Association between the intake of cocaine and a strong physical and emotional stress: a case report of a sudden death

Cocaine is a powerful sympathomimetic agent, that determines its effects either by inhibiting synaptic re-uptake of noradrenaline or through the direct stimulation of the release of catecholamines from the adrenal gland. Cocaine abuse is associated with various cardiovascular events including ventricular arrhytmias, systemic hypertension, myocardial infarction and left ventricular hypertrophy. These effects are independent of the dose and route of administration of the substance and can be noticeably enhanced by the synergistic action of factors such as stress, smoking and alcoholism. The case that we report has involved a 48 year old man, who died of acute myocardial infarction, which arose as the result of an intake of a large amount of cocaine and a strong physical and emotional stress

Death connected to paralytic ileus due to the intake of antipsychotic drugs. Case report

Abstract: The aim of this article is to enlarge furtherly the case-studies on the potentially lethal side-effects of second generation atypical antipsychotic drugs. We report the case of a 40-years-old man, under treatment with quietiapine and clozapine because of a psychotic upset, presenting persistent constipation, who died few hours after his arrive at the ER. The autopsy, together with toxicological an histologic exams, allowed to hail the cause of the death from a cardiac upset, fostered by hydroelectric imbalance connected to the sub-occlusion context. This evaluation has been related to the side-effects of these drugs -even if used with therapeutic dosages -that are able to cause in predisposed people, the onset of disorder within the cardiac rhythm, provoking ventricular fibrillation and death. Because of this reason, a constant patients' monitoring -from the first treatment administration through all the therapy -is beneficial, to prevent the onset of these potential lethal episodes

Hypo-Expression of Flice-Inhibitory Protein and Activation of the Caspase-8 Apoptotic Pathways in the Death-Inducing Signaling Complex Due to Ischemia Induced by the Compression of the Asphyxiogenic Tool on the Skin in Hanging Cases

The FLICE-inhibitory protein (c-FLIPL) (55 kDa) is expressed in numerous tissues and most abundantly in the kidney, skeletal muscles and heart. The c-FLIPL has a region of homology with caspase-8 at the carboxy-terminal end which allows the molecule to assume a tertiary structure similar to that of caspases-8 and -10. Consequently, c-FLIPL acts as a negative inhibitor of caspase-8, preventing the processing and subsequent release of the pro-apoptotic molecule active form. The c-FLIP plays as an inhibitor of apoptosis induced by a variety of agents, such as tumor necrosis factor (TNF), T cell receptor (TCR), TNF-related apoptosis inducing ligand (TRAIL), Fas and death receptor (DR). Increased expression of c-FLIP has been found in many human malignancies and shown to be involved in resistance to CD95/Fas and TRAIL receptor-induced apoptosis. We wanted to verify an investigative protocol using FLIP to make a differential diagnosis between skin sulcus with vitality or non-vital skin sulcus in hanged subjects and those undergoing simulated hanging (suspension of the victim after murder). The study group consisted of 21 cases who died from suicidal hanging. The control group consisted of traumatic or natural deaths, while a third group consisted of simulated hanging cases. The reactions to the Anti-FLIP Antibody (Abcam clone-8421) was scored for each section with a semi-quantitative method by means of microscopic observation carried out with confocal microscopy and three-dimensional reconstruction. The results obtained allow us to state that the skin reaction to the FLIP is extremely clear and precise, allowing a diagnosis of unequivocal vitality and a very objective differentiation with the post-mortal skin sulcus

Urokinase Plasminogen Receptor and the Fibrinolytic Complex Play a Role in Nerve Repair after Nerve Crush in Mice, and in Human Neuropathies

Remodeling of extracellular matrix (ECM) is a critical step in peripheral nerve regeneration. In fact, in human neuropathies, endoneurial ECM enriched in fibrin and vitronectin associates with poor regeneration and worse clinical prognosis. Accordingly in animal models, modification of the fibrinolytic complex activity has profound effects on nerve regeneration: high fibrinolytic activity and low levels of fibrin correlate with better nerve regeneration. The urokinase plasminogen receptor (uPAR) is a major component of the fibrinolytic complex, and binding to urokinase plasminogen activator (uPA) promotes fibrinolysis and cell movement. uPAR is expressed in peripheral nerves, however, little is known on its potential function on nerve development and regeneration. Thus, we investigated uPAR null mice and observed that uPAR is dispensable for nerve development, whereas, loss of uPAR affects nerve regeneration. uPAR null mice showed reduced nerve repair after sciatic nerve crush. This was a consequence of reduced fibrinolytic activity and increased deposition of endoneurial fibrin and vitronectin. Exogenous fibrinolysis in uPAR null mice rescued nerve repair after sciatic nerve crush. Finally, we measured the fibrinolytic activity in sural nerve biopsies from patients with peripheral neuropathies. We showed that neuropathies with defective regeneration had reduced fibrinolytic activity. On the contrary, neuropathies with signs of active regeneration displayed higher fibrinolytic activity. Overall, our results suggest that enforced fibrinolysis may facilitate regeneration and outcome of peripheral neuropathies