Acute Pathological Conditions Research Articles

ZeroExpander® effectiveness assessment in PEEK or PA12 in a group of paediatric patients with transverse maxillary deficiency.

The aim of this article is to compare the performance of ZeroExpander® realised using PEEK or PA12 for the expansion of the maxilla in paediatric patients, exploring a new concept for approaching maxillary expansion with a metal-free fixed automatic appliance, based on pre-programmed set-up and anchored on deciduous teeth. It is a retrospective comparative study with a sample of 40 children in early or mixed deciduous dentition and transversal maxillary deficit, 20 treated with ZeroExpander® in PEEK and 20 treated with ZeroExpander® in PA12 with a mean age of 7.3 years old. The intraoral scans at T0 and at the end of the expansion were all performed by the same operator to obtain digital models on which were performed measurements by two other different operators. A descriptive analysis was conducted using frequencies and percentages for nominal variables and means and standard deviations for continuous variables. In cases of allergy or hypersensitivity to metals or to specific chronic or acute pathological conditions, which may require periodic magnetic resonance imaging (MRI), it may not be possible to use traditional and metal fixed expansion devices. Moreover the concept of autonomous driving in paediatric orthodontics is not only possible, but it is and will be more real and very useful in the future. The "ortho-paediatric dentistry concept" will increase the range of benefits for children and their families which, in addition to care and thanks to technology, demand well-being, safety, comfort and quality of life beyond clinics.

Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways.

Persistent cellular stress induced perpetuation and uncontrolled amplification of inflammatory response results in a shift from tissue repair toward collateral damage, significant alterations of tissue functions, and derangements of homeostasis which in turn can lead to a large number of acute and chronic pathological conditions, such as chronic heart failure, atherosclerosis, myocardial infarction, neurodegenerative diseases, diabetes, rheumatoid arthritis, and cancer. Keeping the vital role of balanced inflammation in maintaining tissue integrity in mind, the way to combating inflammatory diseases may be through identification and characterization of mediators of inflammation that can be targeted without hampering normal body function. Pirin (PIR) is a non-heme iron containing protein having two different conformations depending on the oxidation state of the iron. Through exploration of the Pirin interactome and using molecular docking approaches, we identified that the Fe2+-bound Pirin directly interacts with BCL3, NFKBIA, NFIX and SMAD9 with more resemblance to the native binding pose and higher affinity than the Fe3+-bound form. In addition, Pirin appears to have a function in the regulation of inflammation, the transition between the canonical and non-canonical NF-κB pathways, and the remodeling of the actin cytoskeleton. Moreover, Pirin signaling appears to have a critical role in tumor invasion and metastasis, as well as metabolic and neuro-pathological complications. There are regulatory variants in PIR that can influence expression of not only PIR but also other genes, including VEGFD and ACE2. Disparity exists between South Asian and European populations in the frequencies of variant alleles at some of these regulatory loci that may lead to differential occurrence of Pirin-mediated pathogenic conditions.

Regulation of Immune Checkpoint Antigen CD276 (B7-H3) on Human Placenta-Derived Mesenchymal Stromal Cells in GMP-Compliant Cell Culture Media.

Therapies utilizing autologous mesenchymal cell delivery are being investigated as anti-inflammatory and regenerative treatments for a broad spectrum of age-related diseases, as well as various chronic and acute pathological conditions. Easily available allogeneic full-term human placenta mesenchymal stromal cells (pMSCs) were used as a potential pro-regenerative, cell-based therapy in degenerative diseases, which could be applied also to elderly individuals. To explore the potential of allogeneic pMSCs transplantation for pro-regenerative applications, such cells were isolated from five different term-placentas, obtained from the dissected maternal, endometrial (mpMSCs), and fetal chorion tissues (fpMSCs), respectively. The proliferation rate of the cells in the culture, as well as their shape, in vitro differentiation potential, and the expression of mesenchymal lineage and stem cell markers, were investigated. Moreover, we studied the expression of immune checkpoint antigen CD276 as a possible modulation of the rejection of transplanted non-HLA-matched homologous or even xeno-transplanted pMSCs. The expression of the cell surface markers was also explored in parallel in the cryosections of the relevant intact placenta tissue samples. The expansion of pMSCs in a clinical-grade medium complemented with 5% human platelet lysate and 5% human serum induced a significant expression of CD276 when compared to mpMSCs expanded in a commercial medium. We suggest that the expansion of mpMSCs, especially in a medium containing platelet lysate, elevated the expression of the immune-regulatory cell surface marker CD276. This may contribute to the immune tolerance towards allogeneic pMSC transplantations in clinical situations and even in xenogenic animal models of human diseases. The endurance of the injected comparably young human-term pMSCs may promote prolonged effects in clinical applications employing non-HLA-matched allogeneic cell therapy for various degenerative disorders, especially in aged adults.

