Tax Justice Beyond National Borders-International or Interpersonal?

Recent times have seen growing calls for considerations of justice to be given a greater role in international taxation. The main driver of these calls are distributive concerns, although agreement is still missing as to what this means both in principle and in practice. This article asks whether it is the task of international tax law at all to implement principles of distributive justice beyond the national context and gives an overview of how the 'global justice debate' in contemporary political philosophy bears on this question. When it comes to distributive duties with respect to taxing rights, it is crucial to differentiate between the collective and the individual level. Absent a robust assumption of a benevolent and capable government on the recipient side, the reallocation of taxing rights from state to state does not necessarily help when it comes to fulfilling duties of justice towards individuals.

Incidence of hypoglycemia in newborn infants identified as at risk.

Background: Temporary low plasma glucose concentrations are common in healthy newborns. Although there is no uniform definition of neonatal hypoglycemia, there is a consensus in the current literature that plasma glucose concentrations should be measured in infants at risk. Known risk groups for transient neonatal hypoglycemia include infants of diabetic mothers (IDM), large (LGA) or small (SGA) for gestational age and late preterm (LPT) infants.Objectives: The aim of this retrospective trial was to determine the incidence of hypoglycemia and the impact of the application of a 2011 revised guideline in respect of additional feeding or i.v. glucose administration, admission to a neonatal ward and the number of blood samples taken.Methods: During the period 1 January 2015 to 31 January 2016, the plasma glucose concentrations of all infants at risk were determined. They were screened over a period of 24 hours or until plasma glucose concentration was >45 mg/dL on three occasions. Hypoglycemia was defined as a plasma glucose concentration <40 mg/dL, regardless of the age of the infant.Results: One hundred and thirty-six (13.6%) out of 1017 newborns were identified as at-risk patients, 119 (87.5%) of whom were included in the final data evaluation. Ten study participants had more than one risk factor and 32 (26.9%) newborns (male:female = 1.1:1) had a total of 40 hypoglycemic episodes. Three (9.4%) out of these 32 newborns had to be transferred to the neonatal ward for i.v. glucose treatment. The mean number of blood samples taken was 7.6 ± 2.4.Conclusions: The incidence of hypoglycemia in the studied infants at risk was 27%, and 19.7 blood samples had to be taken to detect one episode of low glucose concentration. Neonatal hypoglycemia can be recognized and avoided in time, which justifies the establishment of a standardized plasma glucose measurement protocol in newborn infants at risk.Brief RationaleFollowing a considerable number of sources, it is recommended that infants at risk be identified, low plasma glucose concentrations prevented and, if necessary, the affected neonates cared for. Our data show that the risk group for neonatal hypoglycemia comprised about one-tenth of all infants at our nursery and hypoglycemia occurred in one-fourth. These results are in accordance with the recommendations to implement this protocol as a screening tool in neonates.

Synaptic amplifier of inflammatory pain in the spinal dorsal horn.

Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.