Initial Insult Research Articles

Interleukin-18 and Gelsolin Are Associated with Acute Kidney Disease after Cardiac Catheterization

Patients undergoing cardiac catheterization are at high risk of post-procedure acute kidney injury (AKI) and may experience persistent renal damage after an initial insult, a state known as acute kidney disease (AKD). However, the association between AKD and urinary renal biomarkers has not yet been evaluated in this population. We enrolled 94 patients who underwent elective cardiac catheterization to investigate patterns of urinary renal biomarkers and their associations with post-procedure AKD. Serial urinary renal biomarker levels were measured during pre-procedure, early post-procedure (12-24 h), and late post-procedure (7-10 days) periods. In our investigation, 42.55% of the enrolled patients developed AKD during the late post-procedure period. While the liver-type free-fatty-acid-binding protein level increased sharply during the early post-procedure period, it returned to baseline during the late post-procedure period. In contrast, interleukin-18 (IL-18) levels increased steadily during the post-procedure period. Early post-procedure ratios of IL-18 and gelsolin (GSN) were independently associated with subsequent AKD (odds ratio (95% confidence interval), 4.742 (1.523-14.759) for IL-18 ratio, p = 0.007; 1.812 (1.027-3.198) for GSN ratio, p = 0.040). In conclusion, post-procedure AKD is common and associated with early changes in urinary IL-18 and GSN in patients undergoing cardiac catheterization.

Association Between Admission Ionized Calcium Level and Neurological Outcome of Patients with Isolated Severe Traumatic Brain Injury: A Retrospective Cohort Study.

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Pathophysiological processes following initial insult are complex and not fully understood. Ionized calcium (Ca++) is an essential cofactor in the coagulation cascade and platelet aggregation, and hypocalcemia may contribute to the progression of intracranial bleeding. On the other hand, Ca++ is an important mediator of cell damage after TBI and cellular hypocalcemia may have a neuroprotective effect after brain injury. We hypothesized that early hypocalcemia might have an adverse effect on the neurological outcome of patients suffering from isolated severe TBI. In this study, we aimed to evaluate the relationship between admission Ca++ level and the neurological outcome of these patients. This was a retrospective, single-center, cohort study of all patients admitted between January 2014 and December 2020 due to isolated severe TBI, which was defined as head abbreviated injury score ≥ 4 and an absence of severe (abbreviated injury score > 2) extracranial injuries. The primary outcome was a favorable neurological status at discharge, defined by a modified Rankin Scale of 0-2. Multivariable logistic regression was performed to determine whether admission hypocalcemia (Ca++ < 1.16mmol L-1) is an independent predictor of neurological status at discharge. The final analysis included 201 patients. Hypocalcemia was common among patients with isolated severe TBI (73.1%). Most of the patients had mild hypocalcemia (1 < Ca++ < 1.16mmol L-1), and only 13 (6.5%) patients had Ca++ ≤ 1.00mmol L-1. In the entire cohort, hypocalcemia was independently associated with higher rates of good neurological status at discharge (adjusted odds ratio of 3.03, 95% confidence interval 1.11-8.33, p = 0.03). In the subgroup of 81 patients with an admission Glasgow Coma Scale > 8, 52 (64.2%) had hypocalcemia. Good neurological status at discharge was recorded in 28 (53.8%) of hypocalcemic patients compared with 14 (17.2%) of those with normal Ca++ (p = 0.002). In multivariate analyses, hypocalcemia was independently associated with good neurological status at discharge (adjusted odds ratio of 6.67, 95% confidence interval 1.39-33.33, p = 0.02). Our study demonstrates that among patients with isolated severe TBI, mild admission hypocalcemia is associated with better neurological status at hospital discharge. The prognostic value of Ca++ may be greater among patients with admission Glasgow Coma Scale > 8. Trials are needed to investigate the role of hypocalcemia in brain injury.

