The role of the Patient-Generated Subjective Global Assessment (PG-SGA) and biochemical markers in predicting anemia patients with cancer.

PURPOSE: The causes of anemia and the common side effects of cancer are multifactorial. Malnutrition is one of the alleged components of the aforementioned complications. This study planned to investigate the relationship among biochemical markers, Patient-Generated Subjective Global Assessment (PG-SGA), and anemia in cancer patients. METHODS: This analysis consisted of 234 patients who were enlisted in the Department of Oncology of the First Hospital of Shanxi Medical University between December 2016 and October 2017. The groups were divided into anemic and non-anemic patients. The gathered data primarily discussed the patients' basic information, specifically the age, gender, smoking, alcohol consumption, and nutritional status based on levels of serum biochemical markers and PG-SGA scores. RESULTS: Among the participants, 31.2% of the cancer patients were diagnosed with anemia whereas, according to the scores of PG.SGA, 65.0% of patients experienced malnourishment. The anemia was significantly associated with biochemical markers, expecting a transferrin in univariable analyses. Binary logistic regression analysis between anemic cancer patients and non-anemic cancer patients suggested that high PG-SGA score (odds ratio 1.082; 95% CI 1.027-1.141) implied the risk factor for anemia, and high PG-SGA scores could potentially increase the risk of anemia. The multiple regression analysis showed that hemoglobin concentration (OR 0.575; 95% CI 0.450-0.736) and PG-SGA score (OR 1.231; 95% CI 1.013-1.496) were linked to anemia. However, total protein, albumin, prealbumin, serum iron, transferrin, and transferrin saturation lacked a strong relationship with anemia. CONCLUSION: Anemia prevailed in cancer patients, as nutritionally assessed by PG-SGA, while hemoglobin established a linkage with anemia as they could provide extra predictive information about anemia in patients diagnosed with cancer.

Dynamics of posttranslational modifications of p53.

The latest experimental evidence indicates that acetylation of p53 at K164 (lysine 164) and K120 may induce directly cell apoptosis under severe DNA damage. However, previous cell apoptosis models only studied the effects of active and/or inactive p53, that is, phosphorylation/dephosphorylation of p53. In the present paper, based partly on Geva-Zatorsky et al. (2006) and Batchelor et al. (2008), we propose a new cell apoptosis network, in which p53 has three statuses, that is, unphosphorylated p53, phosphorylated p53, and acetylated p53. The time delay differential equations (DDEs) are formulated based on our network to investigate the dynamical insights of p53-induced cell apoptosis. In agreement with experiments (Loewer et al. (2010)), our simulations indicate that acetylated p53 accumulates gradually and then induces the proapoptotic protein Bax under enough DNA damage. Moreover, phosphorylated p53 oscillates and initiates cell repair during DNA damage.