Spinal osteoid osteoma in the pediatric population: A management algorithm and systematic review.

Purpose: The purpose of this study is to develop an accessible step-wise management algorithm for the management of pediatric spinal osteoid osteomas (OOs) based on a systematic review of the published literature regarding the diagnostic evaluation, treatment, and outcomes following surgical resection. Methods: A systematic review of the literature was conducted on PubMed to locate English language studies reporting on the management of pediatric spinal OOs. Data extraction of clinical presentation, management strategies and imaging, and treatment outcomes were performed. Results: Ten studies reporting on 85 patients under the age of 18 years presenting with OOs were identified. Back pain was the most common presenting symptom, and scoliosis was described in 8 out of 10 studies, and radicular pain in 7 out of 10 studies. Diagnostic, intraoperative, and postoperative assessment included radiographs, computed tomography (CT) scans, magnetic resonance imaging (MRI), bone scans, and frozen section. Treatment options varied, including conservative management, open surgical resection with or without intraoperative imaging, and percutaneous image-guided treatment. All included studies described partial or complete resolution of pain in the immediate postoperative period. Conclusions: The proposed algorithm provides a suggested framework for management of pediatric spinal OOs based on the available evidence (levels of evidence: 3, 4). This review of the literature indicated that a step-wise approach should be utilized in the management of pediatric spinal OOs.

Carnitine, apelin and resveratrol regulate mitochondrial quality control (QC) related proteins and ameliorate acute kidney injury: role of hydrogen peroxide.

Mitochondrial impairment is recognised as a prominent feature in kidney diseases. Therefore, we investigated whether the effects of resveratrol, L-carnitine, and apelin in the acute kidney injury model were associated with modulation of mitochondrial quality control (QC) related proteins, intra-renal renin-angiotensin (RAS) activity, adenosine triphosphate (ATP) and Na+-K+ ATPase gene expression. Rats were randomly assigned to 7 groups: Distilled water injected control group, DMSO injected control group, distilled water injected lipopolysaccharide (LPS) group, DMSO injected LPS group, resveratrol injected LPS group, L-carnitine injected LPS group and apelin 13 injected LPS group. We observed that resveratrol, L-carnitine, and apelin treatments altered mitochondrial (QC) related protein levels (Pink1, Parkin, BNIP-3, Drp1, and PGC1α), decreased intra-renal RAS parameters, increased ATP level and upregulated Na+-K+ ATPase gene expression in renal tissue. Our results provide new insight into the role of mitochondrial quality control and how different antioxidants exert beneficial effects on acute kidney injury.

Hypopigmented Interface T-Cell Dyscrasia and Hypopigmented Mycosis Fungoides: A Comparative Study.

Hypopigmented interface T-cell dyscrasia (HITCD) is a distinct form of lymphoid dyscrasia that may progress to hypopigmented mycosis fungoides (HMF). We compared both diseases as regards their CD4/CD8 phenotype and expression of granzyme B and tumor necrosis factor-alpha (TNF-α) and how these are affected by narrow-band UVB (nb-UVB). The study included 11 patients with HITCD and 9 patients with HMF. They received nb-UVB thrice weekly until complete repigmentation or a maximum of 48 sessions. Pretreatment and posttreatment biopsies were stained using anti CD4, CD8, TNF-α, and granzyme B monoclonal antibodies. Epidermal lymphocytes were CD8 predominant in 54.5% and 66.7% of HITCD and HMF cases, respectively, whereas dermal lymphocytes were CD4 predominant in 63.6% and 66.7%, respectively. Significantly, more dermal infiltrate was encountered in HMF (P = 0.041). In both diseases, granzyme B was only expressed in the dermis, whereas TNF-α was expressed both in the epidermis and dermis. No difference existed as regards the number of sessions needed to achieve repigmentation or cumulative nb-UVB dose reached at end of study. (P > 0.05). Narrow-band UVB significantly reduced only the epidermal lymphocytes in both diseases (P ≤ 0.05) with their complete disappearance in 8 (72.7%) HITCD and 6 (66.7%) HMF cases. In both diseases, nb-UVB did not affect granzyme B or TNF-α expression (P > 0.05). In conclusion, both diseases share the same phenotype, with HITCD being a milder form of T-cell dysfunction. In both diseases, epidermal lymphocytes are mainly CD8-exhausted cells lacking cytotoxicity, whereas dermal cells are mostly reactive cells exerting antitumor cytotoxicity. Tumor necrosis factor-alpha mediates hypopigmentation in both diseases and prevents disease progression. Repigmentation after nb-UVB in both diseases occurs before and independently from disappearance of the dermal infiltrate.

Low dose bisphenol S or ethinyl estradiol exposures during the perinatal period alter female mouse mammary gland development.

Throughout life, mammary tissue is strongly influenced by hormones. Scientists have hypothesized that synthetic chemicals with hormonal activities could disrupt mammary gland development and contribute to breast diseases and dysfunction. Bisphenol S (BPS) is an estrogenic compound used in many consumer products. In this study, CD-1 mice were exposed to BPS (2 or 200 µg/kg/day) during pregnancy and lactation. Mice exposed to 0.01 or 1 µg/kg/day ethinyl estradiol (EE2), a pharmaceutical estrogen, were also evaluated. Mammary glands from female offspring were collected prior to the onset of puberty, during puberty, and in early adulthood. Growth parameters, histopathology, cell proliferation and expression of hormone receptors were quantified. Our evaluations revealed age- and dose-specific effects of BPS that were different from the effects of EE2, and distinct from the effects of BPA that have been reported previously. These assessments suggest that individual xenoestrogens may have unique effects on this sensitive tissue.

Islet amyloid formation is an important determinant for inducing islet inflammation in high-fat-fed human IAPP transgenic mice.

AIMS/HYPOTHESIS: Amyloid deposition and inflammation are characteristic of islet pathology in type 2 diabetes. The aim of this study was to determine whether islet amyloid formation is required for the development of islet inflammation in vivo. METHODS: Human islet amyloid polypeptide transgenic mice and non-transgenic littermates (the latter incapable of forming islet amyloid) were fed a low-fat (10%) or high-fat (60%) diet for 12 months; high-fat feeding induces islet amyloid formation in transgenic mice. At the conclusion of the study, glycaemia, beta cell function, islet amyloid deposition, markers of islet inflammation and islet macrophage infiltration were measured. RESULTS: Fasting plasma glucose levels did not differ by diet or genotype. Insulin release in response to i.v. glucose was significantly greater in both high vs low fat groups, and significantly lower in both transgenic compared with non-transgenic groups. Only high-fat-fed transgenic mice developed islet amyloid and showed a trend towards reduced beta cell area. Compared with islets from low-fat-fed transgenic or high-fat-fed non-transgenic mice, islets of high-fat-fed transgenic mice displayed a significant increase in the expression of genes encoding chemokines (Ccl2, Cxcl1), macrophage/dendritic cell markers (Emr1, Itgax), NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome components (Nlrp3, Pycard, Casp1) and proinflammatory cytokines (Il1b, Tnf, Il6), as well as increased F4/80 staining, consistent with increased islet inflammation and macrophage infiltration. CONCLUSIONS/INTERPRETATION: Our results indicate that islet amyloid formation is required for the induction of islet inflammation in this long-term high-fat-diet model, and thus could promote beta cell dysfunction in type 2 diabetes via islet inflammation.