Search

There is increasing awareness of radiotherapy's potential side effects, such as lymphopenia. Therefore, this study aimed to establish the association between WBRT and the development of lymphopenia in patients with brain metastases undergoing brain radiotherapy (RT), along with evaluating the corresponding clinical outcomes. Including 116 patients with brain metastases undergoing brain radiotherapy, the study collected the absolute lymphocyte counts (ALC) within 2 weeks before brain radiotherapy (pre-radiotherapy, pre-RT), as well as ones at 1 and 2 months after completing RT (post-RT). Univariate and multivariate analyses were performed to identify associations between radiation modality and post-RT ALC. The relationships between post-RT ALC and overall survival were evaluated with Kaplan–Meier analysis and a multivariate Cox regression model. The median ALC definitely decreased at 1 month post-RT, but at 2 months post-RT, gradually rose but not to the pre-RT ALC. The multivariate analysis identified WBRT and lower pre-RT ALC as independent risk factors associated with the decrease in post-RT ALC at 1 month. It also revealed more than 4 brain metastases, G3-4 lymphopenia at 1 month and lower post-RT ALC at 2 months exhibited significantly worse prognosis regardless of the radiation modality. However, there was indeed an independent correlation between radiation modality and the outcome of intracranial progression-free survival (PFS). To approach the feasibility and reasonableness of treatment, clinicians should carefully consider various factors to achieve long-term survival of patients. [ABSTRACT FROM AUTHOR]

The design of highly active photocatalysts for degradation of phenol can be particularly challenging for solar energy utilisation. Herein, a series of mesoporousLaCo1−xCexO3catalysts have been synthesised and studied for degradation of phenol under UV irradiation. Compared with LaCoO3-SG catalyst which is formed through sol-gel method, optimised LaCo1−xCexO3-NC prepared by nanocasting method showed remarkably higher activity for the degradation of phenol due to the higher specific surface area, and the order of degradation rates is LaCo0.85Ce0.15O3-NC > LaCoO3-NC > LaCoO3-SG. Moreover, Au/LaCo1−xCexO3 catalysts were synthesized via Au deposition–precipitation method, and the catalytic activity for photodegradation of phenol increased with the loading of Au on the support.

Introduction: The aim of the study was to analyze the optic nerve head (ONH) microcirculation using optical coherence tomography angiography (OCT-A) and the upstream macrocirculation using color Doppler imaging (CDI) in low-tension and high-tension glaucoma (LTG and HTG, respectively). Methods: This cross-sectional study included 67 eyes of 67 HTG patients, 55 eyes of 55 LTG patients, and 42 eyes of 42 healthy controls. We recorded the complete ophthalmological examination, visual fields, retinal nerve fiber layer (RNFL) thickness, ONH vessel density (VD) measured using OCT-A, peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index (RI) measured using CDI. SPSS software was used for data analysis. Data are presented as mean ± standard deviation or median (interquartile range) and compared using t test or Mann-Whitney U test, as appropriate. Pearson χ2 test or Fisher's exact test was used for comparisons, as appropriate. Pearson correlation analysis was used to evaluate the correlations between variables. p < 0.05 was considered statistically significant. Results: The ONH VD and RNFL thickness were considerably lower in glaucomatous eyes than in healthy eyes (both p < 0.001). Compared with the HTG group, the LTG group had lower VD in the peripapillary region (p = 0.027). Compared with the healthy group, the HTG group had lower PSV (p = 0.029 and = 0.023, respectively), lower EDV (p = 0.023 and <0.001, respectively), and higher RI (p = 0.019 and = 0.006, respectively) of the internal carotid artery (ICA) and central retinal artery (CRA). The LTG group had lower PSV (p = 0.015 and <0.001, respectively) and EDV (p = 0.047 and = 0.001, respectively) of the ophthalmic artery (OA) and CRA. The LTG group had lower PSV of CRA than the HTG group (p = 0.034). In glaucomatous eyes, peripapillary VD had a significant association with the mean defect (p < 0.001) and RNFL thickness (p < 0.001), but not with the other CDI indices (all p > 0.05). Conclusion: The ONH microcirculation and upstream macrocirculation of the large arteries exhibited differences in the blood flow characteristics between the LTG and HTG groups. These differences may improve our understanding of glaucoma. There was no correlation between the characteristics of the ONH microcirculation and the upstream macrocirculation of large vessels in the LTG and HTG groups. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is complicated by the development of a primary cardiomyopathy, which contributes to the excess morbidity and mortality of this disorder. The protein kinase C (PKC) family of isozymes plays a key role in the cardiac phenotype expressed during postnatal development and in response to pathological stimuli. Hyperglycemia is an activating signal for cardiac PKC isozymes that modulate a myriad of cell events including cell death and survival. The [epsilon]-isozyme of the PKC family transmits a powerful survival signal in cardiac muscle cells. Accordingly, to test the hypothesis that endogenous activation of cardiac PKC-[epsilon] will protect against hyperglycemic cell injury and left ventricular dysfunction, diabetes mellitus was induced using streptozotocin in genetically engineered mice with cardiac-specific expression of the PKC-[epsilon] translocation activator [[psi][epsilon]-receptors for activated C kinase ([psi][epsilon]-RACK)]. The results demonstrate a striking PKC-[epsilon] cardioprotective phenotype in diabetic [psi][epsilon]-RACK ([epsilon]-agonist) mice that is characterized by inhibition of the hyperglycemia apoptosis signal, attenuation of hyperglycemia-mediated oxidative stress, and preservation of parameters of left ventricular pump function. Hearts of diabetic [epsilon]-agonist mice exhibited selective trafficking of PKC-[epsilon] to membrane and mitochondrial compartments, phosphorylation/inactivation of the mitochondrial Bad protein, and inhibition of cytochrome c release. We conclude that activation of endogenous PKC-[epsilon] in hearts of diabetic [epsilon]-agonist mice promotes the survival phenotype, attenuates markers of oxidative stress, and inhibits the negative inotropic properties of chronic hyperglycemia. hyperglycemia; diabetes mellitus; protein kinase C; isozymes; translocation activator; cardioprotection

Left ventricular (LV) myocytes were isolated from male mice bearing the Arg403 -> Gln alpha-cardiac myosin heavy chain missense mutation, a model of familial hypertrophic cardiomyopathy. The myocytes indicated impaired contraction and relaxation. The impaired function may be caused, at least in part, by distinct abnormalities of morphology as evidenced by the misalignment of myofibrils. Possibly, the myocytes with abnormal morphology are those that exhibit a more severe phenotype of the Arg403 -> Gln missense mutation.