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Binaural and spatial hearing
Published in Stanley A. Gelfand, Hearing, 2017
The binaural fusion mechanism has been described in terms of a model by Cherry and Sayers (Cherry and Sayers, 1956; Sayers and Cherry, 1957) in which the central auditory nervous system carries out a running cross-correlation between the inputs to the two ears. In other words, the signals entering the ears are viewed as statistical events, and the fusion mechanism operates by looking for commonalities between the inputs coming from the two ears on an ongoing basis.
Human Parainfluenza Virus Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Eric T. Beck, Kelly J. Henrickson
The HN glycoprotein is the second glycoprotein found on the surface of HPIVs. Like all the other HPIV proteins already mentioned, the HN protein has several roles in the HPIV life cycle. Perhaps the most important is its ability to bind to sialic acid-containing residues, especially heparin sulfate, found on the surface of host cells, thus initiating the infection process.43,44 The ability of this protein to bind cell surface receptors is also responsible for the agglutination of red blood cells, which can be used for serodiagnosis of HPIV infection. In addition to binding host cells, the HN protein also cleaves sialic acid residues on the surface of infected cells to prevent viral reattachment to previously infected cells. The dual purpose of the HN protein (namely, binding to and cleavage of sialic acid residues on the host cell surface) is regulated by halide ion concentration and pH.45 The binding/hemagglutination properties of this protein are favored by the halide ion concentrations and relatively neutral pH of the extracellular environment. Meanwhile, the HN protein’s cleavage/neuraminidase properties are favored in the lower pH/halide ion environment within the cell, indicating that this protein may remove sialic acid residues from newly formed viral and host cell membranes as they are being transported to the cell surface.5 A final function of the HN protein is its ability to interact with and activate the fusion mechanism of the HPIV F protein.46–48
Molecular Mediator of Prostate Cancer Progression and Its Implication in Therapy
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Samikshan Dutta, Navatha Shree Sharma, Ridwan Islam, Kaustubh Datta
One of the most common recurrent genomic rearrangement in prostate cancer is the fusion of androgen regulated gene TMPRSS2 to ETS family of transcription factors, the most common one being ERG [61, 63, 64]. Gene fusion is detected in ~50% of prostate cancer patients and occurs due to improper repair of double stranded breaks. Because of TMPRSS2-ERG fusion, the expression of this family of transcription factors is regulated by androgen axis in prostate cancer cells. It has been suggested that AR itself increases the probability of this specific fusion event to occur in cancer cells [51, 65, 66]. Interestingly, ~90 % patients with early onset of prostate cancer have been detected with the fusion and the prostate cancer in these patients is also dependent on AR axis suggesting an AR-dependent fusion mechanism [67–69]. Fusion of other ETS factors such as ETV1, ETV4, and ETV5 with binding factors such as TMPRSS2, HERV-K, KLK2, SLC45A3, CANT1, HERV-K17, DDX5 and FOXP1 have also been reported [51, 61, 63–69]. These ETS transcription factors promote the expression of genes such as MYC, EZH2 and SOX9 involved in proliferation, dedifferentiation, migration, invasion and oncogenesis [70–72]. TMPRSS2-ERG fusion has been detected in both low and high-grade intraepithelial neoplasia (PIN) and is therefore thought to be an early event in prostate cancer [51, 63, 66]. PIN is also detected in mouse prostate when overexpressing prostate-specific ETV1 in transgenic mice. Interestingly, no tumor is developed in this mouse model, suggesting the requirement of other genetic alterations for oncogenic transformation [73–75]. Some studies also reported increased expression of ETS factors in hormone-naïve and castration-resistant metastatic prostate cancer indicating potential roles of fusion genes in advanced cancer [54, 75, 76]. Studies have indicated co-operation between TMPRSS2-ERG fusion and other oncogenic events such as PTEN loss, AKT activation and AR overexpression, which promotes the emergence of advanced prostate cancer [77, 78]. The TMPRSS2-ERG fusion can activate RAS-MAPK and is associated with downregulation of WNT and TGFβ signaling pathways [79–83]. Moreover, removal of these fusion proteins reduces tumor growth in nude mice highlighting the potential of ETS transcription factors as target for prostate cancer [84–86]. Inhibiting upstream signaling kinases and downstream targets of ETS transcription factors are also considered as effective therapeutic target as an alternative of directly targeting the ETS factors [73, 87, 88]. Because of its cancer-specific expression and potential impact on tumor initiation and growth, many studies investigated the prognostic importance of ETS gene rearrangement. The results are conflicting as they reported association of ETS fusions with both aggressive and indolent disease [64, 89–91]. There could be several reasons for this anomaly, including heterogeneity of the prostate tumors, study cohorts and the impact of sampling.
