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The current study focuses on the ability to improve cognitive function after stroke with interventions administered at delayed/chronic time points. In light of recent studies demonstrating delayed GABA antagonists improve motor function, we utilized electrophysiology, biochemistry and neurobehavioral methods to investigate the role of a5 GABAA receptors on hippocampal plasticity and functional recovery following ischemic stroke. Male C57Bl/6 mice were exposed to 45 min transient middle cerebral artery occlusion and analysis of synaptic and functional deficits performed 7 or 30 days after recovery. Our findings indicate that hippocampal long-term potentiation (LTP) is impaired 7 days after stroke and remain impaired for at least 30 days. We demonstrate that ex vivo administration of L655,708 reversed ischemia-induced plasticity deficits and importantly, in vivo administration at delayed time-points reversed stroke-induced memory deficits. Western blot analysis of hippocampal tissue reveals proteins responsible for GABA synthesis are upregulated (GAD65/67 and MAOB), increasing GABA in hippocampal interneurons 30 days after stroke. Thus, our data indicate that both synaptic plasticity and memory impairments observed after stroke are caused by excessive tonic GABA activity, making inhibition of specific GABA activity at delayed timepoints a potential therapeutic approach to improve functional recovery and reverse cognitive impairments after stroke. [ABSTRACT FROM AUTHOR]

B Introduction: b Data on obesity and diabetes in the acute respiratory distress syndrome (ARDS) are mixed. Previously, a metabolic sub-phenotype, characterized by obesity, diabetes, and hypertension, was associated with COVID-19 ARDS development and mortality. B Conclusions: b Obesity, diabetes, and hypertension are equal contributors to a metabolic sub-phenotype of non-COVID-19 ARDS that is significantly associated with lower mortality. [Extracted from the article]

B DISCUSSION: b Differential diagnosis of RV masses include benign or malignant tumors, infectious or inflammatory masses and thrombus. Most reported cases of RV thrombus are almost always associated with Pulmonary embolism (PE) and have a high mortality rate if not treated early. [Extracted from the article]

WHAT "LEADS" TO PLEURAL EFFUSION B INTRODUCTION: b Post-cardiac injury syndrome (PCIS) was first described in 1953 in patients developing fever and pleuritic chest pain after mitral valve surgery.1 It refers to inflammatory response to cardiac injury and is often characterized by pleuro-pericarditis with effusion. We report a patient who developed this syndrome following dual-chamber pacemaker insertion. [Extracted from the article]

B CASE PRESENTATION: b A 53-year-old male with a history of morbid obesity, obesity hypoventilation syndrome (OHS) and obstructive sleep apnea (OSA) was admitted for recurrent falls. While the respiratory failure is due to weakness of respiratory muscles, severe bulbar (oropharyngeal) muscle weakness often accompanies the respiratory muscle weakness or may be the predominant feature in some patients. B CONCLUSIONS: b Even though the patient had obvious causes for hypercapnia like OSA and OHS, complete PFT's with inspiratory and expiratory pressures were done which lead to the diagnosis of MG. [Extracted from the article]

OBJECTIVES: Metabolic syndrome is known to predict outcomes in COVID-19 acute respiratory distress syndrome (ARDS) but has never been studied in non- COVID-19 ARDS. We therefore aimed to determine the association of metabolic syndrome with mortality among ARDS trial subjects. DESIGN: Retrospective cohort study of ARDS trials' data. SETTING: An ancillary analysis was conducted using data from seven ARDS Network and Prevention and Early Treatment of Acute Lung Injury Network randomized trials within the Biologic Specimen and Data Repository Information Coordinating Center database. PATIENTS: Hospitalized patients with ARDS and metabolic syndrome (defined by obesity, diabetes, and hypertension) were compared with similar patients without metabolic syndrome (those with less than three criteria). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The primary outcome was 28-day mortality. Among 4288 ARDS trial participants, 454 (10.6%) with metabolic syndrome were compared with 3834 controls (89.4%). In adjusted analyses, the metabolic syndrome group was associated with lower 28-day and 90-day mortality when compared with control (adjusted odds ratio [aOR], 0.70 [95% CI, 0.55-0.89] and 0.75 [95% CI, 0.60-0.95], respectively). With each additional metabolic criterion from 0 to 3, adjusted 28-day mortality was reduced by 18%, 22%, and 40%, respectively. In subgroup analyses stratifying by ARDS etiology, mortality was lower for metabolic syndrome vs. control in ARDS caused by sepsis or pneumonia (at 28 d, aOR 0.64 [95% CI, 0.48--0.84] and 90 d, aOR 0.69 [95% CI, 0.53-0.89]), but not in ARDS from noninfectious causes (at 28 d, aOR 1.18 [95% CI, 0.70-1.99] and 90 d, aOR 1.26 [95% CI, 0.77-2.06]). Interaction p = 0.04 and p = 0.02 for 28- and 90-day comparisons, respectively. CONCLUSIONS: Metabolic syndrome in ARDS was associated with a lower risk of mortality in non-COVID-19 ARDS. The relationship between metabolic in- flammation and ARDS may provide a novel biological pathway to be explored in precision medicine-based trials. [ABSTRACT FROM AUTHOR]