Smooth muscle cells-specific loss of OCT4 accelerates neointima formation after acute vascular injury.

There is growing evidence that smooth muscle cell (SMC) phenotypic transitions play critical roles during normal developmental and tissue recovery processes and in pathological conditions such as atherosclerosis. However, the molecular mechanisms responsible for these transitions are not well understood. Recently, we found that the embryonic stem cell/induced pluripotent stem cell (iPSC) factor OCT4, which was believed to be silenced in somatic cells, plays an atheroprotective role in SMC, and regulates angiogenesis after corneal alkali burn and hindlimb ischemia by mediating microvascular SMC and pericyte migration. However, the kinetics of OCT4 activation in arterial SMC and its role in acute pathological conditions are still unknown. Here, using an Oct4-IRES-GFP reporter mouse model, we found that OCT4 is reactivated in the carotid artery 18 hours post-acute ligation-induced injury, a common in vivo model of the SMC phenotypic transitions. Next, using a tamoxifen-inducible Myh11-CreERT2 Oct4 knockout mouse model, we found that the loss of OCT4, specifically in SMC, led to accelerated neointima formation and increased tunica media following carotid artery ligation, at least in part by increasing SMC proliferation within the media. Bulk RNA sequencing analysis on the cultured SMC revealed significant down-regulation of the SMC contractile markers and dysregulation of the genes belonging to the regulation of cell proliferation and, positive and negative regulation for cell migration ontological groups following genetic inactivation of Oct4. We also found that loss of Oct4 resulted in suppression of contractile SMC markers after the injury and in cultured aortic SMC. Further mechanistic studies revealed that OCT4 regulates SMC contractile genes, ACTA2 and TAGLN, at least in part by direct binding to the promoters of these genes. These results demonstrate that the pluripotency factor OCT4 is quickly activated in SMC after the acute vascular injury and inhibits SMC hyperproliferation, which may be protective in preventing excessive neointima formation.

Standardisation and future of preclinical echocardiography.

Echocardiography is a non-invasive imaging technique providing real-time information to assess the structure and function of the heart. Due to advancements in technology, ultra-high-frequency transducers have enabled the translation of ultrasound from humans to small animals due to resolutions down to 30µm. Most studies are performed using mice and rats, with ages ranging from embryonic, to neonatal, and adult. In addition, alternative models such as zebrafish and chicken embryos are becoming more frequently used. With the achieved high temporal and spatial resolution in real-time, cardiac function can now be monitored throughout the lifespan of these small animals to investigate the origin and treatment of a range of acute and chronic pathological conditions. With the increased relevance of in vivo real-time imaging, there is still an unmet need for the standardisation of small animal echocardiography and the appropriate cardiac measurements that should be reported in preclinical cardiac models. This review focuses on the development of standardisation in preclinical echocardiography and reports appropriate cardiac measurements throughout the lifespan of rodents: embryonic, neonatal, ageing, and acute and chronic pathologies. Lastly, we will discuss the future of cardiac preclinical ultrasound.

Spinal Hematoma Visualized with Dual-energy CT-derived Electron Density Overlay Maps.

