Parvovirus B19–Associated Microvesicular Eruption

We report on a 3‐year‐old girl with a microvesicular generalized rash in whom primary infection by parvovirus B19 was demonstrated by seroconversion. To our knowledge, this is the first instance of an eruption arising from parvovirus B19 with this peculiar clinical pattern.     

Magnetic detection of sentinel nodes in oral squamous cell carcinoma by means of superparamagnetic iron oxide contrast

The aim was to evaluate sentinel node detection capacity by means of a magnetic probe in 11 patients with oral squamous cell carcinoma at stages T1-T2 received submucosal injections of a superparamagnetic iron oxide contrast agent (SPIO). A magnetic probe was used for sentinel node biopsy. The use of SPIO and magnetic probes in the early stages of oral cancer may offer an alternative to conventional radioisotope techniques and/or elective neck dissection.     

D2 autoreceptor switches CB2 receptor effects on [3H]-dopamine release in the striatum

CB₂ receptors (CB₂R) are expressed in midbrain neurons. To evidence the control of dopamine release in dorsal striatum by CB₂R, we performed experiments of [³H]-dopamine release in dorsal striatal slices. We found a paradoxical increase in K⁺-induced [³H]-dopamine release by CB₂R activation with GW 833972A and JWH 133 two selective agonist. To understand the mechanism involved, we tested for a role of the D₂ autoreceptor in this effect; because in pallidal structures, the inhibitory effect of CB₁ receptors (CB₁R) on GABA release is switched to a stimulatory effect by D₂ receptors (D₂R). We found that the blockade of D₂ autoreceptors with sulpiride prevented the stimulatory effect of CB₂R activation; in fact, under this condition, CB₂R decreased dopamine release, indicating the role of the D₂ autoreceptor in the paradoxical increase. We also found that the effect occurs in nigrostriatal terminals, since lesions with 6-OH dopamine in the middle forebrain bundle prevented CB₂R effects on release. In addition, D₂–CB₂R interaction promoted cAMP accumulation, and the increase in [³H]-dopamine release was prevented by PKA blockade. D₂–CB₂R coprecipitation and proximity ligation assay studies indicated a close interaction of receptors that could participate in the observed effects. Finally, intrastriatal injection of CB₂R agonist induced contralateral turning in amphetamine-treated rats, which was prevented by sulpiride, indicating the role of the interaction in motor behavior. Thus, these data indicate that the D₂ autoreceptor switches, from inhibitory to stimulatory, the CB₂R effects on dopamine release, involving the cAMP → PKA pathway in nigrostriatal terminals.     

Evaluación del seguimiento de niños con hallazgo de hipertransaminasemia

IntroductionAlthough changes in liver function tests can be non-specific in numerous clinical conditions, they can be the first sign of a potentially serious disease in an asymptomatic patient.Material and methodsRetrospective cohort study, performed by reviewing the records of children of a reference hospital central laboratory with alanine aminorransferase enzyme (ALT) elevation during a 6 month aleatory period.Results572 blood tests with serum ALT elevation corresponding to 403 patients had been assessed during the period studied. 98 patients were excluded for presenting abnormal liver test before the study period of comorbidity that could produce ALT elevation. The remaining 305 patients, 22.6% were diagnosed with a medical condition during the first blood test that explained the ALT elevation, although only 33.3% of them were followed up until verifying their normalization. Final study sample consists of 236 patients with abnormal liver test without apparent liver disease. Adequate follow-up was found only in 29% of them. From this group, 9 patients (13%) were diagnosed with liver disease. The rest of the sample were not properly monitored. In patients with higher serum ALT levels, follow-up was early and more appropiate.ConclusionsIn our area, most children without apparent liver disease are no properly monitored. Therefore, an opportunity to diagnosis and treat a potential liver disease was lost in a great number of children. All children with unexplainedhypertransaminasaemia must be studied.     