The patient was intubated for increased work of breathing and put on high PEEP/low tidal volume per ARDSnet ventilation strategy. The patient had a prolonged hospital stay complicated by a bilateral lower extremity DVT requiring an IVC filter placement, ICU delirium and critical illness myopathy. The patient needed re-intubation for airway protection, but the patient was made DNR and eventually died from the same. [Extracted from the article]

B INTRODUCTION: b Fournier's gangrene is a urological emergency characterized by rapidly progressive fulminant necrotizing infection of the genital, perineal and/or perianal regions. IV Vancomycin and Ertapenem were administered on presentation followed by emergent debridement of bilateral scrotum, perineum and left inguinal region. Journal of Medical Microbiology(2009), 58: 965-967.Lamerton, A. J. "Fournier's Gangrene: Non-Clostridial Gas Gangrene of the Perineum and Diabetes Mellitus.". [Extracted from the article]

The article presents a case study of a 53-year-old man with end-stage renal disease who was found to have asymptomatic metastatic pleural calcifications on a chest Computed Tomography (CT) scan. The condition is rare and can be caused by various factors such as prior pleural inflammation or chronic untreated effusions. The patient did not require treatment for the pleural condition.

Activation of blood coagulation pathways as a component of an allergic response has been studied in animal models. In patients with allergic diseases, clot qualities have been noted to be different in terms of denser fibrin clot with reduced plasmin-mediated clot lysis. Correlation between occupational hypersensitivity pneumonitis (HP) with thromboembolic events is scarce in the general patient population. We present a case of a 52-year-old man with recurrent venous thromboembolism with HP secondary to bioaerosol exposure in a compost plant. Biochemical evaluation found no evidence of underlying hypercoagulable state, with only remarkable findings of elevated levels of total serum immunoglobulin E and raised Aspergillus sp. IgG antibodies. The patient decided to change his working environment to one without exposure to compost or other fungal elements. His symptoms and pulmonary function tests gradually improved without any subsequent intervention. The patient chose against the advice of his care providers to discontinue warfarin anti-coagulation that had been recommended for lifelong duration after recurrent pulmonary thromboembolism. At a 4-year follow-up he has remained free of any further episodes of venous thromboembolic events without any anti-coagulation. Repeated imaging studies after cessation of exposure demonstrated clearance of multiple lung nodules and improvement in DLco. [ABSTRACT FROM AUTHOR]

Cryptococcosis is a global invasive mycosis, commonly encountered in patients with HIV/AIDS with low CD4 counts, diabetics, organ and stem-cell transplant recipients, malignancies, and other patients with immunosuppression. The presentation depends on which organ is usually involved although multi-organ involvement may be present. Here, we describe a young female with an enlarging flank mass, found to have disseminated cryptococcosis in the setting of immunosuppression. [ABSTRACT FROM AUTHOR]

Background: Perivascular stromal cells (PSCs) are a recently identified cell type that comprises a small percentage of the platelet derived growth factor receptor-β+ cells within the CNS perivascular space. PSCs are activated following injury to the brain or spinal cord, expand in number and contribute to fibrotic scar formation within the injury site. Beyond fibrosis, their high density in the lesion core makes them a potential significant source of signals that act on neural cells adjacent to the lesion site.Results: Our developmental analysis of PSCs, defined by expression of Collagen1a1 in the maturing brain, revealed that PSCs first appear postnatally and may originate from the meninges. PSCs express many of the same markers as meningeal fibroblasts, including expression of the retinoic acid (RA) synthesis proteins Raldh1 and Raldh2. Using a focal brain ischemia injury model to induce PSC activation and expansion, we show a substantial increase in Raldh1+/Raldh2+ PSCs and Raldh1+ activated macrophages in the lesion core. We find that RA levels are significantly elevated in the ischemic hemisphere and induce signaling in astrocytes and neurons in the peri-infarct region.Conclusions: This study highlights a dual role for activated, non-neural cells where PSCs deposit fibrotic ECM proteins and, along with macrophages, act as a potentially important source of RA, a potent signaling molecule that could influence recovery events in a neuroprotective fashion following brain injury. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a leading cause of death worldwide and clinical data suggest that children may recover from stroke better than adults; however, supporting experimental data are lacking. We used our novel mouse model of experimental juvenile ischemic stroke (MCAO) to characterize age-specific cognitive dysfunction following ischemia. Juvenile and adult mice subjected to 45-min MCAO, and extracellular field recordings of CA1 neurons were performed to assess hippocampal synaptic plasticity changes after MCAO, and contextual fear conditioning was performed to evaluate memory and biochemistry used to analyze Nogo-A expression. Juvenile mice showed impaired synaptic plasticity seven days after MCAO, followed by full recovery by 30 days. Memory behavior was consistent with synaptic impairments and recovery after juvenile MCAO. Nogo-A expression increased in ipsilateral hippocampus seven days after MCAO compared to contralateral and sham hippocampus. Further, inhibition of Nogo-A receptors reversed MCAO-induced synaptic impairment in slices obtained seven days after juvenile MCAO. Adult MCAO-induced impairment of LTP was not associated with increased Nogo-A. This study demonstrates that stroke causes functional impairment in the hippocampus and recovery of behavioral and synaptic function is more robust in the young brain. Nogo-A receptor activity may account for the impairments seen following juvenile ischemic injury. [ABSTRACT FROM AUTHOR]

