The University of Osaka · Medicine
Professor Kentaro Shimizu's research lab focuses on the pathophysiological role of the gut microbiome and intestinal microenvironment in critical illness, particularly in patients with severe systemic inflammatory response syndrome (SIRS), sepsis, and multi-organ dysfunction. The lab investigates how dysbiosis—especially reductions in obligate anaerobes and overgrowth of pathogenic bacteria—contributes to disease progression, septic complications, and mortality. A key research direction involves identifying gut flora and metabolite profiles as potential prognostic biomarkers in critically ill patients. The lab also explores the structural and functional consequences of chronic spinal cord compression, linking mechanical stress and vascular changes to neurological deterioration.
Figures are computed from collected data and may differ slightly.
The gut flora and environment are significantly altered in patients with severe SIRS. Abnormal gut flora and environment may affect systemic inflammatory response after severe insult.
UMIN, R000007633 . Registered on 29 September 2011.
A decrease in total obligate anaerobes and an increase in pathogenic bacteria in the gut are associated with septic complications and mortality in patients with SIRS. The altered gut flora may be a potential prognostic marker in SIRS patients.
Progressive kyphosis of the cervical spine resulted in demyelination of nerve fibers in the funiculi and neuronal loss in the anterior horn due tochronic compression of the spinal cord. These histologic changes seem to be associated with both continuous mechanical compression and vascular changes in the spinal cord.
The gut is an important target organ for stress caused by severe insults such as sepsis, trauma, burn, shock, bleeding and infection. Severe insult to the gut is considered to have an important role in promoting infectious complications and multiple organ dysfunction syndrome. These are sequelae of interactions between deteriorated intestinal epithelium, the immune system and commensal bacteria. The gut is the "motor" of multiple organ failure, and now it is recognized that gut dysfunction is a
Gut flora and organic acids were significantly altered in patients with severe SIRS complicated by gastrointestinal dysmotility, which was associated with higher septic mortality in SIRS patients.
Bacterial translocation is a major cause of multiple organ dysfunction syndrome in critical illness, and its management is an important therapeutic strategy. In this study, we focused on the key factors responsible for bacterial translocation including the intestinal microbiome and investigated the impact of molecular hydrogen therapy as a countermeasure against bacterial translocation in a murine model of sepsis. The experimental protocols were divided into the sham, saline treatment (control),
Patients suffering from critical illness have host inflammatory responses against injuries, such as infection and trauma, that can lead to tissue damage, organ failure, and death. Modulation of host immune response as well as infection and damage control are detrimental factors in the management of systemic inflammation. The gut is the motor of multiple organ failure following injury, and it is recognized that gut dysfunction is one of the causative factors of disease progression. The gut microb
Quite a few changes and challenges have arisen in society in general as technology has advanced and the aging population has increased. These can lead to the recognition of the shortcomings of a society's traditional systems and the various changes that are needed, especially in providing emergency medical care. A super-aged society has been developing in Japan, and the emergency care system needs to change according to these new demographics and society's needs. The focus has been shifting from
Gram-stained fecal flora can be classified into three patterns and are associated with both cultured bacterial counts and clinical information. Gram-stained fecal bacteria can be used as a quick bedside diagnostic marker for severe SIRS patients.
Regulation of the slowly activating component of delayed rectifier K + current ( I Ks ) by intracellular guanosine 3′5′ cyclic monophosphate (cGMP) was investigated in guinea‐pig sino‐atrial (SA) node cells using the whole‐cell patch‐clamp method. When a cell was dialyzed with pipette solution containing 100 μ M cGMP, I Ks started to gradually increase and reached a maximum increase of a factor of 2.37±0.39 ( n =4) about 10–15 min after rupture of patch membrane. Atrial natriuretic peptide (ANP,
Open papers in the app to read, cite, and organize with AI.
