18 research outputs found
Catheter Care Bundle and Low Catheter Infection Rates in a Home Parenteral Nutrition Population: A 4 Year Observational Study
Abstract
Background
Home Parenteral Nutrition (HPN) is often a life-saving therapy for patients. One of the most common complications for HPN is catheter-related blood stream infections (CRBSI). In the home setting there is no single defined “care bundle” for the on-going maintenance of central venous catheters (CVC) for the prevention of CRBSI. We evaluated the impact of a standardized catheter care bundle in patients receiving HPN on the incidence of CRBSI.
Methods
Data collection included use of standardized tools and processes to capture patient demographics, catheter complications including CRBSI and some associated risk factors. Reported data was collected and analyzed annually and compared year-to-year from the years 2014–2017 from one national home infusion company. CRBSI reported as number of infections/1000 catheter days
Results
The CRBSI rate/1000 days was reported as 0.43, 0.31, 0.30 and 0.23 (2014, 2015, 2016, 2017 respectively). The type of catheter, number of catheter lumens and type of nursing care provided had importance. In general, single lumen central venous catheters had numerically less CRBSI than double lumen central venous catheters; peripherally-inserted central venous catheters were the most common catheter used but also had the highest percentage of CRBSI.
Conclusion
The use of a catheter care bundle in an HPN population resulted in a 4- year reported outcomes of low and continuously declining CRBSI in a large, diverse United States-based HPN population.</jats:p
Catheter Care Bundle and Low Catheter Related Bloodstream Infection Rates in a Home Parenteral Nutrition Population; a&nbsp;&nbsp;4 Year Observational Study
Abstract
Home Parenteral Nutrition (HPN) is often a life-saving therapy for patients. One of the most common complications for HPN is catheter-related blood stream infections (CRBSI). In the home setting there is no single defined “care bundle” for the on-going maintenance of central venous catheters (CVC) for the prevention of CRBSI. We evaluated the impact of a standardized catheter care bundle in patients receiving HPN on the incidence of CRBSI. Methods: Data collection included use of standardized tools and processes to capture patient demographics, catheter complications including CRBSI and some associated risk factors. Reported data was collected and analyzed annually and compared year-to-year from the years 2014-2017 from one national home infusion company. CRBSI reported as number of infections/1000 catheter days Results: The CRBSI rate/1000 days was reported as 0.43, 0.31, 0.30 and 0.23 (2014, 2015, 2016, 2017 respectively) statistically significant difference (p < .05) between the years 2014 and 2017. CRBSI. Conclusion: The use of a catheter care bundle in an HPN population may have contributed to a 4- year reported outcomes of low and continuously declining CRBSI in a large, diverse United States-based HPN population.</jats:p
Perspective on This Article from Rapamycin Is a Potent Inhibitor of Skin Tumor Promotion by 12-<i>O</i>-Tetradecanoylphorbol-13-Acetate
Perspective on This Article from Rapamycin Is a Potent Inhibitor of Skin Tumor Promotion by 12-O-Tetradecanoylphorbol-13-Acetat
Supplementary Figure 1 from Metformin Inhibits Skin Tumor Promotion in Overweight and Obese Mice
PDF file - 1781K, Effect of metformin on epidermal phospho-ULK1 in the absence or presence of TPA treatment.</p
Preventing ovariectomy-induced weight gain decreases tumor burden in rodent models of obesity and postmenopausal breast cancer
ABSTRACTObesity and adult weight gain are linked to increased breast cancer risk and poorer clinical outcomes in postmenopausal women, particularly for hormone-dependent tumors. Menopause is a time when significant weight gain occurs in many women, and clinical and preclinical studies have identified menopause (or ovariectomy) as a period of vulnerability for breast cancer development and promotion. We hypothesized that preventing weight gain after ovariectomy (OVX) may be sufficient to prevent the formation of new tumors and decrease growth of existing mammary tumors. Here, we tested this hypothesis in a rat model of obesity and carcinogen-induced postmenopausal mammary cancer and validated our findings in a murine xenograft model with implanted human tumors. In both models, preventing weight gain after OVX significantly decreased obesity-associated tumor development and growth. Importantly, we did not induce weight loss in these animals, but simply prevented weight gain. In both lean and obese rats, preventing weight gain reduced visceral fat accumulation and associated insulin resistance. Similarly, the intervention decreased circulating tumor-promoting growth factors and inflammatory cytokines (ie, BNDF, TNFα, FGF2), with greater effects in obese compared to lean rats. In obese rats, preventing weight gain decreased adipocyte size, adipose tissue macrophage infiltration, reduced expression of the tumor-promoting growth factor FGF-1, and reduced phosphorylated FGFR in tumors. Together, these findings suggest that the underlying mechanisms associated with the anti-tumor effects of weight maintenance are multifactorial, and that weight maintenance during the peri-/post-menopausal period may be a viable strategy for reducing obesity-associated breast cancer risk and progression in women.</jats:p
Regular exercise potentiates energetically expensive hepatic de novo lipogenesis during early weight regain
