Progressive Acute Lower Extremity Ischemia Resulting From Cardiac Myxoma Embolization: A Case Report.

Cardiac myxomas are the most common primary benign tumors of the heart. The occlusion of peripheral arteries and complete obstruction of the abdominal aorta by a tumor embolus presents with distinct clinical manifestations. Herein, we present the case of a 38-year-old male with acute paresthesia, muscle weakness, erythematous, and violaceous changes in skin color localized to the dorsum of the left forefoot initially treated as cutaneous vasculitis. Further studies revealed the total occlusion of the terminal abdominal aorta by a saddle embolus from a cardiac myxoma. A multidisciplinary team consisting of cardiothoracic and vascular surgeons were involved in treating the patient, which resulted in full resolution of the case. This paper details the progression of acute bilateral limb ischemia to chronic limb threatening ischemia resulting from the total occlusion of the terminal abdominal aorta by a saddle embolus.

Effect of Photobiomodulation on an Experimental Model of Lower Limb Ischemia.

Photobiomodulation (PBM) has been shown to be promising for the promotion of angiogenesis. The present study investigated the effects of PBM on vascularization in an animal model of peripheral artery disease. Wistar rats were divided into three groups. The control group received no procedures. The ischemia group was submitted to ligation of the femoral artery of the hindleg. The ischemia + PBM group was submitted to ligation of the femoral artery followed by PBM (660 and 808 nm, 100 mW, 4 J) over the site. Animals with ischemia treated with PBM exhibited comparable results to the control group with regards to the diameter of the α-SMA+ vessels, cross-sectional area of muscle fibers, percentage of collagen and serum concentration of IL-17A, as well as similarities in terms of vertical mobility, temperature of the hindleg, number of acts of grooming, and percentage of movement, indicating a condition like that of limbs unaffected by ischemia.

Analysis of two reperfusion techniques in uterine transplantation in an experimental model.

INTRODUCTION: Uterine transplantation was developed for the treatment of absolute uterine factor infertility. As it is a new modality of transplantation, there is still room for technical improvement. A factor that impacts graft survival in organ transplantation is the warm ischemia time. In uterine transplantation specifically, at least two vascular anastomoses are performed on each side of the uterus, and the graft revascularization takes place when the vascular clamps of the arteries and veins are released on both sides simultaneously. For this reason, the warm ischemia time in uterine transplant is expected to be considerably long. The purpose of this study was to compare the sequential technique of uterine graft revascularization, which aims to reduce the warm ischemia time of the procedure, with the simultaneous revascularization technique. MATERIAL AND METHODS: For the procedure, the uterine auto-transplantation technique was performed using 10 non-pregnant adult ewes weighing about 45 kg, divided into two groups: simultaneous revascularization group (5 animals) and sequential revascularization group (5 animals). To evaluate the groups, we analyzed the procedure and warm ischemia times, graft macroscopy, hemodynamic, laboratory, and histological parameters of the uterus. RESULTS: The sequential revascularization technique group had similar surgical procedure times, and the warm ischemia time was significantly shorter with medians of 32 min in the sequential group versus 72 min in the simultaneous group (p < 0.008). The graft macroscopy and hemodynamic, laboratory, and histological parameters evaluated were similar between the groups. CONCLUSIONS: The sequential revascularization technique proved to reduce the warm ischemia time in the sheep uterine auto-transplantation model without compromising graft viability.

Neuroprotective effect of Bouvardia ternifolia (Cav.) Schltdl via inhibition of TLR4/NF-κB, caspase-3/Bax/Bcl-2 pathways in ischemia/reperfusion injury in rats.