EVALUATION OF PROGNOSTIC SIGNIFICANCE OF CRP, IONIC CALCIUM,AND SERUM ALBUMIN IN ACUTE PANCREATITIS

Introduction: Acute pancreatitis is defined as an inflammatory process of pancreas with possible peripancreatic tissue involvement and multi organ dysfunction syndrome with increasing mortality rate. In response to initial insult, acinar cells release proinflammatory cytokines, such as TNF a, IL-1, 2 and 6, and anti-inflammatory mediators such as IL-10 and IL-1 receptor antagonist. Acute pancreatitis is best diagnosed clinically in a patient presenting with 2 of the 3 following criteria.(1) Symptoms consistent with pancreatitis,(2) Serum lipase or amylase levels more than 3 times the laboratorys upper range of normal, and (3) Radiologic features suggestive of pancreatitis, usually using CECT. Usually, the first two criteria are present, and CECT is not required for diagnosis. Aims &amp; Objective: 1. To determine the prognosis of acute pancreatitis on the basis of quantitative value of CRP,SERUM ALBUMIN AND IONIC CALCIUM in admitted patients of HIMS on day of admission and after 48hours.2. To assess the severity of acute pancreatitis as mild,moderate,severe form(as per REVISED ATLANTA CLASSIFICATION 2013) and compare it with values of CRP,SERUM ALBUMIN AND IONIC CALCIUM. Methodology: The study will be conducted over a period of 18months (January 2021 to July 2022) in which all patients coming to General Surgery department at Hind Institute of Medical Sciences, Barabanki, UP with diagnosis of acute pancreatitis will be included. Result: We found that male population was higher than the female population. which was statistically significant. Higher number of patients had Pain in Abdomen Since 3 Days and patients were Alcoholic but this was statistically significant.Association of CRP Value with Day is statistically significant.Association of serum albumin value with Day is statistically significant. Association of Ionic Calcium value with Dayis statistically significant. This study shows that there is relation between se.CRP,se.Albumin and ionic calcium to assess the severity of Acute Pancreatitis.

SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock.

Irrespective of the reason for hypoperfusion, hypocoagulable and/or hyperfibrinolytic hemostatic aberrancies afflict up to one-quarter of critically ill patients in shock. Intensivists and traumatologists have embraced the concept of SHock-INduced Endotheliopathy (SHINE) as a foundational derangement in progressive shock wherein sympatho-adrenal activation may cause systemic endothelial injury. The pro-thrombotic endothelium lends to micro-thrombosis, enacting a cycle of worsening perfusion and increasing catecholamines, endothelial injury, de-endothelialization, and multiple organ failure. The hypocoagulable/hyperfibrinolytic hemostatic phenotype is thought to be driven by endothelial release of anti-thrombogenic mediators to the bloodstream and perivascular sympathetic nerve release of tissue plasminogen activator directly into the microvasculature. In the shock state, this hemostatic phenotype may be a counterbalancing, yet maladaptive, attempt to restore blood flow against a systemically pro-thrombotic endothelium and increased blood viscosity. We therefore review endothelial physiology with emphasis on glycocalyx function, unique biomarkers, and coagulofibrinolytic mediators, setting the stage for understanding the pathophysiology and hemostatic phenotypes of SHINE in various etiologies of shock. We propose that the hyperfibrinolytic phenotype is exemplified in progressive shock whether related to trauma-induced coagulopathy, sepsis-induced coagulopathy, or post-cardiac arrest syndrome-associated coagulopathy. Regardless of the initial insult, SHINE appears to be a catecholamine-driven entity which early in the disease course may manifest as hyper- or hypocoagulopathic and hyper- or hypofibrinolytic hemostatic imbalance. Moreover, these hemostatic derangements may rapidly evolve along the thrombohemorrhagic spectrum depending on the etiology, timing, and methods of resuscitation. Given the intricate hemochemical makeup and changes during these shock states, macroscopic whole blood tests of coagulative kinetics and clot strength serve as clinically useful and simple means for hemostasis phenotyping. We suggest that viscoelastic hemostatic assays such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are currently the most applicable clinical tools for assaying global hemostatic function-including fibrinolysis-to enable dynamic resuscitation with blood products and hemostatic adjuncts for those patients with thrombotic and/or hemorrhagic complications in shock states.