HomeRadiologyRecently Published PreviousNext Reviews and CommentaryFree AccessImages in RadiologySpinal Hematoma Visualized with Dual-energy CT-derived Electron Density Overlay MapsChristian Nelles, Simon Lennartz Christian Nelles, Simon Lennartz Author AffiliationsInstitute for Diagnostic and Interventional Radiology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Strasse 62, 50937 Cologne, Germany.Address correspondence to S.L. (email: [email protected]).Christian NellesSimon Lennartz Published Online:Apr 11 2023https://doi.org/10.1148/radiol.222680MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In A 67-year-old man was admitted to the hospital with spontaneous, sudden-onset, severe thoracic back pain, radiating to the neck and lower back, accompanied by an episode of transient paraplegia of unknown severity, which lasted for 30–45 minutes. Three years prior, he had undergone mechanical aortic valve replacement with resection of an ascending aortic aneurysm associated with a bicuspid aortic valve. Consecutively, he had been treated with phenprocoumon for anticoagulation, with an international normalized ratio value of 4.5 at the time of admission (therapeutic range: 2.0–3.0). As the symptoms raised suspicion for aortic dissection, CT angiography of the chest and abdomen was performed with dual-layer dual-energy CT (dlDECT). dlDECT is a detector-based dual-energy CT technique in which a stacked scintillator registers lower energetic photons in the upper layer, whereas higher energetic photons are detected within the subjacent layer (1). The examination did not show signs of aortic dissection or other acute vascular pathologic conditions. Apart from persistent back pain, the patient’s symptoms receded. He was kept under surveillance for 3 days, after which worsening of the pain and the development of new high-grade paraplegia occurred, prompting an emergency MRI examination of the spine. The MRI scan showed extensive spinal hematoma, ranging from T1 to L1, with the maximum diameter and spinal cord compression at the level of T4-6 but without abnormal signal intensity of the spinal cord (Figure, A). The hematoma could not unequivocally be assigned to either the epi- or subdural space. Additionally, subarachnoid hemorrhage was noted along the cauda equina. The patient underwent successful emergency surgical evacuation of the hematoma, which during surgery showed extension to both the epi- and subdural as well as the subarachnoid space. Because digital subtraction angiography scans showed no vascular cause of the hematoma, spontaneous hemorrhage due to over-anticoagulation was determined as the most likely cause. After surgery, the pain and neurologic symptoms resolved rapidly, and the patient was discharged for subsequent rehabilitation. At retrospective review, different spectral data were reconstructed to determine if any of them might have facilitated earlier diagnosis of spinal hematoma with CT. Besides conventional images, virtual noncontrast and iodine images were also unremarkable. However, electron density overlay maps (Figure, B) clearly depicted the hematoma. The increased content of hemoglobin within the hematoma results in a higher material density at this location with a lesser effect on the average atomic number. There is only one study that showed that electron density maps may improve detection of prevertebral hematoma (2), which is in line with the finding in the case presented here. However, the application for detecting intraspinal hematoma has not been described yet. This might be a promising topic for systematic scientific evaluation, as electron density maps could improve CT-based detection of spinal hematoma in the emergency setting, potentially decreasing morbidity by enabling earlier treatment.(A) MRI scans of the spine in a 67-year-old man. Sagittal T2-weighted (top left) and T1-weighted (top right) images and axial contrast-enhanced, fat-saturated, T1-weighted image (bottom) show extensive spinal hematoma (arrows). The maximum diameter is located at the level of thoracic vertebrae T4-6 with effacement of the perimedullary cerebrospinal fluid and spinal cord compression. (B) Dual-layer dual-energy CT reconstructions show the corresponding CT angiography scans of the chest. Electron density overlay images (left) clearly depict the hematoma (green; arrows) that is protruding in the spinal canal. Conventional images (right) in the sagittal and axial plane. The hematoma is almost entirely imperceivable (arrows).Download as PowerPointOpen in Image Viewer Disclosures of conflicts of interest: C.N. No relevant relationships. S.L. Senior deputy editor for Radiology In Training; member of the Radiology editorial board.

