Cell Pathology最新文献

{"title":"Intramuscular hydatid cyst of thigh masquerading as a soft tissue tumour diagnosed by fine needle aspiration cytology","authors":"K. Amita, T. Rajini, M. Sanjay, M. Abhishek, K. Prashantha","doi":"10.1515/ersc-2021-0003","DOIUrl":"https://doi.org/10.1515/ersc-2021-0003","url":null,"abstract":"Abstract Introduction. Hydatid cyst, caused by Echinococcus granulosa, occurs rarely in the musculoskeletal region. Most of the time, clinically and radiologically it is diagnosed as a soft tissue tumor, benign or malignant. There are a few case reports of hydatid cyst presenting as an intramuscular thigh mass, which has been diagnosed at fine needle aspiration cytology (FNAC). Accurate pre-operative diagnosis is essential in view of specific therapeutic options for this disease. Here we report a case of hydatid cyst occurring in an unusual location (thigh) and masquerading as a soft tissue tumour, diagnosed at FNAC. Case Report. 56-year-old male patient presented with gradually increasing swelling of the left thigh since 3 years. On examination, there was a firm non-tender 25 × 20 cm swelling on the posterior aspect of left thigh extending from the gluteal region to five cm above the knee joint. An ultrasound diagnosis of a soft tissue tumor was made. At FNAC, fluid was aspirated and smears showed granulomas along with multiple hyaline acellular membrane-like fragments, few showing vague laminations. A diagnosis of hydatid cyst was made at FNAC which was corroborated at histopathology. Conclusion. Intramuscular hydatid cyst of the thigh is a very rare manifestation. The possibility of hydatid cyst should be considered while aspirating any soft tissue mass lesion, especially when fluid is obtained and microscopy shows acellular hyaline membrane-like material, even when fewer laminations are noted.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76862505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhinoscleroma – A unique masquerader. A retrospective case series","authors":"D. Nayak M, L. Shenoy","doi":"10.1515/ersc-2021-0001","DOIUrl":"https://doi.org/10.1515/ersc-2021-0001","url":null,"abstract":"Abstract Objectives: Rhinoscleroma is a rare infectious disease of the upper respiratory tract caused by Klebsiella rhinoscleromatis. Apart from mandating an appropriate antibiotic therapy, it poses a unique challenge to the pathologists since it can clinically simulate a malignancy. The main objective was to study the cases of rhinoscleroma of the respiratory tract in a period of 3 years with an emphasis on the clinico-pathologic features. Methods: We report a retrospective analysis of 7 cases, histopathologically diagnosed at our centre as rhino-scleroma. The topography ranged from nasal mucosa (3), pharynx (2) and larynx (2). Results: Histopathological examination in all cases showed diffuse aggregates of foamy macrophages (Mikulicz cells) containing intracytoplasmic basophilic organisms; admixed with plasma cells in a fibrotic stroma. The overlying epithelium appeared atrophic to focally hyperplastic. The age ranged from 36–67 years, involving both genders. The significant clinical history included a nasal block without anosmia, atrophic rhinitis with septal perforation to subglottic stenosis, requiring immediate surgical intervention. In 4 of the 7 cases, the working clinical diagnosis was stipulated as a malignancy. Conclusions: Rhinoscleroma can affect different regions in the upper aero digestive tract. A lack of awareness and a delay in the diagnosis of this disease can lead to complications including upper airway obstruction, physical deformity, and rarely, sepsis. In addition, it must be remembered that the treatment of rhinoscleroma is challenging and requires a prolonged course of antibiotics to achieve a definite cure and avoid relapses.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77520244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of zoledronic acid on bone structure and organization of nanocomposites in rats with obesity and limited mobility","authors":"N. Kostyshyn, I. Shtablavyi","doi":"10.1515/ersc-2021-0002","DOIUrl":"https://doi.org/10.1515/ersc-2021-0002","url":null,"abstract":"Abstract Background: Some investigations show that obesity is associated with increase in bone mass due to excessive mechanical exertion. However, these data are contradictory as loss of mineral density of bone tissue and, respectively, the risk of fractures in this population group is higher. The aim of the research was to investigate impact of drug therapy with zoledronic acid on nanostructure of bones in rats with limited mobility and high-calorie diet. Methods: Rats (n = 56) were distributed into three groups: control (n = 18) – standard vivarium conditions, І experimental group (n = 18) – rats, which were on a high-calorie diet with limited mobility (HCD+LM), ІІ experimental group (n = 18) – HCD+LM+zoledronic acid. Zoledronic acid was injected at the dose 0.025 mg/kg intramuscularly every four weeks for six months. X-ray structure analysis, scanning electron microscopy and atomic absorption spectrometry were used for investigation of ultrastructure and quantitative assessment of mineral component loss in the femoral neck. Results: Obesity and limited mobility reduced the level of the mineral component in the femoral neck (−31.5%) compared with control. It is significant that zoledronic acid did not permit decrease in mineral component of the bone throughout the entire experiment compared with group I (+41.8%), and all parameters were higher than in control group (+15%). Conclusions: Obesity and limited mobility negatively affect mineral bone mass. Zoledronic acid induces increase in the mineral component as a result of remodeling inhibition under conditions of obesity and limited mobility modeling.