Hasil untuk "Cytology"

Natalia Pérez-Escudero, Isabel Cabas, Raúl Corbalán-Vélez et al.

Abstract Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte (KC) hyperproliferation and immune cell infiltration, including neutrophils. While estrogens are known to modulate immune responses, the role of the G protein-coupled estrogen receptor 1 (GPER1) in skin inflammation remains poorly understood. Here, we show that GPER1 signaling is downregulated in lesional skin of psoriasis patients and negatively correlates with both inflammation markers and KC proliferation. Using a zebrafish model of chronic skin inflammation (Spint1a-deficient larvae), we demonstrate that Gper1 deficiency leads to increased KC proliferation and enhanced neutrophil infiltration, without directly modulating inflammatory signaling. Pharmacological inhibition of cell proliferation with palbociclib reduced both KC aggregates and neutrophil infiltration, independently of NF-κB activation. Moreover, Gper1 overexpression in basal KCs, but not in neutrophils, rescued skin alterations, indicating a cell-autonomous effect in KCs. Notably, our results also suggest that epithelial cell proliferation facilitates immune cell infiltration into inflamed tissue. Together, our results identify GPER1 as a negative regulator of keratinocyte hyperproliferation and skin inflammation, suggesting that modulation of this pathway may represent a therapeutic strategy for hyperproliferative inflammatory skin diseases such as psoriasis.

Marie Kristin Mikkelborg, Antonette Skram Helgestad, Roy Ambli Dalmo et al.

Abstract Background Pathogens pose a significant threat to farmed salmon, adversely affecting their health and welfare, which results in substantial economic losses. The outermost skin epithelial cells, including skin keratocytes, serve as a critical defense barrier against environmental stressors, such as bacterial infections. Understanding the features and properties of these cells, particularly skin keratocytes, is essential as they play a crucial role in wound healing and tissue regeneration. Additionally, we were curious whether corneal epithelial cells (corneal keratocytes), which protect the fish eye, exhibit similar features and immune functions. Results To investigate the properties of skin keratocytes, we utilized flow cytometry to analyze scale-derived cells. The analysis revealed that more than 85% of the cells were skin keratocytes, although the remaining cells could not be characterized using this method. Microscopic analysis confirmed that the majority of these cells exhibited the typical morphology of keratocytes and were positive for a pan-keratin antibody. To assess the immune function of skin keratocytes, we exposed scale-derived keratocytes to various fish pathogenic bacteria and evaluated their ability to ingest bacteria and examined the regulation of innate immune genes. Additionally, we analyzed the expression of immune-related markers, including mhcii, in both skin and corneal cells. Conclusion Our findings demonstrated that scale-derived skin keratocytes internalized bacteria within 3–6 hours of exposure. This bacterial interaction led to the significant upregulation of several key immune-related genes. Interestingly, both skin and corneal cells expressed mhcii, suggesting a potential role in adaptive immunity in addition to their participation in innate immune responses. These results highlight the vital role of skin and corneal cells in the innate immune response against bacterial infections and their possible contribution to adaptive immunity.

Chidubem Eneanya, George M. Smith

Goal-directed reaching movements are extremely accurate to the point that the location, placement, and speed of the limbs are specific from trial to trial. These movements require descending motor commands and feedback modulation from ascending sensory information. The descending motor commands and ascending sensory information work in conjunction to ensure that the movement is accurate and precise through an error-corrected process that resides in the cerebellum. Disruptions to this information may cause errors in the precision of forelimb motor targeting. According to the previous literature, the external cuneate nucleus (ECN) and central cervical nucleus (CeCv) are responsible for conveying unconscious sensory information from the forelimbs, shoulders, and neck muscles to the cerebellum. Here, we examined the significance of the ECN and CeCv, separately, in forelimb function. In conjunction with inhibitory DREADDs (hM4Di), we observed an obstruction in single pellet reaching and grasping when ECN activity was repressed, both unilaterally and bilaterally, in normal rats. We also observed reduced reach in the grooming assessment bilaterally. We discovered that the CeCv terminates in the medial cerebellar nucleus (MCN), within the deep cerebellar nuclei (DCN), which, to the best of our knowledge, was previously not clearly defined. Together, this information provides evidence that the requirement of ascending sensory information is important in forelimb function.

