Global Alliance for the Promotion of Physical Activity: the Hamburg Declaration.

Non-communicable diseases (NCDs), including coronary heart disease, stroke, hypertension, type 2 diabetes, dementia, depression and cancers, are on the rise worldwide and are often associated with a lack of physical activity (PA). Globally, the levels of PA among individuals are below WHO recommendations. A lack of PA can increase morbidity and mortality, worsen the quality of life and increase the economic burden on individuals and society. In response to this trend, numerous organisations came together under one umbrella in Hamburg, Germany, in April 2021 and signed the 'Hamburg Declaration'. This represented an international commitment to take all necessary actions to increase PA and improve the health of individuals to entire communities. Individuals and organisations are working together as the 'Global Alliance for the Promotion of Physical Activity' to drive long-term individual and population-wide behaviour change by collaborating with all stakeholders in the community: active hospitals, physical activity specialists, community services and healthcare providers, all achieving sustainable health goals for their patients/clients. The 'Hamburg Declaration' calls on national and international policymakers to take concrete action to promote daily PA and exercise at a population level and in healthcare settings.

Considerations about Hypoxic Changes in Neuraxis Tissue Injuries and Recovery.

Hypoxia represents the temporary or longer-term decrease or deprivation of oxygen in organs, tissues, and cells after oxygen supply drops or its excessive consumption. Hypoxia can be (para)-physiological-adaptive-or pathological. Thereby, the mechanisms of hypoxia have many implications, such as in adaptive processes of normal cells, but to the survival of neoplastic ones, too. Ischemia differs from hypoxia as it means a transient or permanent interruption or reduction of the blood supply in a given region or tissue and consequently a poor provision with oxygen and energetic substratum-inflammation and oxidative stress damages generating factors. Considering the implications of hypoxia on nerve tissue cells that go through different ischemic processes, in this paper, we will detail the molecular mechanisms by which such structures feel and adapt to hypoxia. We will present the hypoxic mechanisms and changes in the CNS. Also, we aimed to evaluate acute, subacute, and chronic central nervous hypoxic-ischemic changes, hoping to understand better and systematize some neuro-muscular recovery methods necessary to regain individual independence. To establish the link between CNS hypoxia, ischemic-lesional mechanisms, and neuro-motor and related recovery, we performed a systematic literature review following the" Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA") filtering method by interrogating five international medical renown databases, using, contextually, specific keywords combinations/"syntaxes", with supplementation of the afferent documentation through an amount of freely discovered, also contributive, bibliographic resources. As a result, 45 papers were eligible according to the PRISMA-inspired selection approach, thus covering information on both: intimate/molecular path-physiological specific mechanisms and, respectively, consequent clinical conditions. Such a systematic process is meant to help us construct an article structure skeleton giving a primary objective input about the assembly of the literature background to be approached, summarised, and synthesized. The afferent contextual search (by keywords combination/syntaxes) we have fulfilled considerably reduced the number of obtained articles. We consider this systematic literature review is warranted as hypoxia's mechanisms have opened new perspectives for understanding ischemic changes in the CNS neuraxis tissue/cells, starting at the intracellular level and continuing with experimental research to recover the consequent clinical-functional deficits better.

Delayed Diagnosis of Clostridium difficile Colitis in a 48-Year-Old Woman with a Homozygous Mutation of the UGT1A1 Gene While on Chemotherapy for Colorectal Carcinoma.

BACKGROUND There are many causes of chronic colitis and diarrhea, including the effects of chemotherapy. Mutations in the UGT1A1 gene can be associated with increased toxicity from irinotecan-based chemotherapy. This report is of a case of delayed diagnosis of Clostridium difficile (C. difficile) colitis in a 48-year-old woman with a homozygous mutation of the UGT1A1 gene treated with chemotherapy for colorectal carcinoma. CASE REPORT A 48-year-old woman with a low-differentiated colonic adenocarcinoma was treated after surgery with irinotecan, 5 fluorouracil, and panitumumab and had a history of chronic and severe diarrhea. Genetic testing identified a mutation in the UGT1A1 gene associated with increased toxicity to irinotecan, and the EIA tests performed for evaluation of C. difficile toxins A and B showed repeatedly negative results. Replacement of irinotecan with oxaliplatin did not have significant therapeutic results, but these were achieved by the administration of active antibiotics against C. difficile (metronidazole, vancomycin, and fidaxomicin). CONCLUSIONS This report has shown that in complex cases where patients are treated with chemotherapy and have increased susceptibility to drug toxicity, chronic diarrhea may still have an infectious cause. Only when the diagnosis is correctly made can the patient be appropriately treated.