Disorders of Consciousness: An Embedded Ethnographic Approach to Uncovering the Specific Influence of Functional Neurodiagnostics of Consciousness in Surrogate Decision Making

A recent qualitative study published in Neuroethics by Schembs and colleagues explores how functional neurodiagnostics of consciousness inform surrogate decision making in cases of disorders of consciousness. In this commentary, we argue that the chosen methodology significantly limits the scope of the potential conclusions and suggest an embedded ethnographic approach of co-presence as an alternative.

     

Eruption of the central incisor,the intermaxillary suture,and maxillary growth in patients with a single median maxillary central incisor

The occurrence of a single median maxillary central incisor (SMMCI) is a very rare condition and might be a sign of a more severe midline defect, which could be a mild degree of holoprosencephaly. Absence of the internasal and partial absence of the intermaxillary suture has been observed in a fetus with holoprosencephaly. The purpose of this study was to evaluate the intermaxillary suture, the eruption pattern of the single central incisor in the SMMCI condition, and the growth of the maxilla in a group of patients with SMMCI. A similar study was not found in the scientific literature. The material included orthopantomographs, dental radiographs, and lateral cephalometric radiographs from 11 patients with an SMMCI. The orthopantomographs and dental radiographs showed that the intermaxillary suture was abnormal anterior to the incisive foramen; however, the SMMCI erupted within the expected time interval. Superimposition on stable structures on lateral cephalometric radiographs from two untreated patients, in which growth analysis was possible, showed that the horizontal and vertical growth of the maxilla was normal. Due to the sutural midline defect it is suggested that a transversal growth analysis is included in all treatment planning of SMMCI patients.     

Hypertriglyceridemia is associated with insulin levels in adult cystic fibrosis patients

BackgroundRecent studies have identified hypertriglyceridemic cystic fibrosis patients (CF-TG). However, whether hypertriglyceridemia is associated with an altered metabolic profile remains unknown.ObjectiveTo characterize CF-TG and determine whether triglycerides (TG) levels are associated with metabolic alterations.Methods210 adult CF subjects from the Montreal Cystic Fibrosis Cohort without known diabetes were included in the analysis. All subjects underwent an OGTT to assess glucose tolerance, insulin secretion (insulin AUC) and insulin sensitivity (Stumvoll index). Fasting lipid profiles, pulmonary function (%FEV₁) and BMI were determined. Hypertriglyceridemia (TG > 1.7 mmol/L) was observed in 20 CF patients. These subjects were matched for age, sex and glucose tolerance category with 20 CF patients (CF-normal-TG) and 20 healthy controls that had TG levels below 1.7 mmol/L. Pearson correlations were performed in the complete study sample (n = 210) to examine the associations between TG levels and other parameters.ResultsThe prevalence of hypertriglyceridemia was 9.5%. Compared to CF-normal-TG, CF-TG subjects displayed significantly higher %FEV_1, insulin AUC (AUC_0–120, AUC_0–30, AUC_30–120), cholesterol levels and a higher ratio of total cholesterol to HDL-cholesterol. Pearson analysis demonstrated that TG levels were associated with BMI, %FEV₁, fasting insulin, insulin AUC_0–120 and AUC_30–120, Stumvoll index, cholesterol levels and the ratio of total cholesterol to HDL-cholesterol. All these correlations remained significant after correction for BMI except %FEV₁.ConclusionTG levels are associated with a mild alteration of the metabolic profile. Whether these changes will increase the long-term risk of CF patients in developing cardiometabolic complications remains to be investigated.     

Missed isolated volar dislocation of the scaphoid

A patient presented with volar dislocation of the scaphoid, the diagnosis of which had been missed for two weeks. He was treated with open reduction through a combined volar and dorsal approach with decompression of the median nerve, internal fixation, and a cast for eight weeks. One year postoperatively the functional result was good. A radiograph showed no sign of avascular necrosis.     

Adenosine protects against suicidal erythrocyte death

Suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine exposure at the erythrocyte surface. The cell membrane scrambling is triggered by an increase in cytosolic Ca²⁺ activity and activation of protein kinase C (PKC). Phosphatidylserine exposure fosters adherence of affected erythrocytes to the vascular wall. Thus, microcirculation in ischemic tissues may be impaired by the appearance of eryptotic erythrocytes. Ischemia leads to release of adenosine, which in most tissues leads to vasodilation and protects against cell injury. The present experiments explored whether adenosine influences mechanisms underlying eryptosis. Erythrocyte phosphatidylserine exposure was estimated from annexin V binding, cell volume from forward scatter and cytosolic Ca²⁺ activity from Fluo3 fluorescence. Glucose depletion (for 24 or 48 h) significantly increased annexin binding and decreased forward scatter, effects partially reversed by adenosine. The protective effect of adenosine reached statistical significance (s.d.) at ≥30 μM. Low Cl⁻ solution (Cl⁻ exchanged by gluconate for 24 h) similarly increased annexin binding and decreased forward scatter, effects again reversed by adenosine (s.d. at ≥10 and 30 μM, respectively). Similarly, phosphatase inhibitor okadaic acid (OA, 1 μM) and PKC activator phorbol 12-myristate-13-acetate (PMA, 3 μM) significantly enhanced annexin binding and decreased forward scatter. Adenosine significantly blunted the effects of OA and PMA on annexin V binding (s.d. at ≥30 and 10 μM, respectively) and the effect of OA on forward scatter (s.d. at ≥10 μM). In conclusion, adenosine inhibits eryptosis by a mechanism presumably effective downstream of PKC. The effect may participate in the maintenance of microcirculation in ischemic tissue.