Randrupkrog3588
There is an urgent need for health professionals to address the impacts of accelerating global environmental change. Healthcare faculty therefore have to educate the rising generation of health professionals in subjects unfamiliar to themselves, such as planetary health and sustainable healthcare. This creates a new paradigm where faculty have to learn a new subject area and incorporate and teach it within their own material. It is important to develop faculty knowledge and confidence to integrate education for sustainable healthcare into their educational practice, as faculty can rapidly acquire and build on these skills. Partnership between students and faculty can enhance this faculty development as students bring fresh ideas and possibly greater knowledge of the climate and ecological crisis. Under supervision, they can co-create the necessary new learning. Students can also act as partners in advocating for social and environmental fairness and systemic change toward a sustainable healthcare system. We summarize the impact of various activities of health professions students around the world which advocate for institutional change and enhance faculty development in education for sustainable healthcare. Through diverse case studies from different countries, we illustrate faculty development in education for sustainable healthcare, highlighting student involvement which has enhanced educators' learning.Second metatarsal stress fractures are a problematic injury for runners and are formed when the rate of repair of bone is outpaced by the damage accumulated during loading. Measuring the peak stresses on the bone during running gives an indication of damage accumulation but direct measurement is invasive. Finite element modelling is a viable alternative method of accurately estimating bone stresses but tends to be too computationally expensive for use in applied research. This study presents a novel and simple finite element model which can estimate bone stresses on the second metatarsal during the stance phase of walking and running, accounting for joint reaction forces and soft tissue effects. The influence of the forces and kinematic inputs to the model and the presence of the soft tissues was quantified using a sensitivity analysis. The magnitudes of maximum stress from the model are similar to existing finite element models and bone staple strain gauge values collected during walking and running. The model was found to be most sensitive to the pitch angle of the metatarsal and the joint reaction forces and was less sensitive to the ground reaction forces under the metatarsal head, suggesting that direct measurement of external forces should not be assumed to represent internal stresses.Factor Xa (FXa) and thrombin exert non-hemostatic cellular actions primarily mediated through protease-activated receptors (PARs). We investigated the effect of FXa and thrombin on human late-outgrowth endothelial cells (OECs), a type of endothelial progenitor cells (EPCs), and on human umbilical vein endothelial cells (HUVECs). The effect of direct oral anticoagulants (DOACs), rivaroxaban and dabigatran, was also studied. The membrane expression of intercellular adhesion molecule-1 (ICAM-1) and the secretion of monocyte chemoattractant protein-1 (MCP-1) were used as cell activation markers. FXa and thrombin increase the ICAM-1 expression and the MCP-1 secretion on both cells, being higher on OECs. Vorapaxar, a specific PAR-1 antagonist, completely inhibits FXa-induced activation of both cells and thrombin-induced HUVEC activation, but only partially thrombin-induced OEC activation. Furthermore, thrombin-receptor activating peptide; TRAP-6, only partially activates OECs. OECs do not membrane-express PAR-4, therefore it may not be involved on thrombin-induced OEC activation. Rivaroxaban and dabigatran inhibit OEC and HUVEC activation by FXa and thrombin, respectively. Rivaroxaban enhances thrombin-induced OEC and HUVEC activation, which is completely inhibited by vorapaxar. The inhibition of OEC and HUVEC activation by vorapaxar and DOACs may represent a new pleiotropic effect of these drugs. The pathophysiological and clinical significance of our findings need to be established.
Camrelizumab (also known as SHR-1210), a humanized monoclonal antibody against PD-1, has been shown to block the binding of PD-1 to PD-L1 and consequently inhibit the immune escape of tumor cells. learn more Recently, camrelizumab was approved as a second-line drug for previously treated advanced hepatocellular carcinoma in China.
In this paper, the chemical properties, mechanism of action, pharmacokinetics, clinical efficacy, safety, and tolerability of camrelizumab for the treatment of advanced hepatocellular carcinoma are introduced in detail. The strategy for combination therapy and the potential application of camrelizumab in other solid tumors are briefly described. We performed a systematic review of the literature in PubMed and the following keywords were used 'SHR-1210,' 'Camrelizumab,' and 'hepatocellular carcinoma.'
Camrelizumab is a selective, humanized, high-affinity IgG4 kappa mAb against PD-1. Camrelizumab showed promising antitumor activity and manageable toxicities and offers a new second-line drug option for patients with advanced hepatocellular carcinoma. Reactive cutaneous capillary endothelial proliferation is a novel but prevalent immune-related dermatologic toxicity of camrelizumab, which is mild, reversible, and predictable. More clinical trials of camrelizumab are ongoing to develop combination therapy strategies and new indications for malignancies.
