Novel B-DNA dermatophyte assay for demonstration of canonical DNA in dermatophytes: Histopathologic characterization by artificial intelligence.

We describe a novel assay and artificial intelligence-driven histopathologic approach identifying dermatophytes in human skin tissue sections (ie, B-DNA dermatophyte assay) and demonstrate, for the first time, the presence of dermatophytes in tissue using immunohistochemistry to detect canonical right-handed double-stranded (ds) B-DNA. Immunohistochemistry was performed using anti-ds-B-DNA monoclonal antibodies with formalin-fixed paraffin-embedded tissues to determine the presence of dermatophytes. The B-DNA assay resulted in a more accurate identification of dermatophytes, nuclear morphology, dimensions, and gene expression of dermatophytes (ie, optical density values) than periodic acid-Schiff (PAS), Grocott methenamine silver (GMS), or hematoxylin and eosin (H&E) stains. The novel assay guided by artificial intelligence allowed for efficient identification of different types of dermatophytes (eg, hyphae, microconidia, macroconidia, and arthroconidia). Using the B-DNA dermatophyte assay as a clinical tool for diagnosing dermatophytes is an alternative to PAS, GMS, and H&E as a fast and inexpensive way to accurately detect dermatophytosis and reduce the number of false negatives. Our assay resulted in superior identification, sensitivity, life cycle stages, and morphology compared to H&E, PAS, and GMS stains. This method detects a specific structural marker (ie, ds-B-DNA), which can assist with diagnosis of dermatophytes. It represents a significant advantage over methods currently in use.

Comparison of the CPR Feedback Device Effect on the Effective Technique of the CPR in Two Modes of the Device Warning Being On and Off.

INTRODUCTION: Out-of-hospital cardiac arrest is a major public health problem with over 90% case fatality. Although it is known that good quality of cardiopulmonary Resuscitation (CPR) leads to improved patient outcomes, health care practitioners commonly perform sub-optimal CPR. The CPR feedback device is a small device designed to measure the number and depth of chest compressions (CC) and if the rate of compressions or the depth of the compressions is low or high, it will try to correct the CPR operation by announcing a warning to the resuscitator. The aim of this study was to evaluate the effectiveness of this device which was designed and made by the authors' technician study group member in improving CPR operations, to determine the need for it in all hospitals on a routine basis. METHOD: This cross-sectional study was performed on patients who have suffered from cardio-pulmonary arrest in Al-Zahra Hospital in 2020. Patients needed primary CPR for any reason, were randomly divided into two groups using random allocation software. The first group contains patients as the CPR Feedback device is on and alarm is on and warns, if resuscitation is ineffective, the second group also uses the device, but with the difference that the alarm is off. The data was analyzed by general linear model method (repeated measure ANOVA). RESULTS: 80 patients were studied, including 63 men (79%) and 17 women (21%). Patients were divided among two groups. There was no significant difference in demographic characteristics between two groups. The results showed that there was no significant interaction between group and time for the compression depth variable and there was no significant difference in the depth of compressions between the two groups(P>0.05). For the rate of compressions, there was a significant interaction between group and time. These results indicate that turning on the CPR feedback device's warning increases the number of compressions during CPR and, as a result, makes it more effective. The between-group effect which showed the difference in the number of compressions in the two groups, was statistically significant (P<0.001). CONCLUSION: These results indicated that turning on the CPR feedback device's warning increases the rate of compressions during CPR and, as a result, makes it more effective. Therefore, the use of real-time CPR feedback device during chest compression in real-time CPR improves the quality of CPR.