Qin Han, Tongxia Wang, Zhangxin Wu et al.

Background: Cervical intraepithelial neoplasia grade 3(CIN 3) is a precancerous lesion condition with high progression rate and is advised to be treated immediately. Because traditional treatments have limited effects or complications, here we evaluated the efficacy and safety of topical 5-aminolevulinic acid (ALA)–based photodynamic therapy (PDT). Methods: This study consisted of 56 female patients diagnosed with CIN3. A 20 % 5-ALA jelly formation was topically applied to the cervix, followed by 635 nm PDT at 7-14 days intervals. Cytology, human papillomavirus (HPV) genotyping, colposcopy, and pathology were assessed after treatment. Results: Among the 56 patients in our study, 26.8 % (15/56) patients had disease remission after just one course PDT, 69.6 % (39/56) patients had partial remission to CIN2, which suggested a response to the therapy and should be treated with more course. The total pathological regression rate was 89.3 %(50/56). Although6 patients did CKC finally, none of the pathology suggest cervical cancer and 2 of them were LSIL. The HPV clearance rate during the 6-month follow-up was 51.8 %. 4 patients had recurrent disease during the 2-year follow-up time point. The most common adverse event was increased vaginal discharge, other side effects include abdominal pain, vulvar pruritus, and vaginal bleeding. No severe adverse effect was observed during the treatment. Conclusion: ALA-PDT is a treatment option for CIN 3 which meet certain conditions, with the main goal to preserve the struction and founction of cervix.

Long Liu, Yu Zhang, Yuxi Huang et al.

Abstract Local invasion is considered a premonitor of tumor metastasis which cause curative difficulties and undesired prognosis in patients with Pancreatic ductal adenocarcinoma (PDAC). The importance of mRNA N6-methyladenosine (m6A) modification during tumor invasion is controversial as it plays distinct roles which mainly attributed to different m6A reader proteins exert function. In current study, the level of m6A expression in PDAC was analyzed by IHC and ELISA, all m6A-regulated genes in PDAC detected by qPCR. The downstream gene EMP1 was screened by analyzing IGF2BP3 knockdown RNA-seq, IGF2BP3-RIP, MeRIP-seq, and PDAC-survival related genes. And m6A modification sites of EMP1 RNA was verified by MeRIP-qPCR, RIP-qPCR, and dual luciferase assays. EMP1-binding protein VASP was identified by mass spectrometry. Cell migration and invasive activity were detected using cytoskeletal staining, scratch assay, transwell assay, subcutaneous tumor and lung metastasis models. Finally, prognosis and immune microenvironment was analyzed in PDAC by IHC and multiple immunofluorescence staining. This work shows that m6A reader IGF2BP3 is remarkably upregulated in local invasion PDAC and indicates worse prognosis of patients. Mechanistically, IGF2BP3 recognized m6A-modified EMP1 mRNAs to prolong stability of them, which inhibits the hindrance of SMAD7 to SMAD3/4 phosphorylation by promoting the binding of VASP and SMAD7. Finally, a tight correlation of the local invasion/IGF2BP3/EMP1 and infiltration of immune cells in the tumor microenvironment is evidenced in clinical PDAC. In conclusions, IGF2BP3 functions as an invasion driver that induces PDAC development via the EMP1/TGF-β axis. And IGF2BP3/EMP1 axis may be involved in regulating microenvironmental remodeling in pancreatic cancer.

