Comprehensive Tool to Assess Oral Feeding Support for Functional Recovery in Post-acute Rehabilitation

Objective

To determine the influence of the Kuchi-kara Taberu (KT) index on rehabilitation outcomes during hospitalized convalescent rehabilitation.

PET/CT imaging of renal intravascular large B-cell lymphoma

Clinical and Experimental Nephrology -     

Propranolol suppresses gastric cancer cell growth by regulating proliferation and apoptosis

Background

Despite improvements in gastric cancer treatment, the mortality associated with advanced gastric cancer is still high. The activation of β-adrenergic receptors by stress has been shown to accelerate the progression of several cancers. Accordingly, increasing evidence suggests that the blockade of β-adrenergic signaling can inhibit tumor growth. However, the effect of β-blockers, which target several signaling pathways, on gastric cancer remains to be elucidated. This study aimed to investigate the anti-tumor effects of propranolol, a non-selective β-blocker, on gastric cancer.

Methods

We explored the effect of propranolol on the MKN45 and NUGC3 gastric cancer cell lines. Its efficacy and the mechanism by which it exerts anti-tumor effects were examined using several assays (e.g., cell proliferation, cell cycle, apoptosis, and wound healing) and a xenograft mouse model.

Results

We found that propranolol inhibited tumor growth and induced G1-phase cell cycle arrest and apoptosis in both cell lines. Propranolol also decreased the expression of phosphorylated CREB-ATF and MEK-ERK pathways; suppressed the expression of matrix metalloproteinase-2, 9 and vascular endothelial growth factor; and inhibited gastric cancer cell migration. In the xenograft mouse model, propranolol treatment significantly inhibited tumor growth, and immunohistochemistry revealed that propranolol led to the suppression of proliferation and induction of apoptosis.

Conclusions

Propranolol inhibits the proliferation of gastric cancer cells by inducing G1-phase cell cycle arrest and apoptosis. These findings indicate that propranolol might have an opportunity as a new drug for gastric cancer.

     

Evaluation of lymphatic flow pattern using indocyanine green fluorescence imaging in a highly metastatic mouse model

Recently, the feasibility of real‐time indocyanine green (ICG) fluorescence imaging–guided complete mesocolic excision in colon cancer surgery has been demonstrated; however, its application to the evaluation of lymphatic flow in widespread lymph node metastasis is uncertain. This study aimed to evaluate lymphatic flow using the real‐time ICG fluorescence imaging. A mouse model of subcutaneous inoculation of BJMC3879Luc2 cells, which have been demonstrated to highly metastasize to the lymph nodes, was used as an evaluation model. Tumor growth and lymphatic flow were monitored weekly by bioluminescent imaging and near‐infrared (NIR) fluorescence imaging, respectively. After sacrificing the mice, lymph node metastases were evaluated by bioluminescent imaging and histopathology. Lymphatic flows in a model of high lymph node metastasis were evaluated using NIR fluorescence imaging. Pathological metastases of bilateral axillary, femoral, and para‐aortic lymph nodes were detected in all inoculated mice (100%: 5/5). Real‐time NIR fluorescence imaging showed the primary lymphatic vessels staining through the metastatic lymph nodes as before the inoculation of the cancer cells. Hitherto, it has been considered that lymphatic flow was changed using the bypass pathway due to occlusion of the primary lymphatic vessels. In this presented study, real‐time ICG fluorescence imaging showed no changes in lymphatic flow after lymph node metastasis. Our results suggest that real‐time ICG fluorescence imaging may have potential for the guidance of colon cancer surgery in cases of widespread lymph node metastasis.     

Maternal overweight/obesity characteristics and child anthropometric status in Jos,Nigeria

Objective:

This study is to determine the pattern of overweight and obesity and its relationship with childhood anthropometric status in Nigeria.

Materials and Methods:

This cross-sectional study was conducted in Jos, Nigeria. Interviewer administered questionnaire was used in data collection. Maternal and child anthropometric measurements were obtained using standard WHO methods. Child anthropometric Z scores were obtained from WHO Anthroplus while BMI of mothers were also determined. Totally, 262 mother-child pairs were recruited.

Results:

Mean maternal age and mean child age were 30.8 ± 6.3 yrs (15-47 yrs) and 22.3 ± 18.7 months (3-72 months). Prevalence of maternal underweight, overweight and obesity was 4.2% (11/262), 29.4% (77/262) and 25.9% (68/262), respectively. Child overweight/obesity was 5.4% (14/262), severe under-nutrition 5.7% (15/262). Mean maternal BMI was higher in the older, more educated and higher socioeconomic status (SES). Child mean birth-weight, weight-for-age Z-score and BMI-for-age Z-score (BAZ) were higher among mothers with BMI ≥ 25 kg/m². All large-for-age babies were in mothers with maternal BMI ≥ 25 kg/m². Childhood over-nutrition was more common in maternal BMI of ≥25 kg/m². Overall, BAZ was directly related with maternal BMI, maternal age and birth-weight, although it was inversely related with maternal BM I ≥ 25 kg/m².

Conclusion:

Higher BMI is seen in educated and higher SES mothers and this impact on childhood anthropometry.     

Histopathological studies of microtubule disassembling agent-induced myocardial lesions in rats

Microtubule disassembling agents (MDAs) such as colchicine (COL) and vincristine sulfate (VCR) are known to be cardiotoxic. However, few attempts have been made to histopathologically examine cardiac lesions induced by MDAs. In this study, we endeavored to induce myocardial injury in rats by administering MDAs and to clarify the morphological features of these myocardial lesions. Male rats were intravenously administered COL (1.00 or 1.25 mg/kg for 2 days at single daily doses) or VCR (0.50 or 0.75 mg/kg for 2 days at single daily doses). The day after administration, hearts were excised and examined histopathologically, immunohistochemically and electron microscopically. Degeneration and necrosis of myocardial cells with vacuolation were observed in rats administered COL at 1.25 mg/kg or VCR at 0.75 mg/kg. Electron microscopic examination revealed vacuoles in swollen mitochondria. Moreover, there were cells showing pyknosis and karyorrhexis in the interstitium. TUNEL and immunohistochemical staining for endothelial cells and electron microscopic examination identified the apoptotic cells in the interstitium to be vascular endothelial cells. These vascular endothelial lesions were induced by lower doses of MDAs than were myocardial lesions. Furthermore, common sites of cardiac lesions induced by MDAs had almost the same distribution as areas positive for pimonidazole, a marker of hypoxia. These findings indicate that MDAs occasionally damage mitochondria in myocardial cells, and suggest that these changes involve microcirculatory dysfunction induced by endothelial cell injury.