Conjunctival myxoid stromal tumour: a distinctive clinicopathological and immunohistochemical study.

BACKGROUND/AIMS: To describe the clinicopathological and immunohistochemical characteristics of 10 patients representing a new entity of benign conjunctival myxoid stromal tumours. METHODS: Retrospective review of clinical findings, histopathological and immunohistochemical studies identified 10 cases of low-grade conjunctival myxoid stromal tumours. Specimens were routinely processed and stained with H&E. Immunohistochemical stains for CD34, CD68, vimentin, S100, smooth muscle actin (SMA), myosin, desmin, actin, Bcl-2 and Ki-67 were performed. Specific stains for Alcian-blue periodic acid-Schiff (AB-PAS) and aldehyde fuchsin stains were also performed. RESULTS: Ten patients with an average age of 45.6±11.1 years had a tender white or faint yellow to red mass on the bulbar conjunctiva. All the lesions were completely removed, and none of the patients relapsed. Histologically, all neoplasms consisted of spindle-shaped cells that showed signs of pseudonuclear inclusions, multinuclear cells and had no atypia. The stroma consisted of a large amount of mucus and was infiltrated with delicate to ropey collagens, a few mast cells and new vessels. Immunohistochemical stains were positive for CD34, vimentin and Bcl-2; partial positive for CD68; very low for Ki-67; and negative for S100, SMA, myosin, desmin and actin. AB-PAS suggested that the stroma was mucinous. CONCLUSIONS: These rare benign mesenchymal conjunctival tumours are mostly unilateral and occur in the bulbar conjunctiva. Complete resection is the radical treatment. These lesions are characterised by multiple spindle cells, a large amount of mucus, and sharing similar basic histopathological features with conjunctival myxoma and conjunctival stromal tumour. We suggest naming these lesions 'conjunctival myxoid stromal tumours'.

Safety of femtosecond laser-assisted cataract surgery: assessment of aqueous humour and lens capsule.

PURPOSE: To investigate the effect of femtosecond laser-assisted cataract surgery (FLACS) on aqueous humour and lens capsule. METHODS: This prospective randomized comparative study enrolled 19 eyes that underwent FLACS as the trial group and 20 eyes that underwent conventional phacoemulsification as the control group. The femtosecond laser platform (LLS-fs 3D; LensAR, Orlando, FL, USA) was used to generate capsulotomy (laser energy 8 µJ) and lens fragmentation (laser energy 10 µJ). Morphology of the cutting edge and cells of anterior capsule was assessed by light microscopy. The proteins in the aqueous humour were identified by mass spectrometry (Ultraflex III TOF/TOF; Bruker Dalton, Bremen, Germany). Electrolyte in the aqueous humour was detected by a chemistry analyzer (Aeroset Clinical Chemistry Analyzer; Abbott Laboratories, Abbott Park, IL, USA). RESULTS: The cutting edge of anterior capsule was saw-tooth-shaped under magnification of 200× and 400× in the trial group, while it was smooth in the control group. Intact cells were found in the boundary area next to the cutting edge of anterior capsule in both groups. ß-Crystallin B1, γ-crystallin S and transferrin were detected in the aqueous humour in the trial group. The concentrations of K+ , Na+ and Cl- in the aqueous humour in the trial group differed significantly from those in the control group (p = 0.02, 0.03 and 0.04, respectively). CONCLUSION: Femtosecond laser-assisted cataract surgery (FLACS) causes release of transferrin and crystallin from lens to aqueous humour and results in significant changes in the concentrations of K+ , Na+ and Cl- in aqueous humour. However, these changes due to FLACS have no clinical significance or toxicity.

Ratcheting behavior of articular cartilage under cyclic unconfined compression.