Made Gede Adi Surya Saputra, Sri Kayati Widyastuti, Putu Ayu Sisyawati Putriningsih

Background: Conjunctivitis is an inflammation of the conjunctiva that is common in dog, which also known as pink eyes. Conjunctivitis can be caused by infectious agents such as bacteria, chlamydia, and virus, and can also be induced by allergies or due to trauma. Bilateral infection may indicate they are caused by an infectious agent or allergy. Purpose: This study aims to provide veterinarians with insight into the treatment of conjunctivitis cases and the factors that hinder therapy. Case: A seven-year-old female Shih-Tzu dog has had eye problems for six months since April 2023. Physical examination revealed redness in the left and right eyes with mucopurulent exudate. Laboratory examination using an impression smear followed by cytology confirmed inflammation in the eye with many neutrophil cells and coccus-shaped bacteria. The dog was diagnosed with bacterial conjunctivitis with a good prognosis. Case Management: The therapy consisted of the administration of topical antibiotics in the form of Erlamycetin plus® (chloramphenicol and dexamethasone) eye drops for five days, followed by Erlamycetin® (chloramphenicol) eye ointment. Conclusion: After 12 days of therapy, there was no redness in the dog's eyes and only a small amount of exudate was observed. However, on day 14, the owner reported that exudates were observed in the dog's eyes. The therapy resulted in improvements but was not optimal because the owner did not consistently follow the recommendations.

Xiangdong Xu, Yaofeng Zheng, Linting Luo et al.

Abstract Glioblastoma stem cells (GSCs) play a key role in glioblastoma (GBM) resistance to temozolomide (TMZ) chemotherapy. With the increase in research on the tumour microenvironment, exosomes secreted by GSCs have become a new focus in GBM research. However, the molecular mechanism by which GSCs affect drug resistance in GBM cells via exosomes remains unclear. Using bioinformatics analysis, we identified the specific expression of ABCB4 in GSCs. Subsequently, we established GSC cell lines and used ultracentrifugation to extract secreted exosomes. We conducted in vitro and in vivo investigations to validate the promoting effect of ABCB4 and ABCB4-containing exosomes on TMZ resistance. Finally, to identify the transcription factors regulating the transcription of ABCB4, we performed luciferase assays and chromatin immunoprecipitation-quantitative PCR. Our results indicated that ABCB4 is highly expressed in GSCs. Moreover, high expression of ABCB4 promoted the resistance of GSCs to TMZ. Our study found that GSCs can also transmit their highly expressed ABCB4 to differentiated glioma cells (DGCs) through exosomes, leading to high expression of ABCB4 in these cells and promoting their resistance to TMZ. Mechanistic studies have shown that the overexpression of ABCB4 in GSCs is mediated by the transcription factor ATF3. In conclusion, our results indicate that GSCs can confer resistance to TMZ in GBM by transmitting ABCB4, which is transcribed by ATF3, through exosomes. This mechanism may lead to drug resistance and recurrence of GBM. These findings contribute to a deeper understanding of the mechanisms underlying drug resistance in GBM and provide novel insights into its treatment.

Natalia López-González del Rey, Miguel Ángel García-Cabezas

Degeneration of neurons and circuits across the striatum shows stereotyped time-course and spatial topography patterns that are distinct for Huntington's disease, Parkinson's disease, or the Tauopathies. These patterns of neurodegeneration in humans have not yet been systematically related to developmental, connectional, cellular, and chemical factors studied in human and non-human primates, that may underlie potential differences in selective vulnerability across striatal sectors. Relating primate anatomy to human pathology could provide new venues for identifying molecular, cellular, and connectional factors linked to the degeneration of striatal neurons and circuits. This review describes and summarizes several developmental, cellular, structural, and connectional features of the primate striatum in relation to patterns of neurodegeneration in the striatum of humans and of non-human primate models. We review (1) the types of neurons in the primate striatum, (2) the cyto-, myelo-, and chemoarchitecture of the primate striatum, (3) the developmental origin of the striatum in light of modern patterning studies, (4) the organization of corticostriatal projections in relation to cortical types, and (5) the topography and time-course of neuron loss, glial reaction, and protein aggregation induced by neurodegenerative diseases in humans and in non-human primate models across striatal sectors and their corresponding cortical areas. We summarize current knowledge about key aspects of primate striatal anatomy and human pathology and indicate knowledge gaps that should be addressed in future studies. We aim to identify factors for selective vulnerability to neurodegeneration of striatal neurons and circuits and obtain hints that could help elucidate striatal pathology in humans.