Introduction: Bouvardia ternifolia is a plant known for its traditional medicinal uses, particularly in treating inflammation and oxidative stress. Recent studies have explored its potential in neuroprotection, especially in the context of cerebral ischemia/reperfusion injury, a condition where blood supply returns to the brain after a period of ischemia, leading to oxidative stress and inflammation. This damage is a major contributor to neuronal death and neurodegenerative diseases. Methods: A BCCAO/reperfusion model was induced, followed by treatment with B. ternifolia extract. Various molecular biology methods were employed, including Western blot analysis, gene expression assessment via RT-qPCR, and the measurement of oxidative stress mediators. Results: In the BCCAO/reperfusion model, the compounds in the dichloromethane extract work by targeting various signaling pathways. They prevent the activation of iNOS and nNOS, reducing harmful reactive oxygen and nitrogen species, and boosting antioxidant enzymes like catalase and superoxide dismutase. This lowers oxidative stress and decreases the expression of proteins and genes linked to cell death, such as Bax, Bcl-2, and caspase-3. The extract also blocks the TLR4 receptor, preventing NF-κB from triggering inflammation. Additionally, it reduces the activation of microglia and astrocytes, as shown by lower levels of glial activation genes like GFAP and AiF1. Conclusion: The dichloromethane extract of B. ternifolia demonstrated significant neuroprotective effects in the BCCAO/reperfusion model by modulating multiple signaling pathways. It effectively reduced oxidative stress, inhibited inflammation, and attenuated apoptosis, primarily through the downregulation of key proteins and genes associated with these processes. These findings suggest that the extract holds therapeutic potential for mitigating ischemia/reperfusion-induced neuronal damage.

Ozone therapy mitigates parthanatos after ischemic stroke.

BACKGROUND: Stroke is a leading cause of death worldwide, with oxidative stress and calcium overload playing significant roles in the pathophysiology of the disease. Ozone, renowned for its potent antioxidant properties, is commonly employed as an adjuvant therapy in clinical settings. Nevertheless, it remains unclear whether ozone therapy on parthanatos in cerebral ischemia-reperfusion injury (CIRI). This study aims to investigate the impact of ozone therapy on reducing parthanatos during CIRI and to elucidate the underlying mechanism. METHODS: Hydrogen peroxide (H2O2) was utilized to mimic the generation of reactive oxygen species (ROS) in SH-SY5Y cell reperfusion injury in vitro, and an in vivo ischemic stroke model was established. Ozone saline was introduced for co-culture or intravenously administered to mice. Apoptosis and oxidative stress were assessed using flow cytometry and immunofluorescence. Western blotting was utilized to examine the expression of parthanatos signature proteins. The mechanism by which ozone inhibits parthanatos was elucidated through inhibiting PPARg or Nrf2 activity. RESULTS: The findings demonstrated that ozone mitigated H2O2-induced parthanatos by either upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) or activating peroxisome proliferator-activated receptorg (PPARg). Furthermore, through the use of calcium chelators and ROS inhibitors, it was discovered that ROS directly induced parthanatos and facilitated intracellular calcium elevation. Notably, a malignant feedback loop between ROS and calcium was identified, further amplifying the induction of parthanatos. Ozone therapy exhibited its efficacy by increasing PPARg activity or enhancing the Nrf2 translation, thereby inhibiting ROS production induced by H2O2. Concurrently, our study demonstrated that ozone treatment markedly inhibited parthanatos in stroke-afflicted mice. Additionally, ozone therapy demonstrated significant neuroprotective effects on cortical neurons, effectively suppressing parthanatos. CONCLUSIONS: These findings contribute valuable insights into the potential of ozone therapy as a therapeutic strategy for reducing parthanatos during CIRI, highlighting its impact on key molecular pathways associated with oxidative stress and calcium regulation.

Ultrasonography in the management of lip complications caused by hyaluronic acid.

Ultrasonography is highly accurate for evaluating soft tissues. Given that minimally invasive aesthetic procedures are on the rise, complications have become more prevalent. Thus, ultrasonography holds promise for assisting in the diagnosis and management of complications arising from these interventions. This report highlights the importance of ultrasonography in the treatment of complications caused by hyaluronic acid injection. A patient visited a dental office 24 hours after hyaluronic acid application, presenting pain and bruising in the middle and inferior thirds of the face on the right side. To evaluate blood vessels, the surgeon used Doppler-mode ultrasonography, which enabled the precise application of hyaluronidase to reestablish blood perfusion and preserve adjacent structures. Therefore, to avoid severe outcomes, such as necrosis or even amaurosis, the use of ultrasonography is suggested, improving the precision and safety of these procedures.

