Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

Background: According to the ventricular myocardial band model, the diastolic isovolumetric period is a contraction phenomenon. Our objective was to employ speckle-tracking echocardiography (STE) to analyze myocardial deformation of the left ventricle (LV) and to confirm if it supports the myocardial band model. Methods: This was a prospective observational study in which 90 healthy volunteers were recruited. We evaluated different types of postsystolic shortening (PSS) from an LV longitudinal strain study. Duration of latest deformation (LD) was calculated as the time from the start of the QRS complex of the ECG to the latest longitudinal deformation peak in the 18 segments of the LV. Results: The mean age of our subjects was 50.3 ± 11.1 years. PSS was observed in 48.4% of the 1620 LV segments studied (19.8%, 13.5%, and 15.1% in the basal, medial, and apical regions, respectively). PSS was more frequent in the basal, medial septal, and apical anteroseptal segments (>50%). LD peaked in the interventricular septum and in the basal segments of the LV. Conclusions: The pattern of PSS and LD revealed by STE suggests there is contraction in the postsystolic phase of the cardiac cycle. The anatomical location of the segments in which this contraction is most frequently observed corresponds to the main path of the ascending component of the myocardial band. This contraction can be attributed to the protodiastolic untwisting of the LV.

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Physical examination showed decreased ventilation at the right base, tachypnoea (respiratory rate 26 breaths/minute) and tachycardia (heart rate 120 beats/minute). The haemoglobin and a biochemical screen were normal. Arterial blood gas tensions when breathing room air were Pao, 4 93 kPa, Paco, 4-26 kPa, HCO3-24 mEq/l, and pH 7-48. A chest radiograph showed elevation of the right hemidiaphragm with paradoxical movement during inspiration which increased with the sniff manoeuvre. An electrocardiogram revealed sinus tachycardia with anterior hemiblock and incomplete right bundle branch block. Abdominal and thoracic ultrasonography and computed tomographic scanning excluded subphrenic and hepatic pathology. Pulmonary function tests revealed a mild restrictive ventilatory defect (vital capacity 2-761 (67% predicted), FEVI/FVC 77%, total lung capacity 4-561 (79%)). The single breath transfer factor for carbon monoxide (TLCO) was normal (109%). A right-to-left shunt was detected while the patient breathed 100% oxygen in the sitting position (Po2 7.73 kPa, Pco, 4-8 kPa). Maximal static inspiratory mouth pressure (Pimax) was reduced (-72 cm H,O) while expiratory mouth pressure (PEmax) was normal (165 cm H2O). Electromyographic studies of the right hemidiaphragm with stimulation of the phrenic nerve suggested the occurrence of a neurapraxia. A ventilationperfusion scan showed defects which were consistent with the radiographic findings. Pulmonary arteriography was normal. Transoesophageal echocardiography (figure) showed a patent foramen ovale with a right-to-left shunt from the inferior vena cava towards the foramen ovale in the interatrial septum, later confirmed by arterial angiography. Cardiac catheterisation showed normal pressures and resistance in the pulmonary artery.Another chest radiograph taken six weeks later, while the patient was being assessed for surgical correction, showed the right diaphragmatic paralysis to have resolved. Arterial blood gas tensions when breathing room air were Po, 10-4 kPa, Pco, 4-2 kPa and, after breathing 100% oxygen, Po, 75-7 kPa, Pco, 5-8 kPa (Qs/QT of 6% with an assumed arteriovenous oxygen content difference of 5 ml%).Transoesophageal echocardiography confirmed the disappearance of the right-to-left shunt. DiscussionPatent foramen ovale is a common finding among healthy people, its incidence ranging from 20% to 35% in necropsy series.3 It is often overlooked because no abnormalities are found on physical, electrocardiographic, or radiological examination; nevertheless, the importance of patent foramen ovale is that any condition causing a higher pressure in the right atrium than the left may lead to a right-to-left shunt with systemic arterial desaturation and possibly paradoxical emboli.4 This may occur during crying in the neonate,5 the Valsalva manoeuvre,6 during positive end expiratory