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81908174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Index","authors":"","doi":"10.1016/b978-0-12-822481-6.09991-6","DOIUrl":"https://doi.org/10.1016/b978-0-12-822481-6.09991-6","url":null,"abstract":"","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87313184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"List of abbreviations","authors":"","doi":"10.1016/b978-0-12-822481-6.09992-8","DOIUrl":"https://doi.org/10.1016/b978-0-12-822481-6.09992-8","url":null,"abstract":"","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73258592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tubarial or not to be – a potential new organ in the pharynx","authors":"A. Turk","doi":"10.1515/ersc-2020-0002","DOIUrl":"https://doi.org/10.1515/ersc-2020-0002","url":null,"abstract":"In an elegantly presented and thought-provoking manuscript published by the journal Radiotherapy and Oncology, Valstar et al. characterize previously unreported structures comprising salivary gland tissue near the torus tubarius [1]. The authors present their findings in three stages. First, they identify these entities in patients with prostate or urethral gland cancer who underwent positron emission tomography / computed tomography with prostate-specific membrane antigen ligands (PSMA PET/ CT), which technique—despite its name—demonstrates avidity for salivary glands. The investigators then evaluate these glands using human cadavers, and finally assess the effect of radiation therapy involving this region in head & neck cancer (HNC) patients. Ultimately, the authors proffer two conclusions from their findings. First, they propose recognition of this region as newly identified paired organs, suggesting the designation of “tubarial glands.” Second, they underscore the importance of sparing this area from the toxic effects of radiation therapy, to whatever extent feasible. Whereas the second of these points seems more resonant and straightforward, the authors appear to emphasize the first, in terms of coverage and explication. The dichotomy between these claims, and the relative prominence of the purported anatomic contribution within the manuscript, potentially detract from study’s significant clinical impact. The anatomic issue—whether these glands more closely resemble major or minor salivary glands—is an interesting question. In terms of features shared in common with major glands, the authors discuss several analogies between the tubarial glands and sublingual glands. For instance, the tubarial glands lack a capsule, and the sublingual glands show only partial encapsulation. The authors also demonstrate the tubarial glands’ “multiple macroscopically visible draining duct openings in the dorsolateral pharyngeal wall” in Figure 4. The sublingual gland secretes its products through multiple ducts as well. However, these features (absence of a fibrous capsule, and presence of multiple ducts) pertain to minor salivary glands as well as the sublingual gland, and therefore may not distinguish the tubarial glands as major versus minor. Conversely, the tubarial glands exhibit several aspects analogous to the minor salivary glands of the palate, potentially suggesting a designation as minor rather than major glands for the region in question. The authors concede these resemblances, stating “the tubarial glands have many similarities with the palatal conglomerate of microscopic glands.” From the perspective of a pathologist, anyway (and based on the text), the relationship between the radiologic features of the tubarial and palatal glands is difficult to discern. The authors alternately describe the PET avidity of the tubarial glands as “consistently more than the uptake in the palate,” and/or as “comparable to the mucous aspect and PSMA-ligand uptake o","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79386780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive outlook of Cell Pathology","authors":"G. Su","doi":"10.1515/ersc-2020-0001","DOIUrl":"https://doi.org/10.1515/ersc-2020-0001","url":null,"abstract":"Pathology is one of the oldest medical disciplines, one that can be arguably rooted early in Egyptian medicine and Traditional Chinese Medicine 5,000 years ago [1,2]. In ancient times, documentation of diseases relied on the understandings of anatomy and observations of abnormalities that deviated from normal physiology. For many centuries ensued, vast knowledge was accumulated from observations of pathological conditions and autopsies, it is this wealth of information that laid the foundation for the modern medicine we see today. In the early beginning, pathology focused on morphological abnormalities. Random documentation of broken bones, abnormal masses, skin discoloration evolved into systematic gross anatomy in modern pathology in the 19th century [2,3]. The invention of the microscope in the 19th century was undoubtedly another force that propelled pathology and medicine forward, moving us from organbased to cell-based pathology with this “new technology”. Along with the microscope, other technological advances such as tissue fixation, embedding, microtomes, and biological stains, all enabled the practice of histopathology possible. However, for a century, despite the improvement of microscopes and a plethora of ancillary diagnostic tests (i.e. electron microscopy, fluorescent microscopy, immunohistochemistry, cytogenetics), the importance of detecting morphological abnormalities remained constant and central to scientific discoveries, journal publications, and patient care as research focuses moved from organs to cells, from organelles to chromosomes. In recent decades, we have seen an explosion of technologies in science, which enabled comparisons of normal vs. diseased states at molecular levels. Soon, analyses of DNA (single nucleotide polymorphism profiling, whole exome sequencing, cell-free