Assessment of genotoxic effects of (4-methoxyphenyl)(3,4,5-trimethoxyphenyl)methanone in human lymphocytes

(4-Methoxyphenyl)(3,4,5-trimethoxyphenyl)methanone (PHT) belongs to the phenstatin family. This compound has been studied due to its potent cytotoxicity and ability to inhibit tubulin assembly. The present study aimed to evaluate the mutagenic potential of PHT in human lymphocytes. PHT displayed cytotoxicity in human lymphocytes with an IC₅₀ value of 5.68 μM, and therefore, concentrations of 0.25, 0.5, 1.0, 2.0, and 4.0 μM were used for all protocols. The alkaline comet assay and chromosome aberration (CA) analysis were performed in different phases of the cell cycle (G₁, G₁/S, transition, and G₂), to evaluate the DNA-damaging and clastogenic effects of PHT, respectively. CA analysis was carried out in the presence or absence of colchicine to evaluate the action of PHT in the mitotic phase. PHT was cytotoxic and significantly reduced the mitotic index with drug exposure in all phases of cell cycle. Interestingly, it induced an increase in mitotic index in experimental protocols without colchicine, corroborating its action as an antitubulin agent. It also induced DNA damage and was clastogenic with drug exposure in all phases of the cell cycle, in the presence or absence of colchicine. In conclusion, PHT induces DNA damage and exerts clastogenic effects in human lymphocytes.     

Biological and genetic landscape of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL)

Breast implant–associated anaplastic large cell lymphoma (BIA-ALCL) is an uncommon form of non-Hodgkin lymphoma (cancer of the immune system) that can develop around breast implants. Breast implants are among the most commonly used medical devices for cosmetic or reconstructive purposes. In the past few years, the number of women with breast implants diagnosed with anaplastic large cell lymphoma (ALCL) has increased, and several studies have suggested a direct association between breast implants and an increased risk of this disease. Although it has been hypothesized that chronic stimulation of the immune system caused by implant materials and biofilms as well as a possible genetic predisposition play an important role in this disease, the cellular and molecular causes of BIA-ALCL are not fully understood. This review aims to describe the current understanding around the environmental and molecular drivers of BIA-ALCL as well as the genetic and chromosomal abnormalities identified in this disease to date.     

Characteristics of Pseudomonas aeruginosa isolates from intensive care unit

The study looked at the antimicrobial resistance patterns, serotypes, molecular types, metallo beta-lactamase, and chromosomal betalactamase enzymes of P. aeruginosa strains isolated from the patients and the staffs of the intensive care unit. P. aeruginosa isolates from the patients as nosocomial pathogens and from the staffs were evaluated for their susceptibilities to the antimicrobials by the disk diffusion and E-test methods. Metallo beta-lactamase enzymes were investigated by E-test, the inducibility of β - lactamase enzymes were detected by the disk antagonism test. Serotyping was performed by slide agglutination method. The P. aeruginosa isolates were typed by pulsed field gel electrophoresis. Twenty-five P. aeruginosa strains from the patients and three from the staffs were isolated. Fifteen P. aeruginosa, eleven of which composed of MDR bacteria, were found in serogroup E, 7 strains in G, 4 strains in B, and 1 strain in serogroup A. In all 12 bacteria in the MDR and serogroup E, metallo beta-lactamase enzyme was found to be positive. And in other 15 strains, except the bacterium which could not be serotyped, chromosomal beta-lactamase was found to be positive. The result of the molecular typing showed PFGE A pattern. In conclusion, a pattern in PFGE which included bacteria from MDR and serogroup E, G which was observed in the P. aeruginosa strains which was isolated from the staff’s hands and from the 5 patients, and PFGE F pattern were found to be observed the most. Finally, the two different clonal strains were found to be established in the intensive care.     

Accounting for the phase,spatial frequency and orientation demands of the task improves metrics based on the visual Strehl ratio

Advances in ophthalmic instrumentation have allowed high order aberrations to be measured in vivo. These measurements describe the distortions to a plane wavefront entering the eye, but not the effect they have on visual performance. One metric for predicting visual performance from a wavefront measurement uses the visual Strehl ratio, calculated in the optical transfer function (OTF) domain (VSOTF) (Thibos et al., 2004). We considered how well such a metric captures empirical measurements of the effects of defocus, coma and secondary astigmatism on letter identification and on reading. We show that predictions using the visual Strehl ratio can be significantly improved by weighting the OTF by the spatial frequency band that mediates letter identification and further improved by considering the orientation of phase and contrast changes imposed by the aberration. We additionally showed that these altered metrics compare well to a cross-correlation-based metric. We suggest a version of the visual Strehl ratio, VS_combined, that incorporates primarily those phase disruptions and contrast changes that have been shown independently to affect object recognition processes. This metric compared well to VSOTF for letter identification and was the best predictor of reading performance, having a higher correlation with the data than either the VSOTF or cross-correlation-based metric.     

超声检查评估胎儿肝强回声的价值及预后分析

目的探讨胎儿肝强回声变化规律和病因，为临床咨询提供帮助。 方法采用回顾性研究方法，收集自2016年1月1日至2019年12月31日在首都医科大学附属北京妇产医院和首都医科大学附属北京潞河医院产前超声检查发现胎儿肝存在强回声灶的单胎孕妇63例。记录孕妇基本信息，胎儿大小测值，强回声病灶的大小、位置、数量，是否合并胎儿其他结构异常，胎盘、羊水、脐带、胎儿脐动脉血流等情况。随访入组病例的染色体检查结果及母体病毒系列（TORCH）检查结果及胎儿强回声灶随孕周的变化及妊娠结局。所有活产婴儿都详细记录新生儿出生信息，出生后生长发育及肝超声复查情况。总结、整理产前产后资料，探讨肝强回声变化特征和病因。采用秩和检验比较出生后回声消失与否2组病例的出生前病灶长径的差异。 结果63例胎儿中合并胎儿其他结构异常者17例（27%，17/63），孤立性肝强回声灶46例（73%，4/63）；染色体异常2例（3%，2/63），均为21-三体；母体病毒感染3例（5%，3/63）；胎粪性腹膜炎1例（2%，1/63）。17例合并胎儿其他结构异常的病例中有2例终止妊娠，1例新生儿死亡，2例生后接受手术治疗。共随访到52例生后信息：27例出生时强回声灶仍存在，出生前病灶平均长径为0.70 cm，中位数为0.60（0.60，0.80）cm，25例出生时已消失，出生前病灶平均长径为0.47 cm，中位数为0.50（0.40，0.60）cm，二者差异具有统计学意义（Z=3.54，P＜0.001）。所有活产病例结局均良好。 结论胎儿肝强回声灶并不罕见，部分胎儿肝强回声灶（长径较小）可自发消失。孤立性病灶病例占比比既往文献高，且预后良好。母体病毒感染主要为巨细胞病毒感染。当合并胎儿其他结构异常时，建议通过无创DNA或羊水穿刺进行胎儿染色体检查，必要时还需进行染色体微阵列分析。     

Chordoma: an update on the pathophysiology and molecular mechanisms

Chordoma is a rare low-grade primary malignant skeletal tumor, which is presumed to derive from notochord remnants. The pathogenesis of chordoma has not been fully elucidated. However, recent advances in the molecular biology studies have identified brachyury underlying the initiation and progression of chordoma cells. More efforts have been made on accumulating evidence of the notochordal origin of chordoma, discovering signaling pathways and identifying crucial targets in chordomagenesis. In this review, we summarize the most recent research findings and focus on the pathophysiology and molecular mechanisms of chordoma.