ATR-FTIR spectroscopy to evaluate serum protein expression in a murine cerebral ischemia model.

Stroke is a prevalent vascular disease that causes disability and death worldwide. Molecular techniques have been developed to assess serum concentrations of biomarkers associated with this disease, such as some proteins. ATR-FTIR was proposed as an alternative technique to determine protein expression during the early stages of stroke. Serum samples from sham, ischemic, and ischemic treated with estradiol benzoate (EB; as a neuroprotective agent) male rats were evaluated at 0, 2-, 4-, 6-, 12-, and 24-hours post-ischemia. The analysis was developed in the mid-infrared region but mainly focused on the protein region (1500-1700 cm-1), where it was possible to observe the modulation in the absorbance intensity. The peaks at 1545, 1645, 1635, and 1650 cm-1 associated with amide II, amide I, ß-sheets, and α-helixes, respectively, were prominent peaks where protein modulation was observed. The results demonstrate that infrared spectroscopy could be a good alternative technique to determine the modulation of protein expression during stroke events.

Angiotensin-converting enzyme 2 activation attenuates inflammation and oxidative stress in brain death donor followed by rat lung transplantation.

Brain death (BD) provides most of the donor organs destined for lung transplantation (LTx). However, the organs may be affected by inflammatory and oxidative processes. Based on this, we hypothesize that the angiotensin-converting enzyme 2 (ACE2) activation can reduce the lung injury associated with LTx. 3 h after BD induction, rats were injected with saline (BD group) or an ACE2 activator (ACE2a group; 15 mg/kg-1) and kept on mechanical ventilation for additional 3 h. A third group included a control ventilation (Control group) prior to transplant. After BD protocol, left LTx were performed, followed by 2 h-reperfusion. ACE2 activation was associated with better oxygenation after BD management (p = 0.01), attenuating edema (p = 0.05) followed by the reduction in tissue resistance (p = 0.01) and increase of respiratory compliance (p = 0.02). Nrf2 expression was also upregulated in the ACE2a group (p = 0.03). After transplantation, ACE2a group showed lower levels of TNF-α (p = 0.02), IL-6 (p = 0.001), IL-1ß (p = 0.01), ROS (p = 0.004) and MDA (p = 0.002), in addition to higher CAT activity (p = 0.04). In conclusion, our study suggests that ACE2 activation improves anti-inflammatory and antioxidant activity in a model of LTx.

Linking head and heart health: the association between psychiatric outcomes for patients with major depressive disorder and myocardial ischemia - a systematic review.

INTRODUCTION: The development of depression after myocardial infarction is associated with a 2- to 2.5-fold increased risk of all-cause mortality, cardiovascular mortality, and cardiovascular events. The objective of this study was to investigate, through a broad search of the literature, whether major depression is associated with worse psychiatric outcomes in middle-aged patients with myocardial ischemia. METHODS: An extensive search for studies on the association between major depression and myocardial ischemia was conducted in the PubMed, Embase, PsycINFO, and Web of Science databases. Randomized clinical trials of middle-aged patients with myocardial ischemia and concomitant depressive symptoms were included. RESULTS: The 14 articles included in this systematic review did not confirm an association between myocardial ischemia and depression with worse psychiatric outcomes in middle-aged patients. However, worse cardiovascular outcomes have been observed in patients with depression after myocardial infarction. CONCLUSIONS: The findings of this study suggest that major depression increases cardiovascular risk in patients after acute myocardial infarction, possibly because of a more pronounced increase in inflammatory markers. REGISTRATION: This systematic review was registered in the International Prospective Registry of Systematic Reviews (PROSPERO) under the number CRD: 511650.

The Ethanolic Extract of Polygala paniculata L. Blocks Panx1 Channels and Reduces Ischemic Brain Infarct in a Dose- and Sex-Dependent Way.