Syphilis, also known as the "the great masquerader," is a re-emerging infectious disease in the Western world, and may present with various signs and symptoms, making it difficult to distinguish from other diseases. Nephrotic syndrome due to syphilis has been rarely reported in modern times. Here, we describe a young male with acute hearing loss and peripheral edema, found to have acute nephrotic syndrome in the setting of otosyphilis. Given increasing incidence of syphilis, physicians must remain alert to syphilis as a possible cause of nephrotic syndrome. [ABSTRACT FROM AUTHOR]

B Introduction: b Poor metabolic health increases the risk of COVID-19 acute respiratory distress syndrome (ARDS), however, its relationship with non-COVID-19 ARDS remains controversial. We considered metabolic inflammation to reside along the causal pathway between infection and ARDS outcomes, and as such, stratified for primary ARDS etiology (e.g., sepsis or pneumonia as compared to other primary etiologies). B Results: b Among 4,288 ARDS trial participants, 3,205 (74.7%) had primary ARDS etiologies sepsis or pneumonia and 1,083 (25.3%) aspiration, trauma, transfusions, or other causes. [Extracted from the article]

B Introduction: b Poor metabolic health increases the risk of COVID-19 acute respiratory distress syndrome (ARDS), however, its relationship with non-COVID-19 ARDS remains controversial. We considered metabolic inflammation to reside along the causal pathway between infection and ARDS outcomes, and as such, stratified for primary ARDS etiology (e.g., sepsis or pneumonia as compared to other primary etiologies). B Results: b Among 4,288 ARDS trial participants, 3,205 (74.7%) had primary ARDS etiologies sepsis or pneumonia and 1,083 (25.3%) aspiration, trauma, transfusions, or other causes. [Extracted from the article]

Cerebral ischemia caused by loss of blood supply to the brain during cardiac arrest or stroke are major causes of death and disability. Biological sex is an important factor in predicting vulnerability of the brain to an ischemic insult, with males being at higher risk for cardio-cerebrovascular events than females of the same age. However, relative incidence of stroke between the genders appears to normalize at advanced ages. Therefore, many scientists have focused on the mechanisms of sex differences in outcome following brain ischemic injury, with a particular emphasis on the role of sex steroids. The majority of studies indicate that female sex steroids, such as estrogen and progesterone, play important roles in the relative neuroprotection following cerebral ischemia observed in females. However, less is known about male sex steroids and brain damage. This review describes the state of our knowledge of androgen-related contributions to neurological injury and recovery following cerebral ischemia that occurs following stroke. Experimental studies examining the effects of castration, androgenic agonists and antagonists and aging provide valuable insights into the role of androgens in clinical outcome following cerebrovascular events. [ABSTRACT FROM AUTHOR]

Cerebellar Purkinje cells ( PCs) are particularly sensitive to cerebral ischemia, and decreased GABAA receptor function following injury is thought to contribute to PC sensitivity to ischemia-induced excitotoxicity. Here we examined the functional properties of the GABAA receptors that are spared following ischemia in cultured Purkinje cells from rat and in vivo ischemia in mouse. Using subunit-specific positive modulators of GABAA receptors, we observed that oxygen and glucose deprivation ( OGD) and cardiac arrest-induced cerebral ischemia cause a decrease in sensitivity to the β2/3-subunit-preferring compound, etomidate. However, sensitivity to propofol, a β-subunit-acting compound that modulates β1-3-subunits, was not affected by OGD. The α/γ-subunit-acting compounds, diazepam and zolpidem, were also unaffected by OGD. We performed single-cell reverse transcription-polymerase chain reaction on isolated PCs from acutely dissociated cerebellar tissue and observed that PCs expressed the β1-subunit, contrary to previous reports examining GABAA receptor subunit expression in PCs. GABAA receptor β1-subunit protein was also detected in cultured PCs by western blot and by immunohistochemistry in the adult mouse cerebellum and levels remained unaffected by ischemia. High concentrations of loreclezole (30 μ m) inhibited PC GABA-mediated currents, as previously demonstrated with β1-subunit-containing GABAA receptors expressed in heterologous systems. From our data we conclude that PCs express the β1-subunit and that there is a greater contribution of β1-subunit-containing GABAA receptors following OGD. [ABSTRACT FROM AUTHOR]