Milestones in the discovery of hepatitis C

The discovery of hepatitis C has been a landmark in public health as it brought the opportunity to save millions of lives through the diagnosis, prevention and cure of the disease. The combined work of three researchers, Alter H, Houghton M and Rice C, which set the basis for the diagnosis, treatment and prevention of hepatitis C apart from laying the ground work for a new approach to study infections in general and developing new antiviral agents. This is a story of a transfusion-associated infection. A series of clinical studies demonstrated the existence of an infectious agent associated with hepatitis. That was followed by the identification of what was later known to be the hepatitis C virus (HCV) and the development of diagnostic tests. It all preceded the full molecular identification and demonstration of a causal effect. Finally it ended up with the development and discovery of a new class of therapeutic drugs, the direct acting antivirals, which are now used not only to cure the disease but most probably, to eliminate the problem. This work started with Dr Alter H who demonstrated that a new virus was responsible for the majority of post-transfusion hepatitis followed by Houghton M who cloned the virus and developed the blood test to identify those cases that carried the virus. Finally, the work of Rice C demonstrated that a cloned HCV produced after applying molecular biology techniques could cause long-standing infection and cause the same disease as the one observed in humans.     

Retinoic acid improves recovery after nephrectomy and decreases renal TGF‐β1 expression. Gender‐related effects

End‐stage renal disease is a cause for death worldwide. Renal transplant is a therapeutic alternative, restricted by the scant number of donors. Function of the donor kidney is under risk of adverse circumstances such as fibrosis, where profibrotic effect of transforming growth factor beta 1 (TGF‐β1) plays a key role. Efforts to diminish risks of damage in the remnant kidney of the donor are required. Vitamin A represents one alternative. It has beneficial effects on some nephropathies, mainly those related to oxidative stress. It also participates in normal intrauterine renal development. We studied the effect of all‐trans retinoic acid (ATRA), active form of vitamin A, on postnephrectomy compensatory growth, in male or female rats. Compensatory growth and renal function were evaluated on four experimental groups: Control without treatment (CTL), ATRA‐treated intact rats (CTL + RA), nephrectomized rats (NFX), and ATRA‐treated nephrectomized rats (NFX + RA). We evaluated glomerular function (inulin clearance), tubular function (fractional excretions of sodium and potassium), and urinary flow. Renal mass was also estimated. In ATRA‐treated animals, compensatory growth was higher than in nephrectomized rats without treatment. Hyperfiltration after nephrectomy was less intense in ATRA‐treated female than in male rats. In tubular functions, effect of ATRA was more evident in female than in male rats. Glomerular expression of TGF‐β1 was lower in ATRA‐treated animals than in controls. ATRA reduced intensity and duration of compensatory changes after nephrectomy, improving recovery.     

Steroid hyperglycemia: Prevalence,early detection and therapeutic recommendations: A narrative review

Steroids are drugs that have been used extensively in a variety of conditions. Although widely prescribed for their anti-inflammatory and immunosuppressive properties, glucocorticoids have several side effects, being hyperglycemia one of the most common and representative. In the present review, we discuss the main epidemiologic characteristics associated with steroid use, with emphasis on the identification of high risk populations. Additionally we present the pathophysiology of corticosteroid induced hyperglycemia as well as the pharmacokinetics and pharmacodynamics associated with steroid use. We propose a treatment strategy based on previous reports and the understanding of the mechanism of action of both, the different types of glucocorticoids and the treatment options, in both the ambulatory and the hospital setting. Finally, we present some of the recent scientific advances as well as some options for future use of glucocorticoids.     

Hippocampal Insulin Resistance Impairs Spatial Learning and Synaptic Plasticity

Insulin receptors (IRs) are expressed in discrete neuronal populations in the central nervous system, including the hippocampus. To elucidate the functional role of hippocampal IRs independent of metabolic function, we generated a model of hippocampal-specific insulin resistance using a lentiviral vector expressing an IR antisense sequence (LV-IRAS). LV-IRAS effectively downregulates IR expression in the rat hippocampus without affecting body weight, adiposity, or peripheral glucose homeostasis. Nevertheless, hippocampal neuroplasticity was impaired in LV-IRAS–treated rats. High-frequency stimulation, which evoked robust long-term potentiation (LTP) in brain slices from LV control rats, failed to evoke LTP in LV-IRAS–treated rats. GluN2B subunit levels, as well as the basal level of phosphorylation of GluA1, were reduced in the hippocampus of LV-IRAS rats. Moreover, these deficits in synaptic transmission were associated with impairments in spatial learning. We suggest that alterations in the expression and phosphorylation of glutamate receptor subunits underlie the alterations in LTP and that these changes are responsible for the impairment in hippocampal-dependent learning. Importantly, these learning deficits are strikingly similar to the impairments in complex task performance observed in patients with diabetes, which strengthens the hypothesis that hippocampal insulin resistance is a key mediator of cognitive deficits independent of glycemic control.