Zeynep Danisman, Maximilian Linxweiler, Jan Philipp Kühn et al.

IntroductionChronic Rhinosinusitis with nasal polyps (CRSwNP) is a common chronic disease with a high impact on patients’ quality of life. If conservative and surgical guideline treatment cannot sufficiently control disease burden, biologicals can be considered as a comparably new treatment option that has revolutionized CRSwNP therapy since the first approval of Dupilumab in 2019. With the aim to select patients who benefit from this new treatment and to find a marker for therapy monitoring, we investigated the cellular composition of nasal mucous membranes and inflammatory cells of patients suffering from CRSwNP and undergoing Dupilumab therapy using non-invasive nasal swab cytology.MethodsTwenty CRSwNP patients with the indication for Dupilumab therapy have been included in this prospective clinical study. In total, five study visits were conducted with ambulatory nasal differential cytology using nasal swabs starting with the beginning of therapy and followed by visits every 3 months for 12 months. First, these cytology samples were stained with the May-Grunwald-Giemsa method (MGG) and the percentage of ciliated cells, mucinous cells, eosinophil cells, neutrophil cells, and lymphocytes was analyzed. Secondly, an immunocytochemical (ICC) ECP-staining was performed to detect eosinophil granulocytes. Additionally, during each study visit the nasal polyp score, SNOT20 questionnaire, olfactometry, the total IgE concentration in peripheral blood as well as the eosinophil cell count in peripheral blood were recorded. The change of parameters was evaluated over one year and the correlation between clinical effectiveness and nasal differential cytology was analyzed.ResultsIn both MGG (p<0.0001) and ICC analysis (p<0.001) a significant decrease of eosinophils was seen under Dupilumab treatment. When patients were divided into a Eo-low- (<21%) and Eo-high- (≥21%) group according to the percentage eosinophils in nasal swab catology in the first study visit, the Eo-high-group showed a greater change of eosinophils over time (Δ17.82) compared to the Eo-low-group (Δ10.67) but, however, no better response to therapy. The polyp score, SNOT20 questionnaire, and total IgE concentration in peripheral blood showed a significant decrease during the observation period (p<0.0001).DiscussionNasal swab cytology as an easy-to-apply diagnostic method allows detection and quantification of the different cell populations within the nasal mucosa at a given time. The nasal differential cytology showed a significant decrease of eosinophils during Dupilumab therapy and can therefore be used as non-invasvive method for monitoring therapy success of this cost intensive therapy and potentially can allow an optimized individual therapy planning and management for CRSwNP patients. Since the validity of initial nasal swab eosinophil cell count as a predictive biomarker for therapy response was limited in our study, additional studies including larger number of participants will be necessary to further evaluate the potential benefits for clinical practice of this new diagnostic method.

Saleh Jamehdor, Sara Pajouhanfar, Sadaf Saba et al.

Viruses are one of the most important concerns for human health, and overcoming viral infections is a worldwide challenge. However, researchers have been trying to manipulate viral genomes to overcome various disorders, including cancer, for vaccine development purposes. CRISPR (clustered regularly interspaced short palindromic repeats) is becoming one of the most functional and widely used tools for RNA and DNA manipulation in multiple organisms. This approach has provided an unprecedented opportunity for creating simple, inexpensive, specific, targeted, accurate, and practical manipulations of viruses, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human immunodeficiency virus-1 (HIV-1), and vaccinia virus. Furthermore, this method can be used to make an effective and precise diagnosis of viral infections. Nevertheless, a valid and scientifically designed CRISPR system is critical to make more effective and accurate changes in viruses. In this review, we have focused on the best and the most effective ways to design sgRNA, gene knock-in(s), and gene knock-out(s) for virus-targeted manipulation. Furthermore, we have emphasized the application of CRISPR technology in virus diagnosis and in finding significant genes involved in virus-host interactions.