Anti-Inflammatories in the Treatment of Dry Eye Disease: A Review.

Inflammation is an important driver of dry eye disease (DED) pathogenesis. An initial insult that results in the loss of tear film homeostasis can initiate a nonspecific innate immune response that leads to a chronic and self-sustaining inflammation of the ocular surface, which results in classic symptoms of dry eye. This initial response is followed by a more prolonged adaptive immune response, which can perpetuate and aggravate inflammation and result in a vicious cycle of chronic inflammatory DED. Effective anti-inflammatory therapies can help patients exit this cycle, and effective diagnosis of inflammatory DED and selection of the most appropriate treatment are therefore key to successful DED management and treatment. This review explores the cellular and molecular mechanisms of the immune and inflammatory components of DED, and examines the evidence base for the use of currently available topical treatment options. These agents include topical steroid therapy, calcineurin inhibitors, T cell integrin antagonists, antibiotics, autologous serum/plasma therapy, and omega-3 fatty acid dietary supplements.

LINCs Are Vulnerable to Epileptic Insult and Fail to Provide Seizure Control via On-Demand Activation.

Temporal lobe epilepsy (TLE) is notoriously pharmacoresistant, and identifying novel therapeutic targets for controlling seizures is crucial. Long-range inhibitory neuronal nitric oxide synthase-expressing cells (LINCs), a population of hippocampal neurons, were recently identified as a unique source of widespread inhibition in CA1, able to elicit both GABAA-mediated and GABAB-mediated postsynaptic inhibition. We therefore hypothesized that LINCs could be an effective target for seizure control. LINCs were optogenetically activated for on-demand seizure intervention in the intrahippocampal kainate (KA) mouse model of chronic TLE. Unexpectedly, LINC activation at 1 month post-KA did not substantially reduce seizure duration in either male or female mice. We tested two different sets of stimulation parameters, both previously found to be effective with on-demand optogenetic approaches, but neither was successful. Quantification of LINCs following intervention revealed a substantial reduction of LINC numbers compared with saline-injected controls. We also observed a decreased number of LINCs when the site of initial insult (i.e., KA injection) was moved to the amygdala [basolateral amygdala (BLA)-KA], and correspondingly, no effect of light delivery on BLA-KA seizures. This indicates that LINCs may be a vulnerable population in TLE, regardless of the site of initial insult. To determine whether long-term circuitry changes could influence outcomes, we continued testing once a month for up to 6 months post-KA. However, at no time point did LINC activation provide meaningful seizure suppression. Altogether, our results suggest that LINCs are not a promising target for seizure inhibition in TLE.

Platelet-instructed SPP1+ macrophages drive myofibroblast activation in fibrosis in a CXCL4-dependent manner.

Fibrosis represents the common end stage of chronic organ injury independent of the initial insult, destroying tissue architecture and driving organ failure. Here we discover a population of profibrotic macrophages marked by expression of Spp1, Fn1, and Arg1 (termed Spp1 macrophages), which expands after organ injury. Using an unbiased approach, we identify the chemokine (C-X-C motif) ligand 4 (CXCL4) to be among the top upregulated genes during profibrotic Spp1 macrophage differentiation. Invitro and invivo studies show that loss of Cxcl4 abrogates profibrotic Spp1 macrophage differentiation and ameliorates fibrosis after both heart and kidney injury. Moreover, we find that platelets, the most abundant source of CXCL4 invivo, drive profibrotic Spp1 macrophage differentiation. Single nuclear RNA sequencing with ligand-receptor interaction analysis reveals that macrophages orchestrate fibroblast activation via Spp1, Fn1, andSema3 crosstalk. Finally, we confirm that Spp1 macrophages expand in both human chronic kidney disease and heart failure.

