Decreased expression of hyaluronan synthase and loss of hyaluronan-rich cells in the anterior tibial fascia of the rat model of chemotherapy-induced peripheral neuropathy.

Introduction: Previous studies on chemotherapy-induced peripheral neuropathy (CIPN) have focused on neuronal damage. Although some studies have revealed that the fascia is an important sensory organ, currently, we do not know about chemotherapy drug-induced fascial dysfunction. Objectives: This study aimed to explore the fascia as a nonneural cause of mechanical hypersensitivity in CIPN by investigating the expression of hyaluronic acid synthase (HAS) and histology of the fascia in an animal model of CIPN. Methods: Rats were intraperitoneally administered with vincristine (VCR). Mechanical hypersensitivities of the hind paw and the anterior tibial muscle were assessed. The expression of HAS mRNA in the fascia of the anterior tibial muscles was quantitated using reverse transcription polymerase chain reaction. Immunohistochemistry was also performed for HAS2, hyaluronic acid-binding protein, and S100A4 in the fascia. Results: Vincristine administration significantly decreased mechanical withdrawal thresholds in the hind paw and the anterior tibial muscle after day 3. Quantitative polymerase chain reaction showed significant downregulation of HAS mRNAs in the fascia of VCR-treated rats. Immunohistochemical analysis showed that the number of cells with strong HAS2 immunoreactivity, classified as fasciacytes by morphology and colocalized marker S100A4, decreased significantly in the VCR group. Conclusion: Hyaluronic acid plays a critical role in somatic pain sensation. Damaged fascia could be a possible cause of musculoskeletal pain in patients with CIPN. This study suggests that fascia is a nonneural cause and novel therapeutic target for chemotherapy-induced "peripheral neuropathy."

Intrathecal Administration of the α1 Adrenergic Antagonist Phentolamine Upregulates Spinal GLT-1 and Improves Mirror Image Pain in SNI Model Rats.

Mirror image pain (MIP) is a type of extraterritorial pain that results in contralateral pain or allodynia. Glutamate transporter-1 (GLT-1) is expressed in astrocytes and plays a role in maintaining low glutamate levels in the synaptic cleft. Previous studies have shown that GLT-1 dysfunction induces neuropathic pain. Our previous study revealed bilateral GLT-1 downregulation in the spinal cord of a spared nerve injury (SNI) rat. We hypothesized that spinal GLT-1 is involved in the mechanism of MIP. We also previously demonstrated noradrenergic GLT-1 regulation. Therefore, this study aimed to investigate the effect of an α1 adrenergic antagonist on the development of MIP. Rats were subjected to SNI. Changes in pain behavior and GLT-1 protein levels in the SNI rat spinal cords were then examined by intrathecal administration of the α1 adrenergic antagonist phentolamine, followed by von Frey test and western blotting. SNI resulted in the development of MIP and bilateral downregulation of GLT-1 protein in the rat spinal cord. Intrathecal phentolamine increased contralateral GLT-1 protein levels and partially ameliorated the 50% paw withdrawal threshold in the contralateral hind paw. Spinal GLT-1 upregulation by intrathecal phentolamine ameliorates MIP. GLT-1 plays a role in the development of MIPs.

Portal Venous Gas Following Ingestion of Hydrogen Peroxide Successfully Treated with Hyperbaric Oxygen Therapy.

The primary toxicity of hydrogen peroxide results from its interaction with catalase, which liberates water and oxygen. We report the case of a 14-year-old Japanese girl with portal venous gas that was caused by oxygen liberated from intentionally ingested hydrogen peroxide. Although she had a past history of atrial septal defect, recovery without cardiac or neurological sequelae was achieved using hyperbaric oxygen therapy. Emergency physicians must be aware of the danger of liberated oxygen due to hydrogen peroxide ingestion.

Relationship between parents' report rate of twin language and factors related to linguistic development: older sibling, nonverbal play and preschool attendance.

The definition and nature of twin language has been a focus of recent studies concerned with the phenomenon. There has been a call for a tighter definition and understanding of the meaning of twin language (Thorpe et al., 2001). This article sought to identify social factors associated with the parent report of twin language and thus provide further understanding of the phenomenon. Data from 583 mothers of twins aged 25 to 59 months were analyzed using multiple logistic regression. Factors included in the modeling of parent-report twin language included social experience factors such as presence of siblings, attendance at preschool education and reports of nonverbal play. It was found that twin pairs who didn't have an older sibling, who showed frequent nonverbal play and who didn't attend preschool were more likely to have a twin language. Moreover, in the group not having an older sibling, the influence of whether twins attended preschool or not was strong and the odds ratio was 0.589 (95% confidence intervals 0.360-0.963). The findings suggest that social experience factors are important predictors of the parent reporting of twin language.