Activation of Immune System May Cause Pathophysiological Changes in the Myocardium of SARS-CoV-2 Infected Monkey Model.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is an extremely contagious disease whereby the virus damages the host's respiratory tract via entering through the ACE2 receptor. Cardiovascular disorder is being recognized in the majority of COVID-19 patients; yet, the relationship between SARS-CoV-2 and heart failure has not been established. In the present study, SARS-CoV-2 infection was induced in the monkey model. Thereafter, heart tissue samples were collected, and pathological changes were analyzed in the left ventricular tissue by hematoxylin and eosin, trichrome, and immunohistochemical staining specific to T lymphocytes and macrophages. The findings revealed that SARS-CoV-2 infection induces several pathological changes in the heart, which cause cardiomyocyte disarray, mononuclear infiltrates of inflammatory cells, and hypertrophy. Furthermore, collagen-specific staining showed the development of cardiac fibrosis in the interstitial and perivascular regions in the hearts of infected primates. Moreover, the myocardial tissue samples displayed multiple foci of inflammatory cells positive for T lymphocytes and macrophages within the myocardium. These findings suggest the progression of the disease, which can lead to the development of severe complications, including heart failure. Additionally, SARS-CoV-2 antigen staining detected the presence of virus particles in the myocardium. Thus, we found that SARS-CoV-2 infection is characterized by an exaggerated inflammatory immune response in the heart, which possibly contributes to myocardial remodeling and subsequent fibrosis.

HOPX Plays a Critical Role in Antiretroviral Drugs Induced Epigenetic Modification and Cardiac Hypertrophy.

People living with HIV (PLWH) have to take an antiretroviral therapy (ART) for life and show noncommunicable illnesses such as chronic inflammation, immune activation, and multiorgan dysregulation. Recent studies suggest that long-term use of ART induces comorbid conditions and is one of the leading causes of heart failure in PLWH. However, the molecular mechanism of antiretroviral drugs (ARVs) induced heart failure is unclear. To determine the mechanism of ARVs induced cardiac dysfunction, we performed global transcriptomic profiling of ARVs treated neonatal rat ventricular cardiomyocytes in culture. Differentially expressed genes were identified by RNA-sequencing. Our data show that ARVs treatment causes upregulation of several biological functions associated with cardiotoxicity, hypertrophy, and heart failure. Global gene expression data were validated in cardiac tissue isolated from HIV patients having a history of ART. Interestingly, we found that homeodomain-only protein homeobox (HOPX) expression was significantly increased in cardiomyocytes treated with ARVs and in the heart tissue of HIV patients. Furthermore, we found that HOPX plays a crucial role in ARVs mediated cellular hypertrophy. Mechanistically, we found that HOPX plays a critical role in epigenetic regulation, through deacetylation of histone, while the HDAC inhibitor, Trichostatin A, can restore the acetylation level of histone 3 in the presence of ARVs.

Monitoring training in women's volleyball: Supine or seated heart rate variability?

We aimed to examine changes in resting heart rate variability, submaximal exercising heart rate (HRex), countermovement-jump height (CMJ), perceptual wellbeing, and internal load throughout preparatory training in elite women's volleyball players. We also aimed to determine which HRV measurement position (supine vs. seated) provided greater associations with the various markers of training adaptation. Thirteen players (age = 25.8 ± 3.0 years, height = 178.1 ± 6.7 cm, weight = 69.7 ± 7.6 kg) were monitored throughout four successive training camps preceding the Asia Cup. Daily measures of the root-mean square of successive differences were used to calculate the mean (LnRMSSDM) and coefficient of variation (LnRMSSDCV) for each camp. Averages were also determined for Hooper's Index and session ratings of perceived exertion (sRPE). HRex and CMJ were tested at the start of each camp. RESULTS: Seated LnRMSSDCV, HRex, CMJ, and sRPE increased at camp 3 (p < 0.05), then reverted to values similar to camp 2. Changes in seated LnRMSSDM were associated with changes in HRex (r = -0.68 to -0.71, p < 0.05). Occasional associations (p < 0.05) were observed between LnRMSSDCV and Hooper's Index (r = 0.59) and CMJ (r = -0.57), and changes in HRex (r = 0.69) and HRR (r = -0.62). CONCLUSIONS: A reduced cardiorespiratory response to a standardized submaximal workload was associated with increased seated LnRMSSDM. Higher seated LnRMSSDCV was observed in response to increased sRPE and was often associated with decrements in various status markers. Seated LnRMSSD provided more associations with indicators of training adaptation than supine measures.