Regenerative Effects of Exosomes-Derived MSCs: An Overview on Spinal Cord Injury Experimental Studies.

Spinal cord injury (SCI) is a devastating condition usually induced by the initial mechanical insult that can lead to permanent motor and sensory deficits. At present, researchers are investigating potential therapeutic strategies to ameliorate the neuro-inflammatory cascade that occurs post-injury. Although the use of mesenchymal stromal/stem (MSCs) as a potential therapy in application to regenerative medicine promoted anti-inflammatory and neuroprotective effects, several disadvantages limit their use. Therefore, recent studies have reported the effects of exosomes-derived MSCs (MSC-EXOs) as an innovative therapeutic option for SCI patients. It is noteworthy that MSC-EXOs can maintain the integrity of the blood-spinal cord barrier (BSCB), promoting angiogenic, proliferative, and anti-oxidant effects, as well as immunomodulatory, anti-inflammatory, and antiapoptotic properties. Therefore, in this study, we summarized the preclinical studies reported in the literature that have shown the effects of MSC-EXOs as a new molecular target to counteract the devastating effects of SCI.

Stem Cell Therapies for Functional Recovery After Spinal Cord Injury: Mechanisms, Challenges, and Applications

Context: Spinal cord injury (SCI), a debilitating and catastrophic condition, leads to sensory motor impairments, paralysis, and high mortality. It consists of initial physical insult and secondary injury. Despite much research on SCI treatment, it is still one of the incurable damages because of its complex pathophysiology and limited neuronal regeneration ability. In recent years, stem cell therapy has been a promising and exciting strategy for SCI treatment. Evidence Acquisition: In this review, the articles published in PubMed, Google Scholar, Science Direct, and Scopus from 2000 to 2022 were collected using keywords such as spinal cord injury, stem cell therapy, neuroprotection, neuroregeneration, neurotrophic factors, anti-inflammatory cytokines, and neural cell death. The articles whose full texts were available and met the inclusion criteria were examined. According to the inclusion criteria, 30 articles were analyzed. Results: Stem cell therapy can promote neuroplasticity and neuroregeneration in the damaged spinal cord. Grafted cells can reconstruct nerves and create new circuits after SCI. Stem cell transplantation can also replace lost oligodendrocytes, thus promoting axon remyelination. Many neurotrophic factors and anti-inflammatory cytokines are secreted by transplanted stem cells to decrease secondary injury and neural cell death, thus inhibiting the glial scar formation after SCI. Stem cells also have antioxidant, anti-inflammatory, immunomodulatory, and anti-apoptotic effects. Grafted stem cells can block microglial activation and astrocyte reactivity and enhance revascularization. Conclusions: Stem cells isolated from different tissues can be promising candidates and attractive options for treating the injured spinal cord. Despite remarkable progress in animal studies, cell transplantation's clinical efficacy and adequacy for SCI remain limited and dubitable. Many essential challenges must be considered in translation to the clinic. It is hoped that the invention of new methods and the anti-inflammatory, anti-apoptotic, antioxidant, and neuronal repair properties of stem cells can effectively improve the sensorimotor function of patients with SCI.

Deep Brain Stimulation for Holmes Tremors and Literature Review.

Deep Brain Stimulation for Holmes Tremors and Literature Review.

Role of inflammation in neurological damage and regeneration following spinal cord injury and its therapeutic implications.

Spinal cord injury (SCI) is an incurable trauma that frequently results in partial or complete loss of motor and sensory function. Massive neurons are damaged after the initial mechanical insult. Secondary injuries, which are triggered by immunological and inflammatory responses, also result in neuronal loss and axon retraction. This results in defects in the neural circuit and a deficiency in the processing of information. Although inflammatory responses are necessary for spinal cord recovery, conflicting evidence of their contributions to specific biological processes have made it difficult to define the specific role of inflammation in SCI. This review summarizes our understanding of the complex role of inflammation in neural circuit events following SCI, such as cell death, axon regeneration and neural remodeling. We also review the drugs that regulate immune responses and inflammation in the treatment of SCI and discuss the roles of these drugs in the modulation of neural circuits. Finally, we provide evidence about the critical role of inflammation in facilitating spinal cord neural circuit regeneration in zebrafish, an animal model with robust regenerative capacity, to provide insights into the regeneration of the mammalian central nervous system.