Do Synthetic Fragrances in Personal Care and Household Products Impact Indoor Air Quality and Pose Health Risks?

Fragrance compounds (synthetic fragrances or natural essential oils) comprise formulations of specific combinations of individual materials or mixtures. Natural or synthetic scents are core constituents of personal care and household products (PCHPs) that impart attractiveness to the olfactory perception and disguise the unpleasant odor of the formula components of PCHPs. Fragrance chemicals have beneficial properties that allow their use in aromatherapy. However, because fragrances and formula constituents of PCHPs are volatile organic compounds (VOCs), vulnerable populations are exposed daily to variable indoor concentrations of these chemicals. Fragrance molecules may trigger various acute and chronic pathological conditions because of repetitive human exposure to indoor environments at home and workplaces. The negative impact of fragrance chemicals on human health includes cutaneous, respiratory, and systemic effects (e.g., headaches, asthma attacks, breathing difficulties, cardiovascular and neurological problems) and distress in workplaces. Pathologies related to synthetic perfumes are associated with allergic reactions (e.g., cutaneous and pulmonary hypersensitivity) and potentially with the perturbation of the endocrine-immune-neural axis. The present review aims to critically call attention to odorant VOCs, particularly synthetic fragrances and associated formula components of PCHPs, potentially impacting indoor air quality and negatively affecting human health.

Special Populations in Orthobiologics: Athletic, Elderly, and Pediatrics Populations.

This section is devoted to a review of the literature regarding the usage of orthobiologics in the special populations of elite athletes, the elderly, and pediatrics. The prospect of these regenerative options is encouraging to help provide alternative options that may enhance recovery and healing of acute and degenerative pathologic conditions. The goal is to provide the readers an overview of the existing literature highlighting areas with growing research and others that are still lacking.

Acylated Ghrelin Receptor Agonist HM01 Decreases Lean Body and Muscle Mass, but Unacylated Ghrelin Protects against Redox-Dependent Sarcopenia.

Sarcopenia, the progressive loss of muscle mass and dysfunction, universally affects the elderly and is closely associated with frailty and reduced quality of life. Despite the inevitable consequences of sarcopenia and its relevance to healthspan, no pharmacological therapies are currently available. Ghrelin is a gut-released hormone that increases appetite and body weight upon acylation, which activates its receptor GHSR1a. Recent studies have demonstrated that acyl and unacylated ghrelin are protective against acute pathological conditions of skeletal muscle. We hypothesized that both acyl ghrelin receptor agonist (HM01) and unacylated ghrelin ameliorate muscle atrophy and contractile dysfunction in oxidative stress-induced sarcopenia. HM01, unacylated ghrelin, or saline was delivered via osmotic pump. HM01 increased food consumption transiently, while the body weight remained elevated. It also decreased lean body mass and muscle mass of wildtype and Sod1KO. In contrast, unacylated ghrelin ameliorated loss of muscle mass by 15-30% in Sod1KO mice without changes in food consumption or body weights. Contractile force was decreased by ~30% in Sod1KO mice, but unacylated ghrelin prevented the force deficit by ~80%. We identified downregulation of transcription factor FoxO3a and its downstream E3 ligase MuRF1 by unacylated ghrelin. Our data show a direct role of unacylated ghrelin in redox-dependent sarcopenia independent of changes of food consumption or body weight.

Quick cell-free DNA testing for the prediction of postconcussion syndrome: a single-center prospective pilot trial.