Fabienne Burger, Daniela Baptista, Aline Roth et al.

<b>Background</b>: Atherosclerosis is a chronic inflammatory disease where macrophages participate in the progression of the disease. However, the role of resident-like macrophages (res-like) in the atherosclerotic aorta is not completely understood. <b>Methods:</b> A single-cell RNA sequencing analysis of CD45⁺ leukocytes in the atherosclerotic aorta of apolipoprotein E–deficient (<i>Apoe</i>^−/−) mice on a normal cholesterol diet (NCD) or a high cholesterol diet (HCD), respecting the side-to-specific predisposition to atherosclerosis, was performed. A population of res-like macrophages expressing hyaluronan receptor LYVE-1 was investigated via flow cytometry, co-culture experiments, and immunofluorescence in human atherosclerotic plaques from carotid artery disease patients (CAD). <b>Results:</b> We identified 12 principal leukocyte clusters with distinct atherosclerosis disease-relevant gene expression signatures. LYVE-1⁺ res-like macrophages, expressing a high level of CC motif chemokine ligand 24 (CCL24, eotaxin-2), expanded under hypercholesteremia in <i>Apoe</i>^−/− mice and promoted VSMC phenotypic modulation to osteoblast/chondrocyte-like cells, ex vivo, in a CCL24-dependent manner. Moreover, the abundance of LYVE-1⁺CCL24⁺ macrophages and elevated systemic levels of CCL24 were associated with vascular calcification and CAD events. <b>Conclusions:</b> LYVE-1 res-like macrophages, via the secretion of CCL24, promote the transdifferentiation of VSMC to osteogenic-like cells with a possible role in vascular calcification and likely a detrimental role in atherosclerotic plaque destabilization.

Francisco Prista von Bonhorst, David Gall, Geneviève Dupont

Alzheimer’s disease is characterized by a marked dysregulation of intracellular Ca²⁺ homeostasis. In particular, toxic β-amyloids (Aβ) perturb the activities of numerous Ca²⁺ transporters or channels. Because of the tight coupling between Ca²⁺ dynamics and the membrane electrical activity, such perturbations are also expected to affect neuronal excitability. We used mathematical modeling to systematically investigate the effects of changing the activities of the various targets of Aβ peptides reported in the literature on calcium dynamics and neuronal excitability. We found that the evolution of Ca²⁺ concentration just below the plasma membrane is regulated by the exchanges with the extracellular medium, and is practically independent from the Ca²⁺ exchanges with the endoplasmic reticulum. Thus, disruptions of Ca²⁺ homeostasis interfering with signaling do not affect the electrical properties of the neurons at the single cell level. In contrast, the model predicts that by affecting the activities of L-type Ca²⁺ channels or Ca²⁺-activated K⁺ channels, Aβ peptides promote neuronal hyperexcitability. On the contrary, they induce hypo-excitability when acting on the plasma membrane Ca²⁺ ATPases. Finally, the presence of pores of amyloids in the plasma membrane can induce hypo- or hyperexcitability, depending on the conditions. These modeling conclusions should help with analyzing experimental observations in which Aβ peptides interfere at several levels with Ca²⁺ signaling and neuronal activity.

Zhimei Qiu, Yan Wang, Weiwei Liu et al.