A Multiple Gunshot Suicide Case and the Ability to Act after the Initial Shot: A Forensics Case Report

Multiple gunshot suicides are uncommon and require careful examination, as oftentimes, a single gunshot wound is usually enough to lead to immediate incapacitation. However, an individual’s ability to act after the initial or even more shots is still possible and thus should be acknowledged as it is observed in various cases such as this one. These incidences could be attributed to different reasons, one being the location of the initial insult. In this case report, we present a case of suicide of a 71-year-old male with two gunshot wounds–one to the abdomen and the other to the right temporal area of the head. The characteristics and localization of the wound, type of firearm, and environment are discussed. Such cases pose a challenge to forensic pathologists and require a thorough investigation to be able to make a proper distinction between homicide and suicide.

Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review

The definition of acute kidney injury (AKI), despite improvements in criteria, continues to be based on the level of serum creatinine and urinary output that do not specifically indicate tubular function or injury, or glomerular function or injury that is not significant enough to warrant acute hospitalization of the patient. Finding novel biomarkers of AKI has become a major focus nowadays in nephrology to overcome the further complications of end stage renal disease (ESRD). Many compounds, such as KIM 1, IL 18, NGAL, uromodulin, calprotectin, vanin 1, galactin 3, platelet-derived growth factor (PDGF), urinary Na+/H+ exchanger isoform 3 (NHE3), retinol binding protein (RBP) and Cystatin C, are released from the renal tubules and thus any alterations in tubular function can be detected by measuring these parameters in urine. Additionally, glomerular injury can be detected by measuring immunoglobulin G, nephrin, podocalyxin, podocin, transferrin, netrin-1, pyruvate kinase M2, etc. in urine. These novel biomarkers will be useful for timing the initial insult and assessing the duration of AKI. According to available research, these biomarkers could be applied to assess the onset of AKI, distinguishing between kidney injury and dysfunction, directing the management of AKI, and enhancing disease diagnosis. Therefore, we intend to present recent developments in our understanding of significant biomarkers implicated in various aspects of renal damage. Numerous biomarkers are implicated in various pathophysiological processes that follow renal injury, and can improve prognosis and risk classification.

Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage.

Subarachnoid haemorrhage (SAH) is a common cerebrovascular disease with high disability and mortality rates worldwide. The pathophysiological mechanisms involved in an aneurysm rupture in SAH are complex and can be divided into early brain injury and delayed brain injury. The initial mechanical insult results in brain tissue and vascular disruption with hemorrhages and neuronal necrosis. Following this, the secondary injury results in diffused cerebral damage in the peri-core area. However, the molecular mechanisms of neuronal death following an aneurysmal SAH are complex and currently unclear. Furthermore, multiple cell death pathways are stimulated during the pathogenesis of brain damage. Notably, particular attention should be devoted to necrosis, apoptosis, autophagy, necroptosis, pyroptosis and ferroptosis. Thus, this review discussed the mechanism of neuronal death and its influence on brain injury after SAH.

Dyslipidemia and Inflammation as Hallmarks of Oxidative Stress in COVID-19: A Follow-Up Study.

