Increased expression of glucose transporter-1 (Glut-1) and glucose transporter-3 (Glut-3) has been reported in many human cancers. The mechanism of glucose entry into oral squamous cell carcinoma (OSCC) remains unclear. In this study we investigated, in untreated human OSCC, the relationship between tumour fluorine-18 fluoro-2-deoxy-D-glucose (FDG) accumulation and the expression of Glut-1 and Glut-3, as well as the association between the expression of Glut-1 and of Glut-3. All patients underwent FDG positron emission tomography (PET) pre-operatively. Standardised uptake values (SUVs) were used for evaluation of tumour FDG uptake. Final diagnoses were established by histology. Immunohistochemical staining results were evaluated according to the percentage (%) of positive area, intensity and staining score. Tumour sections were stained by immunohistochemistry for Glut-1 and Glut-3. Glut-1 immunostaining revealed that 18 (94.7%) of the 19 tumours stained positively, while Glut-3 immunostaining yielded positive findings for 16 (84.2%) tumours. Overall, a relatively low level of agreement (36.8%) in the staining score was observed between Glut-1 and Glut-3 expression. No relationship was found between the staining pattern and tumour differentiation or T grade classification in either Glut-1 or Glut-3 immunostaining. Furthermore, no relationship was found between increased FDG SUV and tumour differentiation, but the former did correlate with T grade. In conclusion, high FDG uptake values were seen in OSCC with overexpression of Glut-1 and Glut-3. However, no significant correlation was found between FDG SUV and Glut-1 or Glut-3 expression.

Alterations in cell proliferative activity are a common phenomenon in oral carcinogenesis. In this study, the expression of the cell cycle‐associated proteins p16, pRb, p53, p27 and Ki‐67 were examined by immunohistochemistry in precancerous and cancerous oral lesions, including verrucous carcinomas (VCs). Generally, expression of pRb, p53 and Ki‐67 increased according to the cell proliferative activity or tumor progression, but p27 expression showed an inverse relationship. Comparing squamous cell carcinomas (SCCs) with VCs, there was a great difference in expression levels of p27, Ki‐67 and p53, which seemed to reflect the different cell proliferative activities of these two tumors. Expression of p16 was low in both dysplasia and SCCs, whereas p16 expression was high in VCs. The high immunohistochemical expression for both p16 and pRb in VC is quite different compared with SCC, which may indicate a possible relationship between VC and human papillomavirus (HPV) infection.

The current study demonstrates the feasibility of assessing cardiovascular function quantitatively by combining clinical data with a cardiovascular model. In particular, the assessment utilizes the measurements already in use or available in clinical settings, enhancing the clinical potential of the proposed method.

Mediastinal irradiation has been reported to induce cardiac diseases such as pericardial disease, accelerated arteriosclerosis of the coronary arteries, valvular disease, conduction abnormalities, and calcification of the aorta. We experienced four cases of radiation-induced valvular disease. All patients had histories of radiation therapy and had aortic valve disease. All patients had marked fibrosis of the mediastinum and hypertrophy of pericardium. The aortic valve leaflets were tricuspid and fibrotic with focal dystrophic calcification and markedly thickened. In the pathological findings, certain rheumatic endocarditis changes such as endocardial reduplication and vascularization were not found in all aortic valves. The mechanism of radiation-induced cardiac disease is not clear. However, those changes seem to progress very slowly. Thus, long-term follow-up care is particularly important for patients undergoing radiation therapy. Fortunately, today's irradiation techniques are much less harmful; therefore, radiation-induced cardiac disease will likely become more rare in the future.

Aims/IntroductionTo explore the relationships between periodontitis and microvascular complications as well as glycemic control in type 2 diabetes patients.Materials and MethodsThis multicenter, hospital‐based, cross‐sectional study included 620 patients with type 2 diabetes. We compared the prevalence and severity of periodontitis between patients with ≥1 microvascular complication and those without microvascular complications. We also compared the prevalence and severity of periodontitis among patients with different degrees of glycemic control.ResultsAfter adjusting for confounding factors, multiple logistic regression analysis showed that the severity of periodontitis was significantly associated with the number of microvascular complications (odds ratio 1.3, 95% confidence interval 1.1–1.6), glycated hemoglobin ≥8.0% (64 mmol/mol; odds ratio 1.6; 95% confidence interval 1.1–2.3), and older age (≥50 years; odds ratio 1.7; 95% confidence interval 1.1–2.6). However, the prevalence of periodontitis was not significantly associated with the number of microvascular complications, but was associated with male sex, high glycated hemoglobin (≥8.0% [64 mmol/mol]), older age (≥40 years), longer duration of diabetes (≥15 years) and fewer teeth (≤25). Furthermore, propensity score matching for age, sex, diabetes duration and glycated hemoglobin showed that the incidence of severe periodontitis was significantly higher among patients with microvascular complications than among those without microvascular complications (P < 0.05).ConclusionsThe number of microvascular complications is a risk factor for more severe periodontitis in patients with type 2 diabetes, whereas poor glycemic control is a risk factor for increased prevalence and severity of periodontitis.