A 2020 Update on 20/20 X 2: Diplopia after Ocular Surgery Diplopia after Iatrogenic Monovision
Published in Journal of Binocular Vision and Ocular Motility, 2021
This patient had strabismus prior to her monovision pseudophakia surgery and should have been advised to avoid monovision. Patients with intermittent strabismus and an unreliable fusion mechanism may experience decompensation of a previously well-controlled strabismus.5 The likelihood of postoperative binocular sensorimotor decompensation is higher among those patients with preexisting binocular issues.5,7 In fact, most diplopia-related visual complaints irrespective of surgical procedure for iatrogenic monovision are usually due to a misdiagnosed preoperative disorder. Monovision should not be offered to patients who have a history of strabismus, diplopia, prism use, extraocular muscle (EOM) surgery, EOM restriction, or a significant phoria greater than 8 prism diopters.8
Exploring the contribution of mitochondrial dynamics to multiple acyl-CoA dehydrogenase deficiency-related phenotype
Published in Archives of Physiology and Biochemistry, 2021
Sofia R. Brandão, Rita Ferreira, Hugo Rocha
Mitochondrial dynamics is regulated by fusion and fission mechanisms (Chan 2006, Gregersen et al.2012), which are reported to be impaired in FAOD (Schmidt et al.2010, 2011, Cornelius et al.2014). The fusion mechanism is regulated by mitofusins (Mfns) and mitochondrial dynamin-like 120 kDa protein (OPA1) (Rojo et al.2002, Chan 2006). Several studies demonstrated that cells lacking these proteins present reduced levels of mitochondrial fusion and thus a dramatic decreased mitochondrial functionality (Chen et al.2003, Cipolat et al.2004, Chen et al.2005). In fact, a down-regulation of Mfn2 was reported in RR-MADD patients, probably due to a survival mechanism that consists in elimination of damaged parts of mitochondria (Cornelius et al.2014). The fission mechanism involves dynamin-related protein 1 (Drp1) and mitochondrial fission 1 protein (Fis1) (Smirnova et al.2001, Lee et al.2004, Chan 2006), although other proteins such as endophilin B1 and mitochondrial membrane protein 18 (MTP18) seem to be involved in this process too (Karbowski et al.2004, Tondera et al.2005). Decreased amounts of these proteins result in elongation of mitochondrial tubules. These and other abnormalities in mitochondrial morphology are suggestive of defects in fission mechanism (Smirnova et al.2001, Karbowski et al.2004, Lee et al.2004, Tondera et al.2005).
Liposome-based combination therapy for acne treatment
Published in Journal of Liposome Research, 2020
İpek Eroğlu, Minela Aslan, Ümran Yaman, Merve Gultekinoglu, Semih Çalamak, Didem Kart, Kezban Ulubayram
In the case of liposomes containing tetracycline and tretinoin (Lipo2Comb coded formulation), MIC values were calculated as 0.016 μg/mL for both bacteria. On the other hand, MIC values of solution (Sol-Comb) were calculated as 0.063 and 0.125 μg/mL for Staphylococcus aureus and Streptococcus epidermidis, respectively. This 3.9-fold reduction for Staphylococcus aureus and 12.8-fold reduction in MIC values clearly indicated that liposomal formulations provide dose attenuation in terms of API amounts. The mechanism of this elevated efficacy possibly depends on the interaction of liposomal structures with the bacterial cells, which is literally named as fusion mechanism (Torres et al.2012). It is a two-sided story in which intracellular concentration of the API is increased; but on the other hand, possibility of bacterial resistance is decreased. As well known, the major advantage of liposome structures is their similarity to cellular membranes; thus, they are allowed to fuse with bacterial membranes depending on this mimicking characteristics (Rukavina et al.2018). At the final point of fusion, the release of API from liposomal formulation might be achieved either inside the membrane or inside the bacteria that leads to more effective treatment with high local API concentration (Rukavina et al.2018).