The ratcheting deformation of articular cartilage can produce due to the repeated accumulations of compressive strain in cartilage. The aim of this study was to investigate the ratcheting behavior of articular cartilage under cyclic compression. A series of uniaxial cyclic compression tests were conducted for online soaked and unsoaked cartilage samples and the effects of stress variation and stress rate on ratcheting behavior of cartilage were investigated. It is found that the ratcheting strains of online soaked and unsoaked cartilage samples increase rapidly at initial stage and then show the slower increase with cyclic compression going on. On the contrary, the ratcheting strain rate decreases quickly at first and then exhibits a relatively stable and small value. Both the ratcheting strain and ratcheting strain rate increase with stress variation increasing or with stress rate decreasing. Simultaneously, the optimized digital image correlation (DIC) technique was applied to study the ratcheting behavior and Young's modulus of different layers for cartilage under cyclic compression. It is found that the ratcheting behavior of cartilage is dependent on its depth. The ratcheting strain and its rate decrease through the depth of cartilage from surface to deep, whereas the Young's modulus increases.

ATP-binding cassette transporter A1 R219K polymorphism and coronary artery disease in Chinese population: a meta-analysis of 5,388 participants.

The ATP-binding cassette transporter A1 (ABCA1) R219K gene polymorphism has been suggested to lower the risk of coronary artery disease (CAD). However, research results remain debatable. Meta-analysis involving 2,730 CAD patients and 2,658 controls was performed to investigate the relationship between ABCA1 R219K gene polymorphism and CAD in Chinese population. A total of 14 studies which were obtained from electronic databases were analyzed. The pooled odds ratios (ORs) and their corresponding 95 % confidence intervals (95 % CIs) were estimated by a random effect model. A significant association between ABCA1 R219K gene polymorphism and CAD was found in the Chinese population under the following genetic models: an allelic genetic model (OR 0.70, 95 % CI 0.62-0.78, P < 0.00001), a recessive genetic model (OR 0.51, 95 % CI 0.41-0.64, P < 0.00001), an additive genetic model (OR 0.816, 95 % CI 0780-0.855, P = 0), a dominant genetic model (OR 1.326, 95 % CI 1.232-1.427, P = 0), a homozygote genetic model (OR 0.640, 95 % CI 0.575-0.712, P = 0), and a heterozygote genetic model (OR 0.640, 95 % CI 0.575-0.712, P = 0). The K allele of the ABCA1 R219K gene has a protective role for CAD risk in Chinese population and is possibly associated with decreased CAD susceptibility.

Regulation of angiotensin-(1-7) and angiotensin II type 1 receptor by telmisartan and losartan in adriamycin-induced rat heart failure.

AIM: To investigate the possible effects of telmisartan and losartan on cardiac function in adriamycin (ADR)-induced heart failure in rats, and to explore the changes in plasma level of angiotensin-(1-7)[Ang-(1-7)] and myocardial expression of angiotensin II type 1/2 receptors (AT(1)R / AT(2)R) and Mas receptor caused by the two drugs. METHODS: Male Sprague-Dawley rats were randomly divided into 4 groups: the control group, ADR-treated heart failure group (ADR-HF), telmisartan plus ADR-treated group (Tel+ADR) and losartan plus ADR-treated group (Los+ADR). ADR was administrated (2.5 mg/kg, ip, 6 times in 2 weeks). The rats in the Tel+ADR and Los+ADR groups were treated orally with telmisartan (10 mg/kg daily po) and losartan (30 mg/kg daily), respectively, for 6 weeks. The plasma level of Ang-(1-7) was determined using ELISA. The mRNA and protein expression of myocardial Mas receptor, AT(1)R and AT(2)R were measured using RT-PCR and Western blotting, respectively. RESULTS: ADR significantly reduced the plasma level of Ang-(1-7) and the expression of myocardial Mas receptor and myocardial AT(2)R, while significantly increased the expression of myocardial AT(1)R. Treatment with telmisartan and losartan effectively increased the plasma level of Ang-(1-7) and suppressed myocardial AT(1)R expression, but did not influence the expression of Mas receptor and AT(2)R. CONCLUSION: The protective effects of telmisartan and losartan in ADR-induced heart failure may be partially due to regulation of circulating Ang-(1-7) and myocardial AT(1)R expression.