Mild traumatic brain injury (mTBI) is a major cause of emergency room (ER) admission. Thirty percent of mTBI patients have postconcussion syndrome (PCS), and 15% have symptoms for over a year. This population is underdiagnosed and does not receive appropriate care. The authors proposed a fast and inexpensive fluorometric measurement of circulating cell-free DNA (cfDNA) as a biomarker for PCS. cfDNA is a proven, useful marker of a variety of acute pathological conditions such as trauma and acute illness. Thirty mTBI patients were recruited for this prospective single-center trial. At admission, patients completed questionnaires and blood was drawn to obtain cfDNA. At 3-4 months after injury, 18 patients returned for cognitive assessments with questionnaires and the Color Trails Test (CTT). The fast SYBR Gold assay was used to measure cfDNA. Seventeen men and 13 women participated in this trial. The mean ± SD age was 50.9 ± 13.9 years. Of the 18 patients who returned for cognitive assessment, one-third reported working fewer hours, 4 (22.2%) changed their driving patterns, and 5 (27.7%) reduced or stopped performing physical activity. The median cfDNA level of the mTBI group was greater than that of the matched healthy control group (730.5 vs 521.5 ng/ml, p = 0.0395). Admission cfDNA concentration was negatively correlated with performance on the CTT1 and CTT2 standardized tests (r = -0.559 and -0.599), meaning that greater cfDNA level was correlated with decreased cognitive performance status. The performance of the patients with normal cfDNA level included in the mTBI group was similar to that of the healthy participants. In contrast, the increased cfDNA group (> 800 ng/ml) had lower scores on the CTT tests than the normal cfDNA group (p < 0.001). Furthermore, patients with moderate/severe cognitive impairment according to CTT1 results had a greater median cfDNA level than the patients with scores indicating mild impairment or normal function (1186 vs 473.5 ng/ml, p = 0.0441, area under the receiver operating characteristic curve = 0.8393). The data from this pilot study show the potential to use cfDNA, as measured with a fast test, as a biomarker to screen for PCS in the ER. A large-scale study is required to establish the value of cfDNA as an early predictor of PCS.

Toxic desomorphine encephalopathy due to the use of “Krokodil”: clinical and neuroimaging features

Background: Toxic desomorphine encephalopathy (TDE) is a pathological condition that develops as a result of the intravenous use of a drug called Krokodil containing desomorphine, made in the artisanal conditions using codeine-containing drugs, organic solvents (gasoline), iodine and red phosphorus. This disease is more often observed in the CIS countries. In addition to the acute and chronic pathological conditions with the damage to various organs, the use of Krokodil is characterized by pronounced extrapyramidal manifestations in the form of dystonia, parkinsonism, postural disorders, as well as the occurrence of cognitive and affective disorders.&#x0D; Aims: To find the clinical and neuroimaging features of toxic desomorphine encephalopathy, as well as possible methods of its treatment.&#x0D; Methods: A clinical analysis of the medical documentation of 21 TDE patients (11 women and 10 men) with a history of the use of Krokodil was carried out, the patients had been under observation from 2014 to 2021. All the patients underwent a clinical physical and neurological examination, 14 of them underwent neuroimaging (brain MRI and/or MSCT). The observation of these patients revealed a number of characteristic clinical and neuroimaging features inherent in the majority of drug addicts.&#x0D; Results: The clinical picture of patients with TDE was dominated by movement disorders. All the patients had pronounced postural disorders and gait disturbance. Parkinsonism was observed in 20 of 21 patients. The hyperkinetic syndrome was presented in 17 patients (80.9%) and was manifested by dystonia of various localization with polymorphic manifestations. The brain MRI data taken from the Krokodil users for 3 years were characterized by symmetrical focal changes in the basal ganglia, brainstem, cerebellum and internal capsule of the thalamus in the form of an increase in the intensity of the MR signal in the T1 mode and attenuation in the T2-weighted images mode (7 of 11 cases), with the subsequent regression of these characteristics based on the results of the subsequent MRI studies.&#x0D; Conclusion: The study results have revealed the clinical manifestations characteristic of TDE polymorphic extrapyramidal disorders, as well as neuroimaging changes reflecting these data.