Exercise is a potent facilitator of long-term weight loss maintenance (WLM), whereby it decreases appetite and increases energy expenditure beyond the cost of the exercise bout. We have previously shown that exercise may amplify energy expenditure through energetically expensive nutrient deposition. Therefore, we investigated the effect of exercise on hepatic de novo lipogenesis (DNL) during WLM and relapse to obesity. Obese rats were calorically restricted with (EX) or without (SED) treadmill exercise (1 h/day, 6 days/wk, 15 m/min) to induce and maintain weight loss. After 6 wk of WLM, subsets of WLM-SED and WLM-EX rats were allowed ad libitum access to food for 1 day to promote relapse (REL). An energy gap-matched group of sedentary, relapsing rats (REL-GM) were provided a diet matched to the positive energy imbalance of the REL-EX rats. During relapse, exercise increased enrichment of hepatic DN-derived lipids and induced hepatic molecular adaptations favoring DNL compared with the gap-matched controls. In the liver, compared with both REL-SED and REL-GM rats, REL-EX rats had lower hepatic expression of genes required for cholesterol biosynthesis; greater hepatic expression of genes that mediate very low-density lipoprotein synthesis and secretion; and greater mRNA expression of Cyp27a1, which encodes an enzyme involved in the biosynthesis of bile acids. Altogether, these data provide compelling evidence that the liver has an active role in exercise-mediated potentiation of energy expenditure during early relapse. </jats:p
Metformin Accumulation Correlates with Organic Cation Transporter 2 Protein Expression and Predicts Mammary Tumor Regression <i>In Vivo</i>
Abstract
Several epidemiologic studies have associated metformin treatment with a reduction in breast cancer incidence in prediabetic and type II diabetic populations. Uncertainty exists regarding which patient populations and/or tumor subtypes will benefit from metformin treatment, and most preclinical in vivo studies have given little attention to the cellular pharmacology of intratumoral metformin uptake. Epidemiologic reports consistently link western-style high fat diets (HFD), which drive overweight and obesity, with increased risk of breast cancer. We used a rat model of HFD-induced overweight and mammary carcinogenesis to define intratumoral factors that confer metformin sensitivity. Mammary tumors were initiated with 1-methyl-1-nitrosourea, and rats were randomized into metformin-treated (2 mg/mL drinking water) or control groups (water only) for 8 weeks. Two-thirds of existing mammary tumors responded to metformin treatment with decreased tumor volumes (P &lt; 0.05), reduced proliferative index (P &lt; 0.01), and activated AMPK (P &lt; 0.05). Highly responsive tumors accumulated 3-fold greater metformin amounts (P &lt; 0.05) that were positively correlated with organic cation transporter-2 (OCT2) protein expression (r = 0.57; P = 0.038). Importantly, intratumoral metformin concentration negatively associated with tumor volume (P = 0.03), and each 10 pmol increase in intratumoral metformin predicted &gt;0.11 cm3 reduction in tumor volume. Metformin treatment also decreased proinflammatory arachidonic acid &gt;1.5-fold in responsive tumors (P = 0.023). Collectively, these preclinical data provide evidence for a direct effect of metformin in vivo and suggest that OCT2 expression may predict metformin uptake and tumor response. Cancer Prev Res; 10(3); 198–207. ©2017 AACR.</jats:p
Preventing ovariectomy-induced weight gain decreases tumor burden in rodent models of obesity and postmenopausal breast cancer
Abstract
Background
Obesity and adult weight gain are linked to increased breast cancer risk and poorer clinical outcomes in postmenopausal women, particularly for hormone-dependent tumors. Menopause is a time when significant weight gain occurs in many women, and clinical and preclinical studies have identified menopause (or ovariectomy) as a period of vulnerability for breast cancer development and promotion.
Methods
We hypothesized that preventing weight gain after ovariectomy (OVX) may be sufficient to prevent the formation of new tumors and decrease growth of existing mammary tumors. We tested this hypothesis in a rat model of obesity and carcinogen-induced postmenopausal mammary cancer and validated our findings in a murine xenograft model with implanted human tumors.
Results
In both models, preventing weight gain after OVX significantly decreased obesity-associated tumor development and growth. Importantly, we did not induce weight loss in these animals, but simply prevented weight gain. In both lean and obese rats, preventing weight gain reduced visceral fat accumulation and associated insulin resistance. Similarly, the intervention decreased circulating tumor-promoting growth factors and inflammatory cytokines (i.e., BDNF, TNFα, FGF-2), with greater effects in obese compared to lean rats. In obese rats, preventing weight gain decreased adipocyte size, adipose tissue macrophage infiltration, reduced expression of the tumor-promoting growth factor FGF-1 in mammary adipose, and reduced phosphorylated FGFR indicating reduced FGF signaling in tumors.
Conclusions
Together, these findings suggest that the underlying mechanisms associated with the anti-tumor effects of weight maintenance are multi-factorial, and that weight maintenance during the peri-/postmenopausal period may be a viable strategy for reducing obesity-associated breast cancer risk and progression in women.
</jats:sec
