Cerebral ischemia/hypoxia induces histopathological changes characterized by nuclear and cytoplasmic condensation and sustained c-for expression. The ischemic changes are thought to be initiated by excessive glutamate released by the ischemic neurons. However, no comparative study has been made between the pathological and molecular changes caused by local injection of excitotoxin and by ischemia. In the present study, we investigated the histopathological changes in rat brains induced by an intracerebral microinjection of kainic acid, a potent analogue of glutamate using two newly available markers for ischemic neurons: Fos immunohistochemistry and EA 50 stain. The rats were sacrificed at intervals from 1 hour (h) to 28 days. We demonstrated that the neurons at the site of injection developed changes typical of ischemia 1 h post-lesion: nuclear and cytoplasmic condensation, strong Fos immunoreactivity and positive EA 50 stain. By 1 day, the neurons underwent necrosis and an infarct-like picture was produced. The neuronal degeneration rapidly spread to the bilateral neocortex, CA3 and CA4 regions of hippocampus, piriform gyrus, amygdala and cerebellar Purkinje cells. After 3 days, there was neovascularization and macrophage production in the lesion center and astrocytic proliferation at the lesion periphery. The CA1 of hippocampus showed delayed neuronal necrosis typical of ischemia. Thus, intracerebral microinjection of KA induces similar histopathological and molecular changes as those occurring in brain infarct and is a simple and reliable model for studying changes related to focal brain infarct.

To the best of our knowledge, there was little information available on pathogen removal using low level disinfectant followed by free chlorine in sequential disinfection (SD). This study investigated Escherichia coli inactivation by four types of disinfection: single step disinfection (SSD), SD, traditional sequential disinfection (TSD) and mixed disinfectant disinfection (MDD). Results indicated that SD had higher ability to inactivate E. coli than the others, indicating there was a positive synergistic effect on chlorine disinfection by prior dosing with a low level of chlorine dioxide (ClO₂). The ONPG assay suggested that the permeability of cell wall rather than the viability of E. coli were changed under 0.02 mg/l ClO₂ treatment. The coexistence of residual ClO₂ and free chlorine also plays an active synergistic effect. Additionally, temperature had a positive effect on E. coli inactivation in SD, while inactivation was reduced in alkaline compared to neutral and acidic conditions.

COVID-19 patients present high incidence of kidney abnormalities, which are associated with poor prognosis and high mortality. Identification of SARS-CoV-2 in kidney of COVID-19 patients suggests renal tropism and direct infection. Presently, it is generally recognized that SARS-CoV-2 initiates invasion through binding of receptor-binding domain (RBD) of spike protein to host cell-membrane receptor ACE2, however, whether there is additional target of SARS-CoV-2 in kidney remains unclear. Kidney injury molecule-1 (KIM1) is a transmembrane protein that drastically up-regulated after renal injury. Here, binding between SARS-CoV2-RBD and the extracellular Ig V domain of KIM1 was identified by molecular simulations and co-immunoprecipitation, which was comparable in affinity to that of ACE2 to SARS-CoV-2. Moreover, KIM1 facilitated cell entry of SARS-CoV2-RBD, which was potently blockaded by a rationally designed KIM1-derived polypeptide. Together, the findings suggest KIM1 may mediate and exacerbate SARS-CoV-2 infection in a ‘vicious cycle’, and KIM1 could be further explored as a therapeutic target.

Regulated cell death is essential for development, tissue homeostasis, host defense, and disease. Beyond apoptosis, it is now clear that other forms of cell death, including ferroptosis, pyroptosis, and necroptosis, also contribute to pathology, often in interconnected rather than isolated ways. Within this broader framework, the transcriptional intermediary factor 1 (TIF1) family, comprising TRIM24, TRIM28, TRIM33, and TRIM66, has emerged as an important group of regulators linking stress adaptation, cell-state control, and cell death susceptibility. Although these proteins belong to the same family, they influence cell death through distinct and context-dependent mechanisms. Across the TIF1 family, apoptosis is by far the most extensively studied cell death phenotype, whereas links to ferroptosis, pyroptosis, and necroptosis remain more limited, more context dependent, and more unevenly distributed across individual members. Cell death often becomes evident when TIF1-dependent stress-buffering programs are disrupted, highlighting both their biological importance and potential therapeutic relevance. At the same time, family-level differences are emerging, while the underlying mechanisms remain incompletely understood, and recent advances in this field have not been synthesized. This review summarizes how TIF1 family members intersect with different cell death programs, discusses emerging translational opportunities and challenges, and highlights key mechanistic questions for future study.