Recent works have demonstrated a significant reduction in cholesterol levels and increased oxidative stress in patients with coronavirus disease 2019 (COVID-19). The cause of this alteration is not well known. This study aimed to comprehensively evaluate their possible association during the evolution of COVID-19. This is an observational prospective study. The primary endpoint was to analyze the association between lipid peroxidation, lipid, and inflammatory profiles in COVID-19 patients. A multivariate regression analysis was employed. The secondary endpoint included the long-term follow-up of lipid profiles. COVID-19 patients presented significantly lower values in their lipid profile (total, low, and high-density lipoprotein cholesterol) with greater oxidative stress and inflammatory response compared to the healthy controls. Lipid peroxidation was the unique oxidative parameter with a significant association with the total cholesterol (OR: 0.982; 95% CI: 0.969-0.996; p = 0.012), IL1-RA (OR: 0.999; 95% CI: 0.998-0.999; p = 0.021) IL-6 (OR: 1.062; 95% CI: 1.017-1.110; p = 0.007), IL-7 (OR: 0.653; 95% CI: 0.433-0.986; p = 0.042) and IL-17 (OR: 1.098; 95% CI: 1.010-1.193; p = 0.028). Lipid abnormalities recovered after the initial insult during long-term follow-up (IQR 514 days); however, those with high LPO levels at hospital admission had, during long-term follow-up, an atherogenic lipid profile. Our study suggests that oxidative stress in COVID-19 is associated with derangements of the lipid profile and inflammation. Survivors experienced a recovery in their lipid profiles during long-term follow-up, but those with stronger oxidative responses had an atherogenic lipid profile.

Sting to the Heart – Acute Pulmonary Edema following Hymenoptera Sting

Hymenoptera stings have been reported earlier to cause mild local reactions to severe systemic reactions such as anaphylactic shock. Myocardial infarction following insect stings has been widely described. In this case, we describe a 64-year-old male patient who presented with pulmonary edema 4 h after the initial insult followed by a new onset myocardial infarction which was considered to be a variant of Kounis syndrome. The patient was managed in intensive care with diuretics, positive pressure ventilation, and glucocorticoids and made a complete recovery.

INNV-13. INDOLENT H3 K27-ALTERED DIFFUSE MIDLINE GLIOMA

Abstract INTRODUCTION H3 K27-altered diffuse midline glioma (DMG) is an aggressive central nervous system tumor that is universally fatal with a median survival of 8-12 months after diagnosis. Here we present a patient who was incidentally found to have a lesion within the right thalamus on brain magnetic resonance imaging (MRI). Twelve years later, she was found to have a brain mass within the same area with pathology consistent with an H3 K27-altered DMG. Case Description: A 14-year-old female presented with new onset left sided numbness and weakness, blurry vision and a right sided temporal headache. Her past medical history is significant for severe persistent asthma and anoxic brain injury secondary to a cardiopulmonary arrest at 2-years-of-age due to an asthma exacerbation. She has had multiple MRIs of her brain since her initial insult which initially showed the presence of a T2/FLAIR hyperintense lesion within the right medial thalamus in addition to chronic central nervous system changes. The right thalamic lesion was stable in size between images obtained at 2-years and 4-years of age. Her current physical exam is significant for decreased strength to her left upper and lower extremities. Brain MRI with and without contrast is obtained, demonstrating partial effacement of the third ventricle due to mass effect from an enlarging mass from the right thalamus. Biopsy of the lesion demonstrated an H3 K27-altered DMG, WHO grade 4. Our patient went on to receive palliative radiation therapy with 59.4 Gy over 33 fractions. DISCUSSION This case illustrates an unusual presentation of an H3 K27-altered DMG with an indolent course, diagnosed twelve years after the initial MRI finding. This proposes the possibility of multiple factors playing a role in the oncogenesis of these aggressive tumors and that further research is warranted.

