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Biomedical subjects

Daniele Lo Coco

Publications and source records attributed to Daniele Lo Coco.

4 recordsLinked to original sources
PubMed2006

Distribution and cellular localization of high mobility group box protein 1 (HMGB1) in the spinal cord of a transgenic mouse model of ALS.

Although the aetiology of amyotrophic lateral sclerosis (ALS) is still elusive, increased attention has been put forward on events related to neuroinflammation and an active participation of glial cells in the ALS pathogenesis has been suggested. However, the specific role of many proinflammatory mediators that usually accompany the inflammatory changes is still largely unknown. High mobility group box protein 1 (HMGB1) is an ubiquitous nuclear protein that exerts numerous extranuclear and extracellular functions, including a proinflammatory activity, able to induce cytokines expression and activate inflammatory cells. To investigate whether this protein may play a role in the inflammatory events in ALS, we examined both expression and localization of HMGB1 in the lumbar spinal cord of SOD1G93A transgenic mice, a well established mouse model of familial ALS, at different stages of the disease. Intense HMGB1 reactivity was detected in ventral horn motor neurons of both non-transgenic and SOD1G93A mice and there was no difference in its expression between presymptomatic SOD1G93A mice and controls. With the progression of the disease, degenerating neurons showed a reduction of HMGB1 immunoreactivity which could reflect an extracellular release of this protein. By contrast, in the reactive glial cells HMGB1 was remarkably expressed in the nucleus, but not in the cytosol, likely contributing to the proliferation and/or hypertrophy of these cells. These results suggest that HMGB1 may have a different involvement in the motor neurons and glial cells in response to the neurotoxic environment in the spinal cord of SOD1G93A mice, and it may contribute to the progression of inflammatory and neurodegenerative processes.

Amyotrophic Lateral Sclerosis↗
PubMed2005

Development of chronic hypoventilation in amyotrophic lateral sclerosis patients.

Early prediction of respiratory muscle involvement and chronic hypoventilation (CH) in amyotrophic lateral sclerosis (ALS) patients can help to plan mechanical ventilatory aids and palliative care interventions well before respiratory failure occurs. To describe the natural history of the progressive pulmonary dysfunction leading to CH, and to identify potential parameters associated with its development in ALS, we prospectively followed 38 ALS patients up to 26 months, starting from their first presentation at our Clinic. At study entry, median FVC was 87% (interquartile range: 72-104%) and declined by 10% after 6 months (range: 2-49%), showing a very high inter-patient variability. Over the 26-months follow-up, 19 patients (50%) presented CH in the first 12 months, and eight patients (21%) developed CH in the remaining 14 months of the study. The remaining 29% of patients did not show signs of CH during the whole period of observation. In the Cox model, the category of disease progression (rapid vs. intermediate and slow), assessed using the Appel ALS Rating Scale (AARS) in the first 3 months after presentation, was the only variable associated with a significantly increased likelihood of CH. We conclude that CH can occur within 1 year from presentation in a great proportion of patients, independently from their initial respiratory status. Including the patients in specific categories of early disease progression, as assessed with the AARS, could be a sensitive method to identify patients with different risk of developing CH, and may help physicians to more efficiently plan the frequencies of respiratory evaluations, initiate mechanical ventilation and discuss advance directives with the patients and their caregivers.

Age Factors↗
PubMed2005

Individual and health-related quality of life assessment in amyotrophic lateral sclerosis patients and their caregivers.

We performed a cross-sectional study aimed to address the quality of life (QoL) and putative associated variables in amyotrophic lateral sclerosis (ALS) patients and their respective caregivers, using both health-related (WHOQOL-BREF) and individual (SEIQoL-DW) QoL instruments. Further, we sought to investigate concordance within patient-caregiver pairs for ratings of respective QoL. Thirty-seven patient-caregiver pairs were included in the study. QoL was rated low by both patients and caregivers, and there was no significant difference between them on scores of overall QoL, even if caregivers showed higher scores on the physical and psychological WHOQOL-BREF domains compared to patients. No correlation could be found between QoL of both patients and caregivers and all the examined socio-demographic variables. Moreover, concordance between patients and respective caregivers was low for ratings of QoL, suggesting that their QoL is not necessarily interrelated, and that these couples do not actually represent a unique psychological entity. Interestingly, physical dysfunction, measured with the ALS-FRS, was not significantly correlated with caregivers' individual QoL scores. The most frequently nominated SEIQoL-DW cues were related to health (physical and psychological) and family for both patients and caregivers, and there was high agreement for the choice of areas important for subject's QoL. Interestingly, patients and caregivers who endorsed spirituality as a significant domain reported better QoL. Our study confirms that ALS has a negative impact on QoL in both patients and caregivers. However, caregivers who present lower QoL levels are not always those who have to look after the most physically or psychologically impaired patients. Major attention on QoL issues of both patients and caregivers, family status, and health perception, integrated with the medical evaluation, could lead to a better understanding of the problems related to the caregiving experience, and could help couples dealing with this life-threatening disease.

Activities of Daily Living↗