Polygala paniculata L. is a native plant from tropical America. The therapeutic potential of the hydroalcoholic extract of P. paniculata (HEPp) has been scientifically explored due to folk medicine reports on its action against several afflictions. HEPp contains several bioactive molecules with neuroprotective activities, making it a promising candidate for stroke treatment. This study used electrophysiological, biochemical, and in vivo experiments to evaluate the molecular mechanisms underlying HEPp as a neuroprotective therapy for stroke targeting Pannexin-1 (Panx1). Panx1 is a non-selective channel that opens during ischemia and contributes to neuronal death. HEPp was not toxic to cortical neurons and pre-treatment with the extract reduced neuronal death promoted by oxygen and glucose deprivation in a dose-dependent manner. Additionally, HEPp blocked Panx1 currents in a dose-dependent manner and the effect, which was shown to be partially due to rutin. Animals submitted to photothrombosis and post-treated with HEPp had reduced infarct volume, and the effective dose was lower in males (1 mg/kg) than in females (10 mg/kg). On the other hand, in Panx1 KD mice (50% Panx1 levels), the acute treatment reduced the infarct volume only in males. Upon chronic treatment with HEPp, a reduction in Panx1 protein levels was observed. The current study provides reliable evidence of the neuroprotective properties of HEPp in both in vitro and in vivo models of stroke. The underlying mechanism involves, at least in part, the inhibition of Panx1 channel function and possibly downregulation of protein levels, suppressing the secondary events that lead to apoptosis and inflammation.

Neuroprotective Effect of Flavonoid Agathisflavone in the Ex Vivo Cerebellar Slice Neonatal Ischemia.

Agathisflavone is a flavonoid that exhibits anti-inflammatory and anti-oxidative properties. Here, we investigated the neuroprotective effects of agathisflavone on central nervous system (CNS) neurons and glia in the cerebellar slice ex vivo model of neonatal ischemia. Cerebellar slices from neonatal mice, in which glial fibrillary acidic protein (GFAP) and SOX10 drive expression of enhanced green fluorescent protein (EGFP), were used to identify astrocytes and oligodendrocytes, respectively. Agathisflavone (10 µM) was administered preventively for 60 min before inducing ischemia by oxygen and glucose deprivation (OGD) for 60 min and compared to controls maintained in normal oxygen and glucose (OGN). The density of SOX-10+ oligodendrocyte lineage cells and NG2 immunopositive oligodendrocyte progenitor cells (OPCs) were not altered in OGD, but it resulted in significant oligodendroglial cell atrophy marked by the retraction of their processes, and this was prevented by agathisflavone. OGD caused marked axonal demyelination, determined by myelin basic protein (MBP) and neurofilament (NF70) immunofluorescence, and this was blocked by agathisflavone preventative treatment. OGD also resulted in astrocyte reactivity, exhibited by increased GFAP-EGFP fluorescence and decreased expression of glutamate synthetase (GS), and this was prevented by agathisflavone pretreatment. In addition, agathisflavone protected Purkinje neurons from ischemic damage, assessed by calbindin (CB) immunofluorescence. The results demonstrate that agathisflavone protects neuronal and myelin integrity in ischemia, which is associated with the modulation of glial responses in the face of ischemic damage.

Donor hepatectomy time and liver transplantation outcomes: An opportunity that cannot be dismissed.

The probability of developing primary dysfunction (PD) is a function of the probability of ischemia/reperfusion (I/R) injury. The probability of I/R injury in turn, is a function of several donor and transplantation process variables, among which is ischemia time. Custodio et al studied the duration of a special type of warm ischemia and showed, contrary to what is known, that a longer duration is not statistically different from a shorter one in PD development. This finding opens the door to the unforeseen opportunity of training fellows in performing hepatectomies, since the duration will not jeopardize liver transplant outcomes, albeit with some precautions.

Case report: persistent bilateral complete sciatic artery associated with aneurysmal degeneration.

