Malignant peritoneal mesothelioma with invasion of the liver is an invariably fatal disease. We aimed to clarify the characteristics of malignant peritoneal mesothelioma cases with liver involvement. The clinical presentation, computed tomography images, and immunohistochemical and histopathological features of 5 patients with malignant peritoneal mesothelioma and liver involvement were evaluated. The diagnosis was established by imaging and immune profiles of the tumours. A review of 8 cases with primary or invading malignant mesothelioma in liver is presented. All 5 mesothelioma cases were asbestos-related. CT images of malignant peritoneal mesothelioma with the liver involvement typically showed that the lesion grew inside the liver along the capsule and was possibly accompanied by capsule breakthrough and extrahepatic infiltration. The tumours exhibited a common epithelioid appearance in all 5 patients and most cases revealed positive Cal, CK, and MC with negative CEA and HeP. Different from our findings, the review of literature revealed that most malignant mesothelioma of liver was due to primary intrahepatic malignant mesothelioma. Finally, we concluded that the diagnosis of malignant peritoneal mesothelioma cases with liver invasion is reliably achieved by the history of asbestos exposure, the characteristic CT imaging, and immune profiles of the tumours.

Neuronal pyroptosis serves an important role in the progress of neurologic dysfunction following subarachnoid hemorrhage (SAH), which is predominantly caused by a ruptured aneurysm. Hydrogen gas has been previously reported to be an effective anti-inflammatory agent against ischemia-associated diseases by regulating mitochondrial function. The objective of the present study was to investigate the potential neuroprotective effects of hydrogen gas post-conditioning against neuronal pyroptosis after SAH, with specific focus on the mitochondrial ATP-sensitive K + (mitoK ATP ) channels. Following SAH induction by endovascular perforation, rats were treated with inhalation of 2.9% hydrogen gas for 2 h post-perforation. Neurologic deficits, brain water content, reactive oxygen species (ROS) levels, neuronal pyroptosis, phosphorylation of ERK1/2, p38 MAPK and pyroptosis-associated proteins IL-1β and IL-18 were evaluated 24 h after perforation by a modified Garcia method, ratio of wet/dry weight, 2',7'-dichlorofluorescin diacetate, immunofluorescence and western blot assays, respectively. An inhibitor of the mitoK ATP channel, 5-hydroxydecanoate sodium (5-HD), was used to assess the potential role of the mitoK ATP -ERK1/2-p38 MAPK signal pathway. Hydrogen gas post-conditioning significantly alleviated brain edema and improved neurologic function, reduced ROS production and neuronal pyroptosis, suppressed the expression of IL-1β and IL-18 whilst upregulating ERK1/2 phosphorylation, but downregulated p38 MAPK activation 24 h post-SAH. These aforementioned effects neuroprotective were partially reversed by 5-HD treatment. Therefore, these observations suggest that post-conditioning with hydrogen gas ameliorated SAH-induced neuronal pyroptosis at least in part through the mitoK ATP /ERK1/2/p38 MAPK signaling pathway.

Background: With the popularity of blue-rich light-emitting diode (LED)-backlit display devices, our eyes are now exposed to more short-wavelength blue light than they were in the past. The goal of this study was to investigate the pathogenesis of cataracts after short-wavelength light exposure. Methods: Sprague-Dawley (SD) rats were selected and randomly divided into a control group (10 rats each for the 4-, 8-, and 12-week groups) and an experimental group (10 rats each for the 4-, 8-, and 12-week groups). The rats in the experimental group were exposed to a short-wavelength blue LED lamp for 12 h per day. After exposure to the blue LED lamp, the rats were maintained in total darkness for 12 h, after which a 12-h light/dark cycle was resumed. The intensity of the lamp was 3000 lx. At the end of the short-wavelength blue LED lamp exposure (for 4, 8, and 12 weeks), the expression levels of caspase-1, caspase-11 and gasdermin D (GSDMD) were examined in rat lens epithelial cells (LECs) using qRT-PCR and Western blot analyses. An illuminance of 2500 lx was used to study the potential effect of blue LED light on HLE-B3 hLECs in vitro. AC-YVAD-CMK, a caspase-1 inhibitor, was used to confirm the pyroptosis of LECs by flow cytometry. Results: After 6 weeks, cataracts developed in the experimental rats (4/20 eyes). The clarity of the lens gradually worsened with the duration of exposure. Twelve weeks later, all of the rat eyes had developed cataracts. The expression levels of caspase-1, caspase-11 and GSDMD at 4, 8, and 12 weeks were significantly higher in the samples from rats exposed to a short-wavelength blue LED lamp than in the samples from control rats (p<0.05). The proportions of double-positive hLECs were significantly increased in the 5-h and 10-h short-wavelength blue light exposure subgroups compared with the 5-h and 10-h caspase-1 inhibitor subgroups (p < 0.05).

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