The aim of this study is to identify the hidden etiologies of the black chromo-shifting transient phenomenon affecting Nile tilapia, Oreochromis niloticus, farmed in RAS-controlled ponds together with the assessment of the immunological reaction against the chronic irritating effects of the invasive agent. A total of 100 Nile Tilapia were collected from a private farm at Kafrelsheikh Province, located on the northern side of the Egyptian Nile Delta. The clinical history of the affected fish farm showed an unknown chromo-shifting phenomenon where tilapias were exhibiting severe black skin coloration, which gradually disappeared after removal from the tank’s water. A comprehensive gross examination of the collected fish; including parasitological examination of skin and gill scraps, was performed. Blood biochemical testing was performed on the infested blackish O. niloticus and control non-infested fish. The current study showed that the monogenean parasite, Gyrodactylus cichlidarum, was the abundant parasite detected in the infested fish leading to abnormal black discoloration of skin and disruption of the immune system represented by significant increase of cortisol levels, lysozyme activity and different liver enzymes compared to the control. Treatment trials have been applied with moderate degrees of success, where the monogenean count was sharply decreased, and the normal skin color was remarkably restored, at the end of day 14 post-treatment. A triple treatment plan was initiated through 7 days’ application of 0.7 g/m3 copper sulfates pentahydrate preceded by 1.5 ml/m3 hydrogen peroxide 40% solution for the same period. One day after the end of the initial treatment, a maintenance dosage of 0.095 ml/m3 of glutaraldehyde (15%)/quaternary ammonium compounds (QACs) mixture was administered for 3 days. As a supportive/immune-stimulant regimen, a weekly dosage of vitamin C (0.45 g g/m3) and Saccharomyces cerevisiae (0.45 g/m3) was added into the tank’s water to improve the general fish health.

BACKGROUND: Huntington's disease (HD) is a progressive neurodegenerative disease that causes motor, cognitive, and psychiatric abnormalities, with no satisfying disease-modifying therapy so far. 3-nitropropionic acid (3NP) induces behavioural deficits, together with biochemical and histological alterations in animals' striata that mimic HD. The role of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in HD pathogenesis remains largely uncharacterized. Parthenolide (PTL), a naturally occurring nuclear factor kappa B (NF-κB) inhibitor, is also known to inhibit NLRP3 inflammasome. Whether PTL is beneficial in HD has not been established yet.

AIM: This study evaluated the possible neuroprotective effects of PTL against 3NP-induced behavioural abnormalities, striatal biochemical derangements, and histological aberrations.

METHODS: Male Wistar rats received PTL (0.5 mg/kg/day, i.p) for 3 weeks and 3NP (10 mg/kg/day, i.p) was administered alongside for the latter 2 weeks to induce HD. Finally, animals were subjected to open-field, Morris water maze and rotarod tests. Rat striata were examined histologically, striatal protein expression levels of glial fibrillary acidic protein (GFAP), cluster of differentiation 45 (CD45) and neuron-specific enolase (NSE) were evaluated immunohistochemically, while those of interleukin (IL)-1β, IL-18, ionized calcium-binding adapter molecule-1 (Iba1) and glutamate were determined by ELISA. Striatal nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein (Keap1), NF-κB, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, S100 calcium-binding protein A10 (S100A10) and complement-3 (C3) were assessed by gene expression analysis.

RESULTS: PTL improved motor, locomotor, cognitive and anxiety-like behaviours, restored neuronal integrity, upregulated Nrf2, and inhibited NLRP3 inflammasome, NF-κB and microglial activation. Additionally, PTL induced astrocyte shifting towards the neuroprotective A2 phenotype.

CONCLUSION: PTL exhibits neuroprotection against 3NP-induced HD, that might be ascribed, at least in part, to its modulatory effects on Keap1/Nrf2 and NF-κB/NLRP3 inflammasome signaling.

PURPOSE: The optimal management of pediatric traumatic macular holes (TMH) is unclear from lack of prospective randomized trials. The literature is divided into early (≤1month post-trauma), delayed (>1 month) pars plana vitrectomy (PPV), and observation. Our aim is to find which group can achieve best-superior spectacle corrected visual acuity (VA), visual gain, and time for hole closure.

DESIGN: Systematic review.

METHODS: This systematic review was registered with PROSPERO (ID:CRD42022383134). The databases searched from inception until July 31, 2023, were MEDLINE OVID, Scopus, Web of Science, Embase, and Google Scholar. The articles were screened for title and abstract then for full text. Risk of bias was also assessed. Three outcome measures were analyzed: final VA, visual gain, and time to closure of macular hole (MH). MH size was divided into small (≤250 µm), medium (>250-500 µm), and large (>500 µm).