Chapter 5 - Types of motor speech impairments associated with neurologic diseases

Speech disturbances are common consequences of acquired brain injury or neurodegenerative impairment. Although sudden difficulties with speech may signal acute pathologic conditions such as cerebrovascular accidents, determining the etiology of insidious disruptions in communication can be less straightforward. The identification of motor speech impairment, independent of difficulties with language, can be useful for diagnosis since there are subtle, albeit distinct, patterns of speech production impairments associated with different neurologic conditions. Furthermore, the identification of impairments specific to speech production can help elucidate the suspected pathologic mechanisms or even the neuroanatomic structures compromised. During a routine clinical evaluation, early warning signs of motor speech impairment may go undetected if a clinician is unaccustomed to examining motor speech or is unaware of its manifestations. Accordingly, this chapter provides clinicians with a concise yet thorough guide for the practical assessment and differential diagnosis of motor speech disorders (MSDs)-apraxia of speech and dysarthrias. This chapter is divided into neurologic conditions associated with disorders of speech planning/programming, execution, and articulatory control. The underlying mechanisms associated with these impairments are presented both from a clinical perspective as well as through a scientific discussion of recent research in the field on MSDs.

CT of the Difficult Acute Aortic Syndrome.

Acute aortic syndrome (AAS) is classically attributed to three underlying pathologic conditions-aortic dissection (AD), intramural hematoma (IMH), and penetrating atherosclerotic ulcer (PAU). In the majority of cases, the basics of image interpretation are not difficult and have been extensively reviewed in the literature. In this article, the authors extend existing imaging overviews of AAS by highlighting additional factors related to the diagnosis, classification, and characterization of difficult AAS cases. It has been well documented that AAS is caused not only by an AD but by a spectrum of lesions that often have overlap in imaging features and are not clearly distinguishable. Specifically, phase of contrast enhancement, flow artifacts, and flapless AD equivalents can complicate diagnosis and are discussed. While the A/B dichotomy of the Stanford system is still used, the authors subsequently emphasize the Society for Vascular Surgery's new guidelines for the description of acute aortic pathologic conditions given the expanded use of endovascular techniques used in aortic repair. In the final section, atypical aortic rupture and pitfalls are described. As examples of pericardial and shared sheath rupture become more prevalent in the literature, it is important to recognize contrast material third-spacing and mediastinal blood as potential mimics. By understanding these factors related to difficult cases of AAS, the diagnostic radiologist will be able to accurately refine CT interpretation and thus provide information that is best suited to directing management. Online supplemental material is available for this article. ©RSNA, 2021.

Additional risk factors for in-hospital ischemic stroke. Hypercoagulation syndrome

The risk of ischemic stroke in inpatients is higher than in the general population. This is due to both the greater comorbidity of inpatients and the presence of additional risk factors, the most studied of which are iatrogenic interventions. At the same time, the higher the probability of developing an ischemic stroke, the more risk factors the patient has. An important link in the pathogenesis of in-hospital ischemic stroke is the activation of the hemostasis system, which is an obligate consequence of a typical pathological process underlying diseases and injuries that led to hospitalization: blood loss, inflammation, mechanical tissue damage, dehydration, etc. In foreign literature, this condition is attributed to the group of acquired thrombophilia, in domestic literature the term hypercoagulation syndrome has become more widespread. Iatrogenic effects can also play an important role in the pathogenesis of hypercoagulation syndrome. It is characterized by increased readiness for thrombosis, clinical and laboratory signs of hypercoagulation, activation of various factors and components of coagulation, decreased fibrinolysis, but without the development of acute thrombosis. Hypercoagulation syndrome is rarely assessed in routine practice as a risk factor for ischemic stroke, however, it can act as an additional and main risk factor for the development of all subtypes of ischemic stroke (according to the TOAST classification), including the ESUS concept. In this regard, it is advisable to distinguish in its structure: chronic (existing before hospitalization: hereditary and/or acquired) and acute (situational, developed as a result of the underlying disease, its complications or iatrogenic effects) hypercoagulation syndromes. To designate a group of acute pathological conditions predisposing to the development of hypercoagulation syndrome, systemic and/or local thrombotic complications, including in-hospital ischemic stroke, and requiring increased preventive measures, it seems pathogenetically justified, understandable and convenient to use the term situational hypercoagulation conditions (1 table, bibliography: 19 refs)