DNA screening, etc.), RNA (RNA-Seq, single cell RNA-Seq, miRNA-Seq, ribosome profiling, etc.), protein (protein microarray, mass spectrometry, quantitative proteomics, etc.), epigenome (ChIPSeq, whole-genome bisulphite sequencing), and metabolome (MS-based metabolites or lipid profiles) at various depths and throughputs became a common practice in experimental approaches and journal publications [4,5]. These molecular analyses not only can identify dysfunctional genes and/or pathways that are responsible or have contributed to the diseased state and structural abnormalities that can be visualized grossly or under a microscope, but may also offer insights for personalized medicine. For instance, in the era of precision medicine for cancer treatment, we have come to recognize that not only there are differential sensitivities to a given therapy among patients, there exists cellular heterogeneity in a patient’s tumor. Therefore, a histological diagnosis of cancer in a patient can be complemented by molecular analyses to devise a personalized therapy that matches the tumor’s molecular profile. It is also the hope that advances in liquid biopsies and ar","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83747035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stressors and Stress Responses in Cystic Fibrosis","authors":"Z. Bebok, Lianwu Fu","doi":"10.1515/ersc-2018-0002","DOIUrl":"https://doi.org/10.1515/ersc-2018-0002","url":null,"abstract":"Abstract Cystic fibrosis (CF) is a life-shortening, genetic disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR). The primary cause of CF is reduced CFTR-mediated chloride and bicarbonate transport, due to mutations in CFTR. However, inflammation and persistent infections influence clinical outcome. Cellular stress response pathways, such as the unfolded protein response (UPR) and the integrated stress response (ISR), referred to here as cellular stress response pathways (SRPs), contribute to the pathology of human disorders. Multiple studies have indicated activation of SRPs in CF tissues. We review our present understanding of how SRPs are activated in CF and their contribution to pathology. We conclude that reduced CFTR function in CF organs establishes a tissue environment in which internal or external insults activate SRPs. SRPs contribute to CF pathogenesis by reducing CFTR expression, enhancing inflammation with consequent tissue remodeling. Understanding the contribution of SRPs to CF pathogenesis is crucial even in the era of CFTR “modulators” that are designed to potentiate, correct or amplify CFTR function, since there is an urgent need for supportive treatments. Importantly, CF patients with established pathology could benefit from the targeted use of drugs that modulate SRPs to reduce the symptoms.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2018-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84782155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress-sensing and regulatory mechanism of the endoplasmic-stress sensors Ire1 and PERK","authors":"Yuki Ishiwata‐Kimata, G. Q. Le, Y. Kimata","doi":"10.1515/ersc-2018-0001","DOIUrl":"https://doi.org/10.1515/ersc-2018-0001","url":null,"abstract":"Abstract Ire1 and its family protein PERK are endoplasmic reticulum (ER)-stress sensors that initiate cellular responses against ER accumulation of unfolded proteins. As reviewed in this article, many publications describe molecular mechanisms by which yeast Ire1 senses ER conditions and gets regulated. We also cover recent studies which reveal that mammalian Ire1 (IRE1α) and PERK are controlled in a similar but not exactly the same manner. ER-located molecular chaperone BiP captures these ER-stress sensors and suppresses their activity. Intriguingly, Ire1 is associated with BiP not as a chaperone substrate, but as a unique ligand. Unfolded proteins accumulated in the ER promote dissociation of the Ire1-BiP complex. Moreover, Ire1 is directly bound with unfolded proteins, leading to its cluster formation and potent activation. PERK also captures unfolded proteins and then forms self-oligomers. Meanwhile, membrane-lipid aberrancy is likely to activate these ER-stress sensors independently of ER accumulation of unfolded proteins. In addition, there exist a number of reports that touch on other factors that control activity of these ER-stress sensors. Such a multiplicity of regulatory mechanisms for these ER-stress sensors is likely to contribute to fine tuning of their activity.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2018-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87753985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Link between endoplasmic reticulum stress and autophagy in neurodegenerative diseases","authors":"Toru Hosoi, J. Nomura, Keigo Tanaka, K. Ozawa, A. Nishi, Y. Nomura","doi":"10.1515/ersc-2017-0004","DOIUrl":"https://doi.org/10.1515/ersc-2017-0004","url":null,"abstract":"Abstract Increasing evidence suggests that endoplasmic reticulum (ER) stress and autophagy play an important role in regulating brain function. ER stress activates three major branches of the unfolded protein response (UPR) pathways, namely inositol-requiring enzyme-1 (IRE1), double stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor 6 (ATF6)-mediated pathways. Recent studies have suggested that these UPR signals may be linked to autophagy. In this review article, we summarize recent evidence and discuss a possible link between ER stress and autophagy with regard to neurodegenerative diseases. Furthermore, possible pharmacological strategies targeting UPR and autophagy are discussed.","PeriodicalId":29730,"journal":{"name":"Cell Pathology","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2017-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78075040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}