Partial body cryotherapy exposure drives acute redistribution of circulating lymphocytes: preliminary findings

Partial body cryotherapy (PBC) is proposed to alleviate symptoms of exercise-induced muscle damage (EIMD) by reducing associated inflammation. No studies have assessed acute PBC exposure on peripheral blood mononuclear cell mobilisation or compared these with cold water immersion (CWI), which may inform how PBC impacts inflammatory processes. This trial examined the impact of a single PBC exposure on circulating peripheral blood mononuclear cells compared to CWI or a control. 26 males were randomised into either PBC (3 min at − 110 to − 140 °C), CWI (3 min at 9 °C), or control (3 min at 24 °C), with blood samples, heart rate, and blood pressure taken before and after exposure. Cytometric analysis determined that CD8+ T-cell populations were significantly elevated after treatments, with PBC increasing CD8+ T cells to a greater degree than either CWI or CON. Natural killer cell counts were also elevated after PBC, with the increase attributed specifically to the CD56loCD16+ cytotoxic subset. This provides the first evidence for the effect of PBC exposure on redistribution of immune cells. An increase in circulating leukocyte subsets such as CD8+ T cells and CD56loCD16+ natural killer cells suggests that PBC may induce a transient mobilisation of lymphocytes. PBC may thus enable a more efficient trafficking of these cells from the circulation to the site of initial cellular insult from exercise, potentially accelerating the process of cellular recovery. This provides novel evidence on the use of PBC as a recovery treatment and may also have applicability in other clinical settings involving the recovery of damaged skeletal muscle.

Management of Facial Second-Degree Burns with Nanocellulose-Based Dressing: A Case Series and Systematic Review.

Previous studies have evaluated the effectiveness of bacterial nanocellulose (BNC) for the treatment of thermal injuries, but the synergic effect of platelet-rich plasma (PRP) with BNC-based dressing for burns still requires further investigation. Herein, we evaluated the effectiveness of BNC dressings in the management of facial burns using PRP. Patients with second-degree facial burns were treated with BNC-based wound dressings after debridement. The burn's depth and epithelialization were evaluated by clinical assessment. Besides using the dressings, we injected PRP subcutaneously into the left-hemifacial burns. The right hemiface was only treated with the dressings. Scar quality was assessed using the Patient and Observer Scar Assessment Scale (POSAS). Eight patients were included with superficial second-degree burns in 75% of the cases and deep second-degree burns in 25%. Overall, dressings were placed 3.25 days after the initial insult. None of the patients presented with complications after dressing placement. Dressing changes were not required, and no further surgical management was necessary. The mean time for epithelialization was 11.4 days. During subgroup analysis, we did not find a significant difference in the epithelialization time when comparing BNC-based dressings (11.8 days) to BNC-based dressings + PRP (11 days, p = 0.429). The mean POSAS scores from a patient (17 vs. 12.3, p = 0.242) and surgeon (13.5 vs. 11.3, p = 0.26) standpoint were not significantly different using BNC-based dressings versus BNC-based dressings + PRP. Nanocellulose-based dressings are effective to treat second-degree facial burns. It enhances reepithelialization with optimal esthetic outcomes with or without PRP.

Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy

Perinatal hypoxic-ischemic encephalopathy (HIE) is an acute disease that may afflict newborns, resulting in variable long- and short-term neurodevelopmental outcomes. Early diagnosis is critical to identifying infants who may benefit from intervention; however, early diagnosis relies heavily on clinical criteria. No molecular or radiological tests have shown promise in detecting early cerebral injury. Studies have shown that magnetic resonance imaging (MRI) can show changes in both blood flow/ischemia and metabolic disruption. However, they have all been used to evaluate the secondary phase of the disease (>12 h) after the onset of the injury. Early diagnosis is critical to rapidly starting therapeutic hypothermia in eligible infants, which is currently recommended to be initiated within 6 h of birth. The rat model of hypoxic-ischemic injury was developed in 1981 and has been validated and used extensively to study changes in brain perfusion, cerebral injury markers, and morphology. However, it has primarily been used as a "late model", evaluating injury several days after the initial ischemic insult. The model has been known to have poor sensitivity in evaluating reliable and reproducible early cerebral changes. The objective of this study was to develop a reliable model to study early gross morphological and radiological markers of HIE using pathological staining and cerebral magnetic resonance imaging/magnetic resonance spectroscopy.