Persistent sciatic artery is a rare congenital anomaly, with few cases described in the literature. This study presents a case of this embryological variation observed in a patient's lower limb circulatory system. The anatomical description is based on a review of medical records and imaging exams. This case report describes a 63-year-old female patient admitted to the emergency department complaining of severe pain in the right lower limb, with a cold, pale extremity and ecchymosis on the dorsum of the foot. Duplex ultrasound showed no detectable flow in the anterior tibial and fibular arteries and a tardus parvus pattern in the posterior tibial artery. The patient developed loss of movement and fixed cyanosis in the right foot and was referred for urgent thromboembolectomy. However, adequate reperfusion was not seen after the procedure. Angiotomography was performed on the first postoperative day, showing bilateral persistence of the sciatic artery, with aneurysmal degeneration, partially thrombosed, and no opacification of the arterial system downstream of the aneurysm. By the third postoperative day, the patient had developed areas of dry necrosis in the limb, with no perfusion to the ankle, and underwent transfemoral amputation. Despite being a rare condition, it is of great clinical importance because of the high complication rates.

Isquemia intestinal con antecedente de infección por SARS COV2. Reporte de un caso / Intestinal ischemia with a history of SARS COV2 infection. Report of a case

El virus y la enfermedad COVID-19 no solo afectan los pulmones, sino que también pueden dañar otros sistemas de órganos, además de causar coagulopatía, esta coagulopatía se puede prolongar a largo plazo siendo ésta una de las secuelas más importantes. La ausencia de factores predisponentes importantes para la formación de tromboembolismo en este paciente sugirió una relación causal entre el antecedente COVID-19 y la isquemia intestinal.

The virus and the COVID-19 disease not only affect the lungs, but can also damage other organ systems, in addition to causing coagulopathy, this coagulopathy can be prolonged in the long term, this being one of the most important sequelae. The absence of important predisposing factors for the formation of thromboembolism in this patient suggested a causal relationship between a history of COVID-19 and intestinal ischemia. Post Acute Syndrome of COVID-19

In Vivo Tracking and 3D Mapping of Cell Death in Regeneration and Cancer Using Trypan Blue.

Tracking cell death in vivo can enable a better understanding of the biological mechanisms underlying tissue homeostasis and disease. Unfortunately, existing cell death labeling methods lack compatibility with in vivo applications or suffer from low sensitivity, poor tissue penetration, and limited temporal resolution. Here, we fluorescently labeled dead cells in vivo with Trypan Blue (TBlue) to detect single scattered dead cells or to generate whole-mount three-dimensional maps of large areas of necrotic tissue during organ regeneration. TBlue effectively marked different types of cell death, including necrosis induced by CCl4 intoxication in the liver, necrosis caused by ischemia-reperfusion in the skin, and apoptosis triggered by BAX overexpression in hepatocytes. Moreover, due to its short circulating lifespan in blood, TBlue labeling allowed in vivo "pulse and chase" tracking of two temporally spaced populations of dying hepatocytes in regenerating mouse livers. Additionally, upon treatment with cisplatin, TBlue labeled dead cancer cells in livers with cholangiocarcinoma and dead thymocytes due to chemotherapy-induced toxicity, showcasing its utility in assessing anticancer therapies in preclinical models. Thus, TBlue is a sensitive and selective cell death marker for in vivo applications, facilitating the understanding of the fundamental role of cell death in normal biological processes and its implications in disease.

[Analysis of the unicentric registry of the Infarction Code program: retrospective cohort]. / Análisis del registro unicéntrico del programa Código Infarto: cohorte retrospectiva.

