Publications by authors named "L H Kurahara"

Background & Aims: Inflammatory bowel disease is associated with carcinogenesis, which limits the prognosis of the patients. The local expression of proteinases and proteinase-activated receptor 1 (PAR) increases in inflammatory bowel disease. The present study investigated the therapeutic effects of PAR antagonism on colitis-associated carcinogenesis.

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Article Synopsis
  • Essential hypertension (HTN) is common, while pulmonary arterial hypertension (PAH) is rare but associated with worse prognosis, higher arrhythmia risk, and sudden cardiac death.
  • Chronic inflammation and oxidative stress contribute to arrhythmia by causing endothelial dysfunction and remodeling in the heart, particularly affecting connexin43 (Cx43) channels.
  • Current treatments for HTN are more advanced than those for PAH, with ongoing research exploring therapies like SGLT2 inhibitors and others to protect the heart and reduce arrhythmia risks.
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Intestinal bacteria play important roles in the progression of colitis-associated carcinogenesis. Colostrum-derived Probio-M9 (Probio-M9) has shown a protective effect in a colitis-associated cancer (CAC) model, but detailed metagenomic analysis had not been performed. Here, we investigated the preventive effects of the probiotic Probio-M9 on CAC-model mice, tracking the microbiota.

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A recombinant L-rhamnose isomerase (L-RhI) from probiotic Lactobacillus rhamnosus Probio-M9 (L. rhamnosus Probio-M9) was expressed. L.

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Our and other studies suggest that myocardial hypertrophy in response to hypertension and hyperthyroidism increases propensity of the heart to malignant arrhythmias, while these are rare in conditions of hypothyroidism or type-1 diabetes mellitus associated with myocardial atrophy. One of the crucial factors impacting the susceptibility of the heart to life-threatening arrhythmias is gap junction channel protein connexin-43 (Cx43), which ensure cell-to-cell coupling for electrical signal propagation. Therefore, we aimed to explore Cx43 protein abundance and its topology in hypertrophic and hypotrophic cardiac phenotype.

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