RYR1-related myopathies: Expanding the spectrum of morphological presentation

Mutations in the RYR1 gene are the most common cause of nondystrophic congenital myopathies. Mutations in RYR1 were initially identified in individuals susceptible to malignant hyperthermia, a pharmacogenetic disorder triggered by volatile anesthetics and succinylcholine. Shortly after, mutations in RYR1 were identified in patients with central core disease, which is the most frequent congenital myopathy, and in other muscle disorders, collectively referred to as RYR1-related myopathies. RYR1 mutations are also responsible of some acute pathological conditions triggered by heat- and exercise-induced stress, named exertional heat stroke and exertional-induced rhabdomyolysis, which, similarly to malignant hyperthermia, occur in otherwise healthy individuals with normal skeletal muscle functions. Hundreds of causative mutations linked to RYR1-related diseases have been identified. These mutations are clustered in three regions that are referred to as the N-terminal, central, and C-terminal hot spots. Recent developments in cryo-EM techniques have provided high-resolution reconstructions of the channel, allowing a much better definition of the structural domains within the large N-terminal cytoplasmic region and in the C-terminal domain containing six transmembrane helices and the pore region of the channel. RYR1 mutations may either activate or inhibit channel function or, in some cases, can reduce the expression levels of RYR1 protein. However, similar clinical phenotypes can result from mutations with opposing effects on RYR1 function, or little or no correlation can be found between the observed clinical phenotype and localization of mutations in the structural domains of the RYR1 channel, even though recent studies indicate that clinically severe cases are mostly recessive or due to mutations located in the bridging solenoid. Recent results on the identification of RYR1 mutations in patients with myopathies will be presented.

LncRNA DANCR improves the dysfunction of the intestinal barrier and alleviates epithelial injury by targeting the miR-1306-5p/PLK1 axis in sepsis.

Intestinal barrier dysfunction often occurs in various acute or chronic pathological conditions and has been identified as an important clinical problem. Herein, we explored the biological role and molecular mechanism of Polo-like kinase 1 (PLK1) and differentiation antagonizing non-protein coding RNA (DANCR) in intestinal barrier dysfunction caused by sepsis. RT-qPCR analysis was used to examine PLK1, miR-1306-5p, and DANCR expression in NCM460 cells after LPS treatment. TUNEL assay and Western blot analysis were performed to explore PLK1 function in cell apoptosis and intestinal barrier in vitro. Hematoxylin and eosin staining, Western blot analysis, and TUNEL assay were used to investigate DANCR function in the intestinal barrier and cell apoptosis in vivo. The interaction between miR-1306-5p and PLK1 (or DANCR) was validated by luciferase reporter assay. As a result, PLK1 overexpression decreased cell apoptosis and promoted intestinal barrier function. Moreover, DANCR was validated as a sponge of miR-1306-5p to target PLK1. In addition, we found that DANCR overexpression decreased intestinal mucosal permeability and colon mucosa epithelial cell apoptosis in vivo. Conclusively, DANCR improved intestinal barrier dysfunction and alleviated epithelial injury by targeting the miR-1306-5p/PLK1 axis in sepsis.

Chest CT Angiography for Acute Aortic Pathologic Conditions: Pearls and Pitfalls

Chest CT angiography (CTA) is essential in the diagnosis of acute aortic syndromes. Chest CTA quality can be optimized with attention to technical parameters pertaining to noncontrast imaging, timing of contrast-enhanced imaging, contrast material volume, kilovolt potential, tube-current modulation, and decisions regarding electrocardiographic-gating and ultra-fast imaging, which may affect the accurate diagnosis of acute aortic syndromes. An understanding of methods to apply to address suboptimal image quality is useful, as the accurate identification of acute aortic syndromes is essential for appropriate patient management. Acute aortic syndromes have high morbidity and mortality, particularly when involving the ascending aorta, and include classic aortic dissection, penetrating atherosclerotic ulcer, and acute intramural hematoma. An understanding of the pathogenesis and distinguishing imaging features of acute aortic syndromes and aortic rupture and some less common manifestations is helpful when interpreting imaging examinations. Related entities, such as ulcerated plaque, ulcerlike projections, and intramural blood pools, and mimics, such as vasculitis and aortic thrombus, are important to recognize; knowledge of these is important to avoid interpretive pitfalls. In addition, an awareness of postsurgical aortic changes can be useful when interpreting CTA examinations when patient history is incomplete. The authors review technical considerations when performing CTA, discuss acute aortic syndromes, and highlight diagnostic challenges encountered when interpreting aortic CTA examinations. ©RSNA, 2021.