Background: Acute coronary syndrome (ACS) is the most serious manifestation of coronary heart disease. The Infarction Code (according to its initialism in Spanish, CI: Código Infarto) program aims to improve the care of these patients. Objective: To describe the clinical presentation and outcomes of CI program in a coronary care unit (CCU). Material and methods: A database of a CCU with 5 years of consecutive records was analyzed. Patients diagnosed with ACS were included. The groups with acute myocardial infarction with and without ST-segment elevation were compared using Student's t, Mann-Whitney U and chi-squared tests. We calculated the relative risk (RR) and 95% confidence intervals (95% CI) of cardiovascular risk factors for mortality. Results: A total of 4678 subjects were analyzed, 78.7% men, mean age 63 years (± 10.7). 80.76% presented acute myocardial infarction with positive ST-segment elevation and fibrinolytic was granted in 60.8% of cases. Percutaneous coronary intervention was performed in 81.4% of patients, which was successful in 82.5% of events. Patients classified as CI presented mortality of 6.8% vs. 11.7%, p = 0.001. Invasive mechanical ventilation had an RR of 26.58 (95% CI: 20.61-34.3) and circulatory shock an RR of 20.86 (95% CI: 16.16-26.93). Conclusions: The CI program decreased mortality by 4.9%. Early fibrinolysis and successful coronary angiography are protective factors for mortality within CCU.

Introducción: el síndrome coronario agudo (SICA) es la manifestación más grave de la enfermedad coronaria. El programa Código Infarto (CI) tiene como objetivo mejorar la atención de estos pacientes. Objetivo: describir la presentación clínica y los resultados del programa CI de una unidad de cuidados coronarios (UCC). Material y métodos: se analizó una base de datos de una UCC con 5 años de registros consecutivos. Se incluyeron pacientes con diagnóstico de SICA. Se compararon los grupos con infarto agudo de miocardio con y sin elevación del segmento ST mediante las pruebas t de Student, U de Mann-Whitney y chi cuadrada. Se calculó el riesgo relativo (RR) y el intervalo de confianza del 95% (IC 95%) de los factores de riesgo cardiovascular para mortalidad. Resultados: se analizaron 4678 sujetos, 78.7% hombres, con media de edad de 63 años (± 10.7). El 80.76% presentó infarto agudo de miocardio con desnivel positivo del segmento ST y se otorgó fibrinolítico en el 60.8% de los casos. Se realizó intervencionismo coronario percutáneo en el 81.4% de los pacientes, el cual fue exitoso en el 82.5% de los eventos. Los pacientes catalogados como CI presentaron mortalidad del 6.8% frente a 11.7%, p = 0.001. La ventilación mecánica invasiva tuvo una RR de 26.58 (IC 95%: 20.61-34.3) y el choque circulatorio una RR de 20.86 (IC 95%: 16.16-26.93). Conclusiones: el programa CI disminuyó 4.9% la mortalidad. La fibrinólisis temprana y la angiografía coronaria exitosa son factores protectores para mortalidad dentro de la UCC.

Hypoxic ischemic encephalopathy (HIE).

Introduction: The morbidity and mortality of acute ischemic hypoxic encephalopathy in newborns have not been dramatically modified over the last 20 years. The purpose of this review is to describe the use of hyperbaric oxygenation therapy (HBOT) in the management of acute ischemic hypoxic encephalopathy in newborns. Methods: A review of the medical literature was conducted on the use of HBOT in the pathophysiology of this condition and its impact on outcomes of patients treated at an early stage. Results: When HBOT is administered promptly, it can promote the survival of the penumbra, modulate the cytokine storm, modify inflammatory cascades, restore mitochondrial function, inhibit apoptosis, reinstate cellular communication and cytoskeleton function, reinstall the functioning of the kinase system, reduce cytotoxic and tissue edema, promote microcirculation, and provide an antioxidant effect. All these secondary mechanisms aid in saving, rescuing, and protecting the marginal tissue. Conclusion: When used promptly, HBOT is a non-invasive adjunct treatment that can preserve the marginal tissue affected by ischemia, hypoxia, meet the metabolic needs of the penumbra, reduce inflammatory cascades, prevent the extension of the damaged tissue, and modulate ischemia-reperfusion injury.

Distinct effects of intravenous bone marrow-derived mesenchymal stem cell therapy on ischemic and non-ischemic lungs after ischemia-reperfusion injury.

