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PuraStat® (3D Matrix, Tokyo, Japan) is a novel, self-assembling peptide hemostatic hydrogel that can be used endoscopically. Hemostasis can be physically obtained by covering bleeding points; however, there are no reports of how long PuraStat remains in the upper gastrointestinal tract. Herein, we report a case wherein esophagogastroduodenoscopy (EGD) was performed 2 hours after PuraStat application. A 73-year-old man underwent EGD for evaluation of lesions in the posterior wall of the stomach. A biopsy was then performed on the gastric lesions; however, massive bleeding occurred. A hemostatic clip was used to stop bleeding but failed; primary hemostasis was obtained by applying PuraStat. EGD performed 2 hours later to determine whether the patient could be discharged revealed that the white-turning PuraStat gel remained firmly in the applied area, confirming complete hemostasis. PuraStat is a hemostatic agent capable of physical hemostasis that reliably remains in the stomach even after a few hours of use and, thus, may replace some conventional hemostasis methods.

The widespread use of Helicobacter pylori eradication therapy in recent years has reduced the H. pylori infection rate, indicating that gastric cancer cases diagnosed in the future may be H. pylori-naïve. The typical endoscopic presentation of signet-ring cell carcinoma, which accounts for the majority of H. pylori-naïve gastric cancer cases, is a discolored, flat, or depressed lesion; it is rarely presented as an elevated lesion. In this study, we treated a patient with elevated signet-ring cell carcinoma in an H. pylori-naïve stomach. Histopathological testing after endoscopic submucosal dissection showed proliferation of fibromuscular tissue in the tumor, which may have caused the formation of the elevated lesion.

Invasive fungal infections, particularly those considered opportunistic, have become a common and significant complication of procedures performed in advanced contemporary medicine. Among such infections, cryptococcosis, which is usually caused by infection with Cryptococcus neoformans and Cryptococcus gattii, is particularly problematic because this fungal infection occurs in immunocompromised and apparently immunocompetent individuals. It has been largely accepted that Cryptococcus species are recognized by cellular receptors and that Th1-type immune responses play an important role in defense mechanisms against the yeast. However, the interaction between the yeast and host tissue varies depending on the characteristics of the yeast and the immune status of the host. To gain a better understanding of the pathophysiology of cryptococcosis, we wish to emphasize the usefulness of histopathological examinations, because it allowed more detailed information of an extremely complex interaction between the causative yeasts and tissue response. In the present review, we describe the pathophysiology of cryptococcosis as largely revealed in our previous histopathological investigations of the experimental infection.