The role of a mineralocorticoid receptor gene functional polymorphism in the symptom dimensions of persistent ADHD

Attention-deficit/hyperactivity disorder (ADHD) affects approximately 5 % of school-aged children and 2.5 % of adults. Genetic studies in ADHD have pointed to genes in different neurobiological systems, with relatively small individual effects. The mineralocorticoid receptor is the main receptor involved in the initial triggering of stress response. Therefore, its encoding gene (NR3C2) is a candidate for psychiatric disorder studies, including ADHD, and behavioral phenotypes. There is evidence that the Val allele of the MRI180V polymorphism (rs5522) increases the risk of depression, attention and cognitive deficits. We investigated the possible role of the mineralocorticoid receptor gene in the symptom dimensions and susceptibility to persistent ADHD. We compared genotype and allele frequencies in 478 adult patients with ADHD and 597 controls and symptom dimensions in 449 patients and 132 controls. Diagnoses were based on the DSM-IV criteria. ADHD symptom dimensions were investigated with SNAP-IV for ADHD severity and Barkley scales for severity and impairment. Carriers of the Val allele presented higher inattention, hyperactivity/impulsivity and impairment scores, while genotype and allele frequencies did not differ between patients and controls. These results are consistent with a possible link between genetic variations in the HPA axis and inattention and hyperactivity measures.     

Non-steroidal and steroidal anti-inflammatory use in the context of orthodontic movement

The early phase of orthodontic tooth movement involves sterile acute inflammation of the periodontal ligament in response to biomechanical forces. Anti-inflammatories are pharmacologic agents used in medical and dentistry clinics. The aim of the study was to analyse the bone remodelling during orthodontic movement under non-steroidal and steroidal treatment. Male Wistar rats (n = 90) were randomly divided into three groups: C (control), non-steroidal anti-inflammatory drug (NSAID; potassium diclofenac), and steroidal anti-inflammatory drug (SAID; dexamethasone dissodium phosphate). The animals of the C group received 0.9 per cent saline solution, the NSAID group received potassium diclofenac CATAFLAM? (5 mg/kg), and the SAID group received dexamethasone dissodium phosphate DEXANIL? (2 mg/kg). Animals were sacrificed 3, 7, or 14 days after placement of the orthodontic appliance. The upper first molars were processed histologically; we quantified the blood vessels, Howship lacunae, and osteoclast-like cells present on the tension and compression sides of the periodontal ligament. Bone formation was evaluated under polarized light microscopy; 4.5 Image Pro-Plus? software calculated the percentage of immature/mature collagen present. The results showed that, in 3 and 7 days, NSAID and SAID groups presented fewer blood vessels, Howship lacunae, and osteoclast-like cells when compared to the control group. On the 7th and 14th days, there was a lower percentage of mature collagen in the SAID group (P < 0.001). These data demonstrate that potassium diclofenac and dexamethasone inhibit bone resorption during the initial period of orthodontic movement and that dexamethasone delays the collagen maturation process in established bone matrix.     

Mechanoelectrical transduction in chondrocytes

Cartilage tissue lines the joints of mammals, helping to lubricate joint movement and distribute mechanical loads. This tissue is comprised of isolated cells known as chondrocytes which are embedded in an extracellular matrix. Chondrocytes produce and maintain the cartilage by sensing and responding to changing mechanical loads. Mechanosensitive ion channels have been implicated in chondrocyte mechanotransduction and recent studies have shown that both PIEZO1 and TRPV4 can be activated by mechanical stimuli in these cells. The 2 channels mediate separate but overlapping mechanoelectrical transduction pathways, PIEZO1 in response to stretch and substrate deflections and TRPV4 in response to substrate deflections alone. These distinct pathways of mechanoelectrical transduction suggest a mechanism by which chondrocytes can distinguish between different stimuli that arise in their complex mechanical environment.     

Genetic characterization of Carnivore Parvoviruses in Spanish wildlife reveals domestic dog and cat‐related sequences

The impact of carnivore parvovirus infection on wild populations is not yet understood; disease signs are mainly developed in pups and assessing the health of litters in wild carnivores has big limitations. This study aims to shed light on the virus dynamics among wild carnivores thanks to the analysis of 213 samples collected between 1994 and 2013 in wild ecosystems from Spain. We determined the presence of carnivore parvovirus DNA by real‐time PCR and sequenced the vp2 gen from 22 positive samples to characterize the strains and to perform phylogenetic analysis. The presence of carnivore parvovirus DNA was confirmed in 18% of the samples, with a higher prevalence detected in wolves (Canis lupus signatus, 70%). Fourteen sequences belonging to nine wolves, three Eurasian badgers (Meles meles), a common genet (Genetta genetta) and a European wildcat (Felis silvestris) were classified as canine parvovirus 2c (CPV‐2c); five sequences from three wolves, a red fox (Vulpes vulpes) and a stone marten (Martes foina) as CPV‐2b; and three sequences from a badger, a genet and a stone marten as feline parvovirus (FPV). This was the first report of a wildcat infected with a canine strain. Sequences described in this study were identical or very close related to others previously found in domestic carnivores from distant countries, suggesting that cross‐species transmission takes place and that the parvovirus epidemiology in Spain, as elsewhere, could be influenced by global factors.     