Abstract Autophagy and apoptosis are involved in myocardial ischemia/reperfusion (I/R) injury. Research indicates that circular RNA HIPK3 (circHIPK3) is crucial to cell autophagy and apoptosis in various cancer types. However, the role of circHIPK3 in the regulation of cardiomyocyte autophagy and apoptosis during I/R remains unknown. Our study aimed to examine the regulatory effect of circHIPK3 during myocardial I/R and investigate its mechanism in cardiomyocyte autophagy and apoptosis. Methods and results. The expression of circHIPK3 was upregulated during myocardial I/R injury and hypoxia/reoxygenation (H/R) injury of cardiomyocytes. To study the potential role of circHIPK3 in myocardial H/R injury, we performed gain-of-function and loss-of-function analyses of circHIPK3 in cardiomyocytes. Overexpression of circHIPK3 significantly promoted H/R-induced cardiomyocyte autophagy and cell injury (increased intracellular reactive oxygen species (ROS) and apoptosis) compared to those in the control group, while silencing of circHIPK3 showed the opposite effect. Further research found that circHIPK3 acted as an endogenous miR-20b-5p sponge to sequester and inhibit miR-20b-5p activity, resulting in increased ATG7 expression. In addition, miR-20b-5p inhibitors reversed the decrease in ATG7 induced by silencing circHIPK3. Conclusions. CircHIPK3 can accelerate cardiomyocyte autophagy and apoptosis during myocardial I/R injury through the miR-20b-5p/ATG7 axis. These data suggest that circHIPK3 may serve as a potential therapeutic target for I/R.

Susan Zhou, Zhengping Jia

P21-activated kinase 3 (PAK3) gene mutations are linked to several neurodevelopmental disorders, but the underlying mechanisms remain unclear. In this study, we used a tetracycline-inducible system to control the expression of a mutant PAK3 (mPAK3) protein in immediate early gene, namely cFos, positive cells to disrupt PAK signaling, specifically in cells activated by social interaction in transgenic mice. We show that the expression of mPAK3-GFP proteins was in cFos-expressing excitatory and inhibitory neurons in various brain regions, such as the cortex and hippocampus, commonly activated during learning and memory. Basal expression of mPAK3-GFP proteins in cFos-positive cells resulted in social recognition memory deficits in the three-chamber social interaction test, without affecting locomotor activity or other forms of memory. The social memory deficit was rescued by doxycycline to halt the mPAK3-GFP transgene expression. In addition, we show that the expression of mPAK3-GFP proteins in a subset of cFos-positive cells, induced by an antecedent short social interaction, termed social pairing, was sufficient to impair social recognition memory. These results indicate that normal PAK signaling in cFos-positive cells activated during social interaction is critical for social memory.

Jian Wan, Shunfang Liu, Wanju Sun et al.

Abstract Background Hepatocellular carcinoma (HCC) is the third cause of cancer death in the world, and few molecularly targeted anticancer therapies have been developed to treat it. The E3 ubiquitin ligase RNF152 has been reported to regulate the activity of the mechanistic target of rapamycin complex 1 (mTORC1), induce autophagy and apoptosis. However, the relationship between RNF152 and HCC is unclear. Methods Transcriptome RNA-sequencing data of HCC samples and normal tissues were used to detect the mRNA expression of RNF152. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were used to determine the transcriptional regulation of RNF152 in HCC by FoxO1. RNAi, cell proliferation, colony formation and transwell assays were used to determine the in vitro functions of RNF152. Mouse xenograft models were used to study the in vivo effects of RNF152. The immunoprecipitation assay was used to determine the interaction between RNF152 and TSPAN12. The in vivo ubiquitination assay was performed to determine the regulation of TSPAN12 by RNF152. Results We found that RNF152 is significantly down-regulated in clinic HCC samples, and its down-regulation is associated with pool overall survival (OS), progression-free survival (PFS) and disease-specific survival (DSS) in HCC patients. The transcription factor FoxO1 was significantly positively correlated RNF152 expression in HCC tissues. FoxO1 recognizes a classic insulin response element (IRE) on the RNF152 promoter to regulate its expression in HCC. RNF152 suppressed HCC cell proliferation, clonogenic survival, invasion in vitro, and tumorigenesis in vivo. Mechanistically, RNF152 interacted with TSPAN12 and targeted it for ubiquitination and proteasomal degradation, thereby inhibiting TSPAN12-dependent CXCL6 expression and HCC progression. Conclusion Collectively, our data revealed a tumor suppressor role of RNF152 and a connection between RNF152 and FoxO1 in HCC. Our results support an important role of the FoxO1-RNF152-TSPAN12 axis in the development of HCC. Therapeutic targeting this axis may be an effective means of treating HCC.