Camrelizumab is a selective, humanized, high-affinity IgG4 kappa mAb against PD-1. Camrelizumab showed promising antitumor activity and manageable toxicities and offers a new second-line drug option for patients with advanced hepatocellular carcinoma. Reactive cutaneous capillary endothelial proliferation is a novel but prevalent immune-related dermatologic toxicity of camrelizumab, which is mild, reversible, and predictable. More clinical trials of camrelizumab are ongoing to develop combination therapy strategies and new indications for malignancies.
Inflammatory bowel diseases (IBD) are chronic and progressive diseases. Long-term complications are demolitive surgery and colon-rectal cancer. A 'treat to target' strategy, in which the treatment aims to achieve objective outcomes, has already been introduced in the management of chronic conditions as rheumatic diseases. This approach is emerging as suitable for ulcerative colitis and Crohn's disease. Targets are predefined therapeutic goals demonstrated to prevent end-organ dysfunction. An optimization or switch of therapy is considered depending on the target's achievement, with regular monitoring.
According to the Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE) indications, mucosal healing and clinical remission are the main targets in IBDs. Histological remission is increasingly being considered as a novel target and has given rise to the new concept of 'disease clearance' which includes clinical, endoscopic and microscopic remission. We aim to review current evidence on the treat-to-target strategy in comparison to a stricter treat-to-clear in the IBD field.
Prospective studies on treat-to-target algorithm are sparse; a treat-to-clear approach is desirable but far from adoption in the daily practice and clinical trials. The ultimate goals of a treat-to-clear strategy differ in UC and in CD, including histological healing and transmural healing, respectively.
Prospective studies on treat-to-target algorithm are sparse; a treat-to-clear approach is desirable but far from adoption in the daily practice and clinical trials. The ultimate goals of a treat-to-clear strategy differ in UC and in CD, including histological healing and transmural healing, respectively.Catastrophic antiphospholipid syndrome (CAPS) involves sudden multiorgan dysfunction from thrombosis due to antibodies that cause platelet activation and endothelial dysfunction. Treatment variably combines anticoagulation, corticosteroid use, therapeutic plasma exchange (TPE), and high-dose intravenous immunoglobulin (IVIG). A 42-year-old male with antiphospholipid syndrome (APS) presented with severe thrombocytopenia, encephalopathy, cardiac ischemia, and acral purpuric cutaneous lesions. CAPS was identified and he received heparin infusion, methylprednisolone, and IVIG. On day 7 he developed new purpuric lesions on his right foot despite detectable arterial pulses representing new microthrombosis refractory to IVIG. He was treated with TPE which resolved the right foot ischemia and eventually his CAPS. To our knowledge, this is the first patient with CAPS reported that failed initial treatment with IVIG and subsequently had excellent response to TPE. Our observations also support recent literature indicating that onset of thrombocytopenia in APS is a warning of progression to CAPS requiring treatment escalation.
Paracetamol (acetaminophen) remains a leading cause of poisoning in Europe, North America, and Australia. For over four decades, acetylcysteine has been the antidote of choice. However, despite the use of acetylcysteine, some patients who ingest very large doses of paracetamol or who reach hospital late in the course of their poisoning, develop acute liver failure. Some will develop metabolic acidosis indicating mitochondrial toxicity.
We review the experimental and clinical data reported with the use of cimetidine, fomepizole, and calmangafodipir in the treatment of paracetamol toxicity to determine if these treatments alone or in combination with acetylcysteine might be of benefit.
We searched Ovid Medline 1946-2020, Embase 1947-2020, Scopus 2004-2020, Cochrane Databases of Systematic Reviews (CDSR), Cochrane Central Register of Controlled Trials (CENTRAL), and clinicaltrials.gov 1997-2020 for records including the concepts of paracetamol poisoning and cimetidine, fomepizole, calmangafodipir, and acetse either as a primary treatment or adjunct therapy in paracetamol poisoning. Calmangafodipir remains investigational.
The vast majority of patients with acute paracetamol overdose enjoy excellent outcomes with acetylcysteine alone. Although cimetidine and fomepizole inhibit CYP 2E1 in animals, there is insufficient evidence to recommend their use either as a primary treatment or adjunct therapy in paracetamol poisoning. Calmangafodipir remains investigational.Individuals with severe self-harm and experiences of lengthy psychiatric admissions often have complex mental health conditions and are at risk of suicide. In this qualitative study, self-harming individuals with >180 days of psychiatric admission over 12 months shared their experiences of Brief Admission (BA), a standardized crisis-management intervention encouraging self-admission and autonomy. Phenomenological hermeneutic analysis formulated BA as a worthy respite, replacing an old system of having to prove need 'in blood' or wait and get worse. Successes and struggles in early help-seeking, interpreted in the light of human rights and person-centered care, suggested that individual development of autonomy depended on perceived focus on recovery and compassion. Future research may consider ethical and health-economic aspects of BA in a broader perspective.