RESULTS: Ninety eight (98) studies with 234 patients in the PPV group and 87 patients in the observation group were included in the review. Final VA (logarithm of the minimum angle of resolution) and visual gain were respectively in PPV vs observation groups: (1) small MH 0.37 ± 0.52 vs 0.42 ± 0.56 (P = .484) and -0.96 ± 0.83 vs -0.49 ± 0.40 (P = .005); (2) medium MH 0.58 ± 0.39 vs 0.34 ± 0.34 (P = .06) and -0.36 ± 0.42 vs -0.74 ± 0.44 (P < .001); (3) large MH 0.62 ± 0.42 vs 0.59 ± 0.35 (P = .337) and -0.31 ± 0.48 vs -0.62 ± 0.37 (P = .11). Small TMH had comparable closure time: 3.21 ± 2.52 months vs 3.49 ± 4.43 (P = .954) in the PPV and observation groups. Early and late PPV yielded comparable final VA 0.67 ± 0.66 vs 0.54 ± 0.35 (P = .576) and visual gain -0.58 ± 0.69 vs -0.49 ± 0.48 (P = .242) in the PPV and observation groups.

CONCLUSIONS: PPV was very effective in closing TMH and VA gain in children throughout a wide range of hole size. Early and delayed PPV yielded similar anatomic and visual results. Observation and PPV yielded comparable final VA and closure time. Clinicians can choose either early PPV or delayed PPV when healing biomarkers are absent on periodic optical coherence tomography.

This study aims to explore the protective machinery of pegylated polymeric micelles of boswellic acid-selenium (PMBS) against secondary neuronal damage triggered by mild repetitive traumatic brain injury (RTBI). After PMBS characterization in terms of particle size, size distribution, zeta potential, and transmission electronic microscopy, the selected formula was used to investigate its potency against experimental RTBI. Five groups of rats were used; group 1 (control) and the other four groups were subjected to RTBI. Groups 2 was RTBI positive control, while 3, 4, and 5 received boswellic acid (BSA), selenium (SEL), and PMBS, respectively. The open-field behavioral test was used for behavioral assessment. Subsequently, brain tissues were utilized for hematoxylin and eosin staining, Nissl staining, Western blotting, and ELISA in addition to evaluating microRNA expression (miR-155 and miR-146a). The behavioral changes, oxidative stress, and neuroinflammation triggered by RTBI were all improved by PMBS. Moreover, PMBS mitigated excessive glutamate-induced excitotoxicity and the dysregulation in miR-155 and miR-146a expression. Besides, connexin43 (Cx43) expression as well as klotho and brain-derived neurotrophic factor (BDNF) were upregulated with diminished neuronal cell death and apoptosis because of reduced Forkhead Box class O3a(Foxo3a) expression in the PMBS-treated group. The current study has provided evidence of the benefits produced by incorporating BSA and SEL in PEGylated polymeric micelles formula. PMBS is a promising therapy for RTBI. Its beneficial effects are attributed to the manipulation of many pathways, including the regulation of miR-155 and miR-146a expression, as well as the BDNF /Klotho/Foxo3a signaling pathway.

INTRODUCTION: Peripilar sign (PPS) is a trichoscopic sign that was first described in androgenetic alopecia (AGA) and is thought to reflect the presence of perifollicular infiltrate (PFI) in histopathology.

OBJECTIVES: To study PPS in a cohort of patients with AGA and to assess its validity as a sign indicative of PFI.

METHODS: One hundred patients with AGA (confirmed by trichoscopic examination) were recruited in this cross-sectional study. From those patients, frontal scalp biopsy was done for two subgroups, 22 patients with PPS and 23 patients without PPS. Both groups were compared as regards the presence of PFI.

RESULTS: Peripilar sign was present in 50% of the 100 studied cases. No significant difference existed between those with and those without PPS as regards PFI. Peripilar sign was significantly more encountered in patients with skin type III (p=0.001). Its absence was significantly associated with lower interpretability of yellow dots (p<0.001) and their scores were significantly positively correlated (r=0.498, p<0.001). Peripilar sign was significantly associated with absent melanophages histopathologically (p=0.011).

CONCLUSION: Peripilar sign as a trichoscopic sign in AGA does not reflect PFI. It represents a dark color more encountered in patients with lighter skin types. This can be explained by the increased contrast between the dark PPS and the lighter surrounding skin in lighter skin types. Further studies using melanocyte markers and Masson Fontana's stain are needed to further verify the cause of this peri-follicular dark color.