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Growing evidence supports an individualised approach rather than radical surgery for conjunctival melanoma (CM). This study aimed to compare the long-term outcome between individualised and conventional exenteration techniques.
Our study retrospectively recruited advanced CM (clinical T3 stage) patients treated with individualised (13 cases) or conventional (18 cases) exenteration from June 2014 to April 2019. The individualised approach preserved at least three quadrants of the orbit, and the conventional procedures removed at least one third of the orbital tissues. The medical records were collected and analyzed during April 2020, including demographics, tumour characteristics, surgical details, postoperative rehabilitation and tumour-related prognosis.
The tumour basal diameter was statistically (P = 0.011) larger in the conventional group (23.3 ± 7.6 mm) than in the individualised group (15.4 ± 6.3 mm). More tissues were preserved in the individualised group, resulting in a shorter duration of wound healing (2.1 ± 0.6 vs. 3.6 ± 2.0 weeks, P = 0.018) and less incidence of hollow appearance (15% vs. 72%, P = 0.003) than the conventional group. After follow-up for 39.3 ± 17.3 months, a comparison of survival curves showed no significant differences (P = 0.638) between the two groups. The 1- and 2-year overall survival rates were estimated as 100% and 80.0% in the individualised group, and 93.8% and 72.5% in the conventional group, respectively. Low or mixed pigmentation was identified as the risk factor for tumour-related mortality based on multivariate regression analysis.
The individualised approach to exenteration offers improved aesthetic results while still maximises the curable chance for advanced CM.
The individualised approach to exenteration offers improved aesthetic results while still maximises the curable chance for advanced CM.
To describe the predisposing factors, pathogens and outcomes in patients with clinical presumed concomitant microbial and herpes simplex keratitis (HSK) at Sydney Eye Hospital, Australia over a 5-year period.
A retrospective case review was conducted. Patients with clinical presumed concomitant microbial and HSK from 2012 to 2016 were identified from pathology and hospital coding databases. Data were extracted from the medical records. VA was converted to the logarithm of the minimum angle of resolution (logMAR). 'Poor' outcome was defined as final VA worse than 6/60, or decrease in VA during treatment, or presence of complication, or needed surgical intervention.
126 episodes in 121 patients were included; median age 70 years (range 18-96); 56% male. Predisposing factors included blepharitis 20/126 (16%) cases, and corneal transplantation 19 (15%). Forty-six (37%) cases had prior HSK. Coagulase-negative staphylococci 51/116 (44%), Staphylococcus aureus 11 (9%), and Pseudomonas aeruginosa 11 (9%) were the most common isolates. The median VA at initial visit was 1.7 logMAR (range 0.04-2.7) and at final visit, 0.98 logMAR (range 0-2.7) (P < 0.05). Complications occurred in 70 episodes persistent epithelial defect in 38 (30%); intraocular pressure elevation in 15 (12%), and corneal perforation in 12 (10%). 'Poor' outcome was recorded in 46/75 (61%) episodes.
Patients with clinical presumed concomitant microbial and HSK face significant ocular morbidity and poor visual outcome. In our setting, previous HSK, corneal and ocular surface disease, were common predisposing factors and Gram-positive bacteria were the most commonly associated organisms.
Patients with clinical presumed concomitant microbial and HSK face significant ocular morbidity and poor visual outcome. In our setting, previous HSK, corneal and ocular surface disease, were common predisposing factors and Gram-positive bacteria were the most commonly associated organisms.
To evaluate longitudinal endothelial cell characteristics of children with posterior polymorphous corneal dystrophy (PPCD).
In this prospective case-control study, children with PPCD were followed with slit-lamp photography and non-contact specular microscopy. Patient's eyes were subdivided according to the clinical subtypes of PPCD (vesicular, band, diffuse, and unaffected) and the number of lesions present on the posterior corneal surface. PF-07104091 Findings were then compared with age-matched controls.
Thirty eyes of 15 patients with PPCD with a mean age 10.5 ± 3.1 years were analysed. Mean follow-up was 3.0 ± 1.0 years. PPCD morphology was vesicular in 40%, diffuse in 37%, band type in 10% and 13% had no detectable lesions despite contralateral involvement. Fourteen eyes (47%) had ≥5 endothelial lesions. Patients with PPCD had significantly lower endothelial cell densities (ECD) at recruitment (1918.9 ± 666.3 vs. 3340.1 ± 286.5 cells/mm
, p < 0.007) and at final follow-up (1793.1 ± 684.6 vs. 3265.2 ± 304.3 cells/mm
, p < 0.007) compared to age-matched controls. The lowest ECDs were found in eyes with diffuse type PPCD and those with ≥5 posterior corneal lesions, while clinically unaffected eyes in patients with confirmed PPCD in fellow eye had a normal ECD. However, the rates of annual ECD decline were not significantly different between eyes with PPCD in general, between the subgroups of PPCD and the normative groups.
Endothelial cell density is significantly reduced among children with PPCD and depends on the clinical subtype and the number of posterior corneal lesions present. However, annual ECD loss is similar between normal eyes and those with PPCD.
Endothelial cell density is significantly reduced among children with PPCD and depends on the clinical subtype and the number of posterior corneal lesions present. However, annual ECD loss is similar between normal eyes and those with PPCD.Convincing evidence supports the premise that reducing α-synuclein levels may be an effective therapy for Parkinson's disease (PD); however, there has been lack of a clinically applicable α-synuclein reducing therapeutic strategy. This study was undertaken to develop a blood-brain barrier and plasma membrane-permeable α-synuclein knockdown peptide, Tat-βsyn-degron, that may have therapeutic potential. The peptide effectively reduced the level of α-synuclein via proteasomal degradation both in cell cultures and in animals. Tat-βsyn-degron decreased α-synuclein aggregates and microglial activation in an α-synuclein pre-formed fibril model of spreading synucleinopathy in transgenic mice overexpressing human A53T α-synuclein. Moreover, Tat-βsyn-degron reduced α-synuclein levels and significantly decreased the parkinsonian toxin-induced neuronal damage and motor impairment in a mouse toxicity model of PD. These results show the promising efficacy of Tat-βsyn-degron in two different animal models of PD and suggest its potential use as an effective PD therapeutic that directly targets the disease-causing process.