract in English.
History, 19th Century ; History, 20th Century ; Humans ; Neuralgia/history/surgery ; Neurophysiology/*history ; Neurosurgery/*history ; Therapeutic Human Experimentation/ethics/*history ; United States

This paper aims to examine the spread of paragonimiasis and the Japanese colonial government's response to it. To consolidate colonial rule, the Japanese colonial government needed medications to cure paragonimiasis. When Dr. Ikeda Masakata invented acid emetine to cure paragonimiasis in Manchuria in 1915, emetine treatment carried the risk of emetine poisoning such as fatigue, inappetence, heart failure, and death. Nonetheless, Japanese authorities forced clinical trials on human patients in colonial Korea during the 1910s and 1920s. The emetine poisoning accident in Yeongheung and Haenam counties in 1927 occurred in this context. The Japanese government concentrated on terminating an intermediary host instead of injecting emetine to repress endemic disease in Japan. However, the Japanese colonial government pushed ahead with emetine injections for healthy men through the Preliminary Bureau of Land Research in colonial Korea in 1917. This clinical trial simultaneously presented the effects and the side effects of emetine injection. Because of the danger emetine injections posed, the colonial government investigated only the actual condition of paragonimiasis, delaying the use of emetine injection. Kobayashi Harujiro(1884-1969), a leading zoologist and researcher of endemic disease for three decades in the Government General Hospital and Keijo Imperial University in colonial Korea, had used emetine while researching paragonimiasis, but he did not play a leading role in clinical trials with emetine injections, perhaps because he mainly researched the intermediary host. Government General Hospital and Keijo Imperial University therefore faced limitations that kept them from leading the research on endemic disease. As the health administration shifted the central colonial government to local colonial government, the local colonial government pressed ahead with emetine injections for Korean patients. Emetine poisoning had something to do with medical power's localization. Nevertheless, the central colonial government still supported emetine injections with funds from the national treasury. The emetine poisoning accident that occurred simultaneously in two different regions resulted from the Japanese colonial government's support. This accident represented the Japanese colonial rule's atrocity, its suppression of hygiene policies, and its disdain for colonial inhabitants. The colonial government sought to accumulate medical knowledge not to cure endemic disease, but to expand the Japanese Empire.
Clinical Trials as Topic/history ; Colonialism/*history ; Emetine/*history/poisoning/therapeutic use ; Endemic Diseases/*history ; History, 20th Century ; Human Experimentation/history ; Humans ; Japan ; Korea ; Male ; Paragonimiasis/drug therapy/*history

Stroke is one of the common causes of death and disability. Despite extensive efforts in stroke research, therapeutic options for improving the functional recovery remain limited in clinical practice. Experimental stroke models using genetically modified mice could aid in unraveling the complex pathophysiology triggered by ischemic brain injury. Here, we optimized the procedure for generating mouse stroke model using an intraluminal suture in the middle cerebral artery and verified the blockage of blood flow using indocyanine green coupled with near infra-red radiation. The first week after the ischemic injury was critical for survivability. The survival rate of 11% in mice without any treatment but increased to 60% on administering prophylactic antibiotics. During this period, mice showed severe functional impairment but recovered spontaneously starting from the second week onward. Among the various behavioral tests, the pole tests and neurological severity score tests remained reliable up to 4 weeks after ischemia, whereas the rotarod and corner tests became less sensitive for assessing the severity of ischemic injury with time. Further, loss of body weight was also observed for up 4 weeks after ischemia induction. In conclusion, we have developed an improved approach which allows us to investigate the role of the cell death-related genes in the disease progression using genetically modified mice and to evaluate the modes of action of candidate drugs.
Animals ; Anti-Bacterial Agents ; Body Weight ; Brain Injuries ; Brain Ischemia ; Cause of Death ; Disease Progression ; Indocyanine Green ; Ischemia ; Mice* ; Middle Cerebral Artery ; Stroke* ; Survival Rate ; Sutures ; Therapeutic Human Experimentation