BACKGROUND: The preclinical efficacy of mesenchymal stem cell (MSC) therapy after intravenous infusion has been promising, but clinical studies have yielded only modest results. Although most preclinical studies have focused solely on the ischemic lung, it is crucial to evaluate both lungs after ischemia-reperfusion injury, considering the various mechanisms involved. This study aimed to bridge this gap by assessing the acute effects of bone marrow MSC(BM) infusion before ischemic insult and evaluating both ischemic and non-ischemic lungs after reperfusion. METHODS: Eighteen male Wistar rats (403 ± 23 g) were anesthetized and mechanically ventilated using a protective strategy. After baseline data collection, the animals were randomized to 3 groups (n = 6/group): (1) SHAM; (2) ischemia-reperfusion (IR), and (3) intravenous MSC(BM) infusion followed by IR. Ischemia was induced by complete clamping of the left hilum, followed by 1 h of reperfusion after clamp removal. At the end of the experiment, the right and left lungs (non-ischemic and ischemic, respectively) were collected for immunohistochemistry and molecular biology analysis. RESULTS: MSC(BM)s reduced endothelial cell damage and apoptosis markers and improved markers associated with endothelial cell integrity in both lungs. In addition, gene expression of catalase and nuclear factor erythroid 2-related factor 2 increased after MSC(BM) therapy. In the ischemic lung, MSC(BM) therapy mitigated endothelial cell damage and apoptosis and increased gene expression associated with endothelial cell integrity. Conversely, in the non-ischemic lung, apoptosis gene expression increased in the IR group but not after MSC(BM) therapy. CONCLUSION: This study demonstrates distinct effects of MSC(BM) therapy on ischemic and non-ischemic lungs after ischemia-reperfusion injury. The findings underscore the importance of evaluating both lung types in ischemia-reperfusion studies, offering insights into the therapeutic potential of MSC(BM) therapy in the context of lung injury.

No small dilemma: small bowel volvulus mimicking acute coronary syndrome.

Acute abdominal pathologies can cause electrocardiogram (ECG) changes mimicking an acute coronary syndrome (ACS), resulting in diagnostic uncertainty and delay. We report a 65-year-old male with multiple risk factors for ACS who presented with four hours of progressive epigastric and chest pain that resolved in the emergency department. ECG findings were concerning for new deeply inverted T-waves with normal troponins, raising concerns for Wellens Syndrome. Emergent heart catheterization was negative but abdominal computed tomography angiography showed occlusion of the superior mesenteric vessels. Subsequent exploratory laparotomy revealed a small bowel volvulus with extensive necrosis, resulting in a 430 cm resection.

Biological Evaluation of Thermosensitive Hydrogels of Chitosan/Hydrolyzed Collagen/ß-GP in an In Vitro Model of Induced Cardiac Ischemia.

Ischemic events can culminate in acute myocardial infarction, which is generated by irreversible cardiac lesions that cannot be restored due to the limited regenerative capacity of the heart. Cardiac cell therapy aims to replace injured or necrotic cells with healthy and functional cells. Tissue engineering and cardiovascular regenerative medicine propose therapeutic alternatives using biomaterials that mimic the native extracellular environment and improve cellular and tissue functionality. This investigation evaluates the effect of thermosensitive hydrogels, and murine fetal ventricular cardiomyocytes encapsulated in thermosensitive hydrogels, on the contractile function of cardiomyocyte regeneration during an ischemic event. Chitosan and hydrolyzed collagen thermosensitive hydrogels were developed, and they were physically and chemically characterized. Likewise, their biocompatibility was evaluated through cytotoxicity assays by MTT, LDH, and their hemolytic capacity. The hydrogels, and cells inside the hydrogels, were used as an intervention for primary cardiomyocytes under hypoxic conditions to determine the restoration of the contractile capacity by measuring intracellular calcium levels and the expressions of binding proteins, such as a-actinin and connexin 43. These results evidence the potential of natural thermosensitive hydrogels to restore the bioelectrical functionality of ischemic cardiomyocytes.