Urgentna ultrasonografska dijagnostika akutnih netraumatskih abdominalnih stanja (urgentni ultrazvuk abdomena)

Ultrasound is an essential and often initial visualization diagnostic procedure in all algorithms for urgent care of acute abdominal conditions. Ultrasound is a fast, accessible, non-invasive diagnostic examination method that does not involve ionizing radiation and can be repeated. It is vital in detecting free fluid in the abdominal cavity, acute pathological conditions of parenchymal and hollow organs, and assessing volemic status. Ultrasound efficiently and accurately diagnoses acute pathological conditions of the hepatobiliary and urogenital system. It certainly makes a significant contribution to the definitive diagnosis of pathological conditions of the gastrointestinal and vascular systems and can help detect pneumoperitoneum as an indication for urgent surgical treatment.

Simultaneous Electroencephalographic and Electocorticographic Recordings of Lateralized Periodic Discharges in Temporal Lobe Epilepsy.

Lateralized periodic discharges (LPDs), which constitute an abnormal electroencephalographic (EEG) pattern, are most often observed in critically ill patients with acute pathological conditions, and are less frequently observed in chronic conditions such as focal epilepsies, including temporal lobe epilepsy (TLE). Here we aim to explore the pathophysiological mechanism of LPD in TLE. We retrospectively selected 3 patients with drug-resistant TLE who simultaneously underwent EEG and electrocorticography (ECoG) and demonstrated LPDs. We analyzed the correlation between the EEG and ECoG findings. In patients 1 and 2, LPDs were recorded in the temporal region of the scalp during the interictal periods, when repeated spikes followed by slow waves (spike-and-wave complexes; SWs) and periodic discharges (PDs) with amplitudes of >600 to 800 µV appeared in the lateral temporal lobe over a cortical area of >10 cm2. In patient 3, when the ictal discharges persisted and were confined to the medial temporal lobe, repeated SWs were provoked on the lateral temporal lobe. When repeated SWs with amplitudes of >800 µV appeared in an area of the lateral temporal lobe of >10 cm2, the corresponding EEG discharges appeared on the temporal scalp. LPDs in patients with TLE originate from repeated SWs and PDs of the lateral temporal lobe, which might represent a highly irritable state of the lateral temporal cortex during both interictal and ictal periods.

Organosulfur Compounds: A Review of Their Anti-inflammatory Effects in Human Health.

Phytonutrients are widely recognized for providing protective human health benefits. Among the phytonutrients, epidemiological and experimental studies show that dietary organosulfur compounds (OSC) play a significant role in preventing various human pathological progressions, including chronic inflammation, by decreasing inflammatory mediators such as nitric oxide (NO), prostaglandin (PG)E2, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-17, which are all typical hallmarks of inflammation. Evidence supports OSC in reducing the expression of these markers, thereby attenuating chronic inflammatory processes. Nuclear factor-kappa B (NF-κB) is a key regulating factor during inflammation, and novel evidence shows that OSC downregulates this transcriptional factor, thus contributing to the anti-inflammatory response. In vitro and in vivo studies show that inflammation is mechanistically linked with acute and chronic pathological conditions including cancer, diabetes, obesity, neural dysfunction, etc. Furthermore, a considerable number of experiments have demonstrated that the anti-inflammatory properties of OSC occur in a dose-dependent manner. These experiments also highlight indirect mechanisms as well as potent co-functions for protective roles as antioxidants, and in providing chemoprotection and neuroprotection. In this brief review, we provided an overview of the anti-inflammatory effects of OSC and elucidated probable mechanisms that are associated with inflammation and chronic disorders.