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Background: Stroke survivors frequently encounter malnutrition, adversely impacting clinical outcomes. Nevertheless, malnutrition and food consumption in post-stroke patients have not been frequently assessed, and their correlation with rehabilitation outcomes remains inadequately explored. The objective of this observational study was to evaluate malnutrition at admission in these patients, assess food consumption during a six-week rehabilitation program, and analyze their correlation with rehabilitation outcomes. Methods: Subacute post-stroke patients were evaluated at admission (T0) and after a six-week rehabilitation treatment (T1). At T0, we assessed clinical and demographic characteristics, and we diagnosed malnutrition according to the Global Leadership Initiative on Malnutrition (GLIM) criteria. Weight, BMI, hematochemical parameters, and activities of daily living with the modified Barthel Index (mBI) were evaluated at both T0 and T1; recovery was registered as a change in the mBI (ΔmBI = mBIT1 − mBIT0). Patients' food consumption was recorded through visual plate waste estimation of three meals a day, 5 days a week, for six weeks of hospitalization for rehabilitation. Results: A total of 109 patients completed the study (51 women, mean age 69 ± 11). According to the GLIM criteria, 105 of these patients were at risk of malnutrition, while 43 were malnourished, with 15 severely malnourished. Malnourished patients wasted more food, with respect to non-malnourished patients, as measured by visual plate waste of total meals (25 ± 17% vs. 15 ± 14%; p = 0.001) and reached a lower ΔmBI. A linear regression analysis found a significant correlation between the ΔmBI, the waste of a "second dish", which contained mainly protein, and serum albumin at admission, even after controlling for age. Conclusions: Malnutrition assessed with the GLIM criteria at admission and food consumption are two important nutritional parameters to evaluate in post-stroke patients hospitalized for rehabilitation due to their association with recovery. [ABSTRACT FROM AUTHOR]

In vitro induction of H1-H1 histone cross-linking by adenosine diphosphate-ribose polymers is discussed. A study has been made into whether and how ADP-ribose polymers, alone, can affect formation of H1-H1 oligomers, normally present in a condensed chromatin structure. Results indicate ADP-ribose polymers are involved in chromatin decondensation.

Sequence alignment is used for identifying three functional poly(ADP-ribose) (PAR)-binding sites in the DEK primary sequence and has confirmed their functionality in PAR binding studies. The studies have helped in the molecular understanding of the DEK-PAR interplay and have supported the existence of a cellular ePAR codeE represented by PAR chain length.

Recent evidence obtained with transgenic knockout mice suggests that the enzyme poly(ADP-ribose)polymerase (PARP) does not play a direct role in DNA break processing [1, 2]. Nevertheless, inactivation of the catalytic or the DNA nick-binding functions of PARP affects cellular responses to genotoxins at the level of cell survival, sister chromatid exchanges and apoptosis [2, 3]. In the present report, we conceptualize the idea that PARP is part of a DNA break signal mechanism [4, 5]. In vitro screening studies revealed the existence of a protein family containing a polymer-binding motif of about 22 amino acids. This motif is present in p53 protein as well as in MARCKS, a protein involved in the regulation of the actin cytoskeleton. Biochemical analyses showed that these sequences are directly targeted by PARP-associated polymers in vitro, and this alters several molecular functions of p53- and MARCKS protein. PARP-deficient knockout mice from transgenic mice were found to exhibit several phenotypic features compatible with altered DNA damage signaling, such as downregulation and lack of responsiveness of p53 protein to genotoxins, and morphological changes compatible with MARCKS-related cytoskeletal dysfunction. The knockout phenotype could be rescued by stable expression of the PARP gene. - We propose that PARP-associated polymers may recruit signal proteins to sites of DNA breakage and reprogram their functions. [ABSTRACT FROM AUTHOR]