This study describes magnetic resonance imaging (MRI) results and changes in lateral ventricular size over time in a canine ischemic stroke model. T1- and T2-weighted (T1W, T2W) imaging and fluid-attenuated inversion recovery (FLAIR) sequence MRI were performed at 3 h and 3, 8, and 35 days after brain infarct induction. Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) mapping were performed at 8 and 35 days. A total of 29 brain lesions were induced successfully in 12 of 14 beagle dogs. At 3 h, T2W and FLAIR detected hyperintense lesions in three randomly selected dogs. On T1W, all lesions appeared hypointense to isointense at 3 h, isointense (18/29) or hypointense (11/29) at 3 days, hypointense to isointense with peripheral hyperintensity (24/26) at 8 days, and hypointense (18/26) at 35 days. Infarcts on DWI/ADC were hypointense to isointense centrally, with the periphery hyperintense/hyperintense (17/26) at 8 days and hypointense/hyperintense (19/26) at 35 days. A marked increase in lateral ventricular size was observed in dogs with cerebral infarcts. In conclusion, T2W and FLAIR were useful for detecting early stage (3 h to 3 days) brain infarction. T1W and DWI were useful for detecting neuronal necrosis and providing supplemental information for phase evaluation.
Animals ; Brain Infarction ; Brain ; Diffusion ; Dogs ; Lateral Ventricles ; Magnetic Resonance Imaging ; Necrosis ; Neurons ; Stroke

Rahnella aquatilis, a saprophytic organism, is a member of the Enterobacteriaceae family. The natural habitat of this organism is fresh water, and it is rarely found in clinical specimens. Clinical conditions ascribed to this organism include bacteremia, respiratory infection, urinary tract infection, wound infection in an immunocompromised host, and infective endocarditis in patients with congenital heart diseases. Here, we report a case of bacteremia due to R. aquatilis in a woman with breast cancer who had received chemotherapy through a chemoport. To our knowledge, this is the second case of bacteremia caused by this organism in a patient with cancer in Korea.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

We previously reported peritoneal innate-like integrin α4 (CD49d)highCD4+ T cells that provided help for B-1a cells. Here we analyzed the expression of various integrin chains on the peritoneal and pleural integrin α4highCD4+ T cells and investigated the functional heterogeneity of the subpopulations based on the integrin expression. Pleural cavity contained a lower ratio of integrin α4highCD4+ T cells to integrin α4lowCD4+ T cells than peritoneal cavity, but the pleural integrin α4highCD4+ T cells have the same characteristics of the peritoneal integrin α4highCD4+ T cells. Most of integrin α4highCD4+ T cells were integrin β1highβ7−, but a minor population of integrin α4highCD4+ T cells was integrin β1+β7+. Interestingly, the integrin α4highβ1highβ7− CD4+ T cells expressed high levels of integrin α4β1 and α6β1, whereas integrin α4highβ1+β7+ CD4+ T cells expressed high levels of integrin α4β1 and α4β7, suggesting an alternative expression of integrin α6β1 or α4β7 in combination with α4β1 in respective major and minor populations of integrin α4highCD4+ T cells. The minor population, integrin α4highβ1+β7+ CD4+ T cells, were different from the integrin α4highβ1highβ7− CD4+ T cells in that they secreted a smaller amount of Th1 cytokines upon stimulation and expressed lower levels of Th1-related chemokine receptors CCR5 and CXCR3 than the integrin α4highβ1 highβ7− CD4+ T cells. In summary, the innate-like integrin α4highCD4+ T cells could be divided into 2 populations, integrin α4β1+α6β1+α4β7− and α4β1+α6β1−α4β7+ cells. The functional significance of serosal integrin α4β7+ CD4+ T cells needed to be investigated especially in view of mucosal immunity.
CD4-Positive T-Lymphocytes ; Cytokines ; Immunity, Mucosal ; Integrin alpha4 ; Peritoneal Cavity ; Pleural Cavity ; Population Characteristics ; Receptors, CCR5 ; Receptors, Chemokine ; Receptors, CXCR3 ; T-Lymphocytes* ; Th1 Cells