Mohammad Reza Sharifian, Mahmoud Mahmoudi, Babak Pourmomenarabi et al.

Introduction:<br /> Otitis media with effusion (OME) is prevalent among children in such a way that it is the most common cause of hearing loss and surgery in childhood. Immunoglobulin E (IgE) mediated hypersensitivity has been proposed as a causative factor in the development of OME; however, there has been contrasting data in this regard. Therefore, the present study aimed to detect the possibilities of interconnection.<br /> Materials and Methods:<br /> In this study, 37 OME children were selected as the case group and 52 children were randomly chosen as the control group. Allergic rhinitis prevalence, serum total IgE concentration, serum eosinophil count, and nasal scraping cytology were evaluated in all the children. Furthermore, the skin prick test was performed in the OME group and suspected allergic rhinitis patients in the control group.<br /> Results:<br /> Allergic rhinitis prevalence was notably higher among OME patients than in the control group (P<em>=</em>0.01). There were no remarkable differences in eosinophil counts and serum IgE concentrations in the two groups. Nasal smear eosinophils did not show any significant difference between the two groups; however, Appreciable difference was observed in the allergic rhinitis patients, compared to other OME patients (P<em>=</em>0.004).<br /> Conclusion:<br /> There may be a correlation between allergic rhinitis and development of OME. Therefore, it seems reasonable to examine allergic rhinitis patients for OME.

D. V. Krinochkin, I. S. Bessonov, V. A. Kuznetsov et al.

Timely performed endovascular revascularization is the main modern method of treating for patients with acute myocardial infarction and elevated ST segment. In most cases, it is possible to achieve rapid recovery of coronary blood flow in the infarct related artery. Nevertheless, 10–40 % of patients manifest diminished myocardial reperfusion despite successful opening of the obstructed epicardial artery – so called the no-reflow phenomenon. The main angiographic features of hypoperfusion in the infarction zone are decrease in the degree of myocardial glow and/or blood flow by the TIMI scale. However, the use of angiographic criteria does not always allow accurate detection of developing no-reflow phenomenon. The presented case demonstrates the possibilities and potential benefits of contrast enhanced echocardiography in assessing the no-reflow phenomenon in a patient with acute myocardial infarction after revascularization.

J. Patterson, W. Stone

Subramanian Kannan, Nalini Raju, Vikram Kekatpure et al.

Context: Fine-needle aspiration cytology is the first step in evaluation of thyroid nodules. Although the Bethesda classification for reporting thyroid cytology has been purported that this uniformity in reporting cytology thereby facilitating clinical decision-making, there are also studies indicating that the reporting percentage and the rates of malignancy in each category vary considerably from center to center making the clinical decision more difficult. Aim and Materials and Methods: We looked at our retrospective cytology and histopathology data of thyroid nodules operated between 2012 and 2014 and then prospectively collected data during 2015–2016. In the prospective arm, for every thyroid nodule that was sampled, there was a discussion between the endocrinologist and the cytopathologist on the risk of thyroid cancer (based on the patient's history, examination findings, sonographic pattern, and the cytological appearance). Results: We noted that there was considerable improvement in reporting standards with the rates of nondiagnostic cytology dropping from 11% to 5%, an increased reporting of Bethesda Category 2 and 6 which are the definitive strata of benign and malignant nodules (38% to 41% in Category 2 and 7% to 11% in Category 6) with a high specificity (100%). There was a decline in numbers of Category 4 and 5 (13% to 9% in Category 4 and 12% to 3% in Category 5). The reporting prevalence of Category 3 increased from 19% to 27%. Conclusions: We conclude that a team approach between the clinician who performs the ultrasound and the reporting cytopathologist improves Bethesda reporting, its predictive value, and thus potentially avoiding unnecessary thyroidectomies in benign thyroid nodules and hemithyroidectomies in thyroid cancers.

Guanglei Li, Yajing Liu, Yanting Zeng et al.