Evidence for an Immune Role on Cognition in Schizophrenia: A Systematic Review

Objective:

Recent evidence has associated immune and inflammatory changes to cognitive performance in many diseases, including schizophrenia. Since this is a new research field where concepts are not yet solid and new questions and hypothesis are still arising, the present study aimed at summarizing the available clinical data associating schizophrenia, cognition and inflammation/immune function.

Methods:

A systematic review of the literature was made by searching the following terms in Medline: “schizophrenia or psychosis or psychotic” AND “inflamm* or immun* or cytokine or IL-* or TNF-* or kynureni* or KYNA”, AND “cognit* or attention or memory or executive function”.

Results:

Seventy five papers were identified using the selected terms, and seven papers were included in the review. Papers excluded focused mainly on basic research or other neuropsychiatric disorders.

Conclusions:

Recent findings link inflammatory markers to cognition in schizophrenia, suggesting that inflammation is associated with worst cognitive performance. Microglial activation, monoaminergic imbalance, brain abnormalities and the kynurenine pathway are possible mechanisms underlying cognitive impairment in schizophrenia. Clinical trials with addition of immunomodulatory drugs have shown promising results, opening new windows to tackle cognition in schizophrenia.     

“Low-intensity laser therapy effect on the recovery of traumatic spinal cord injury”

Scientific advances have been made to optimize the healing process in spinal cord injury. Studies have been developed to obtain effective treatments in controlling the secondary injury that occurs after spinal cord injury, which substantially changes the prognosis. Low-intensity laser therapy (LILT) has been applied in neuroscience due to its anti-inflammatory effects on biological tissue in the repairing process. Few studies have been made associating LILT to the spinal cord injury. The objective of this study was to investigate the effect of the LILT (GaAlAs laser—780 nm) on the locomotor functional recovery, histomorphometric, and histopathological changes of the spinal cord after moderate traumatic injury in rats (spinal cord injury at T9 and T10). Thirty-one adult Wistar rats were used, which were divided into seven groups: control without surgery (n?=?3), control surgery (n?=?3), laser 6 h after surgery (n?=?5), laser 48 h after surgery (n?=?5), medullar lesion (n?=?5) without phototherapy, medullar lesion?+?laser 6 h after surgery (n?=?5), and medullar lesion?+?laser 48 h after surgery (n?=?5). The assessment of the motor function was performed using Basso, Beattie, and Bresnahan (BBB) scale and adapted Sciatic Functional Index (aSFI). The assessment of urinary dysfunction was clinically performed. After 21 days postoperative, the animals were euthanized for histological and histomorphometric analysis of the spinal cord. The results showed faster motor evolution in rats with spinal contusion treated with LILT, maintenance of the effectiveness of the urinary system, and preservation of nerve tissue in the lesion area, with a notorious inflammation control and increased number of nerve cells and connections. In conclusion, positive effects on spinal cord recovery after moderate traumatic spinal cord injury were shown after LILT.     

RCT of a promising vocational/employment program for high-risk juvenile offenders

Juvenile offenders with substance use problems are at high risk for deleterious long-term outcomes. This study evaluated the capacity of a promising vocational and employment training program in the building sector (i.e., Community Restitution Apprenticeship-Focused Training, CRAFT) to mitigate such outcomes through enhanced employment and education. Participants were 97 high-risk juvenile offenders (mean age = 15.8 years) randomized to CRAFT versus education as usual (EAU) intervention conditions. Multi-method procedures measured employment, education, substance use, mental health, and criminal outcomes through a 30-month post-baseline follow-up. CRAFT was significantly more effective than EAU at increasing rates of youth employment and GED attendance. Intervention effects were not observed, however, for months employed, hours worked, or hourly wage. Measures of youth substance use, mental health symptoms, and criminal activity showed no favorable or iatrogenic effects. The potential of CRAFT was modestly supported, and suggestions were made for future research.     

Wilson's disease: Revisiting an old friend

Wilson's disease(WD) is a rare condition caused by copper accumulation primarily in the liver and secondly in other organs, such as the central nervous system. It is a hereditary autosomal recessive disease caused by a deficiency in the ATP7 B transporter. This protein facilitates the incorporation of copper into ceruloplasmin. More than 800 mutations associated with WD have been described. The onset of the disease frequently includes manifestations related to the liver(as chronic liver disease or acute liver failure) and neurological symptoms, although it can sometimes be asymptomatic. Despite it being more frequent in young people, WD has been described in all life stages. Due to its fatal prognosis, WD should be suspected in all patients with unexplained biochemical liver abnormalities or neurological or psychiatric symptoms. The diagnosis is established with a combination of clinical signs and tests, including the measurement of ceruloplasmin, urinary copper excretion, copper quantification in liver biopsy, or genetic assessment. The pharmacological therapies include chelating drugs, such as D-penicillamine or trientine, and zinc salts, which are able to change the natural history of the disease, increasing the survival of these patients. In some cases of end-stage liver disease or acute liver failure, liver transplantation must be an option to increase survival. In this narrative review, we offer an overview of WD, focusing on the importance of clinical suspicion, the correct diagnosis, and treatment.