Current treatment for spinal cord injury (SCI) is supportive at best; despite great efforts, the lack of better treatment solutions looms large on neurological science and medicine. Curcumin, the active ingredient in turmeric, a spice known for its medicinal and anti-inflammatory properties, has been validated to harbor immense effects for a multitude of inflammatory-based diseases. However, to date there has not been a review on curcumin's effects on SCI. Herein, we systematically review all known data on this topic and juxtapose results of curcumin with standard therapies such as corticosteroids. Because all studies that compare the two show superior results for curcumin over corticosteroids, it could be true that curcumin better acts at the inflammatory source of SCI-mediated neurological injury, although this question remains unanswered in patients. Because curcumin has shown improvements from current standards of care in other diseases with few true treatment options (e.g., osteoarthritis), there is immense potential for this compound in treating SCI. We critically and systematically summarize available data, discuss clinical implications, and propose further testing of this well-tolerated compound in both the preclinical and the clinical realms. Analyzing preclinical data from a clinical perspective, we hope to create awareness of the incredible potential that curcumin shows for SCI in a patient population that direly needs improvements on current therapy.

Coronavirus disease 2019 (COVID-19) has spread to more than 70 countries around the world since its discovery in 2019. More than 2.5 million cases and more than 130,000 deaths have been reported in the United States alone. The common radiological presentation in this disease is noted to be the presence of ground glass opacities and/or consolidations. We report a case of 40-year-old male admitted for COVID-19 and rapidly deteriorated into severe acute respiratory distress syndrome requiring intubation and mechanical ventilation with no prior history of smoking or lung disease. The patient had normal imaging 3 days prior to admission to the hospital and rapidly developed a large pneumatocele with pneumothorax requiring chest tube placement that later on resolved. This is a unique radiologic finding in COVID-19 and likely related to severe inflammation secondary to SARS-CoV-2 infection.

AIM:To study clinical and histopathological features of nonalcoholic fatty liver disease (NAFLD) in patients with and without type 2 diabetes mellitus (T2DM) using updated nonalcoholic steatohepatitis clinical research network (NASH-CRN) grading system.

Though acute pulmonary manifestations of COVID-19 infection are well documented, the long-term sequelae from this viral infection are unclear. We report a case of a patient presenting with persistent respiratory failure after recovery from COVID-19 infection with imaging showing evidence of new onset pulmonary fibrosis. CASE PRESENTATION: 56 year-old Hispanic male with Diabetes Mellitus presents to ED for shortness of breath on exertion after recent hospitalization 16 days ago for Covid-19 infection. He reports progressive dyspnea since discharge, interfering with daily activities including walking to the bathroom and preparing food. He denies dyspnea at rest, cough, constitutional symptoms, or exposure to sick contacts. On his last visit, he was hospitalized for 24 days for Covid-19 pneumonia, and finished a course of antibiotics, hydroxychloroquine and steroids. PaO2/Fio2 ratio was 250, and oxygen requirements were met with nasal cannula, with gradual improvement to 95% saturation on room air. He denied previous hospitalizations, family history, occupational exposures and substance abuse. Vital Signs showed blood pressure 137/91 mmHg, Pulse 116 BPM, RR 22 Temperature 98.4 F. Physical exam was pertinent for fine velcro-like inspiratory and expiratory crackles auscultated at lung bases, saturating 94% on room air at rest but desaturating to 85% after walking 5 steps. Labs revealed chest x-ray showed patchy opacities diffusely worsened from previous visit. CTPE showed no pulmonary embolism, but diffuse bilateral patchy infiltrates with ground glass opacities and bronchiectasis. WBC was 8.64 [K/mm3], absolute lymphocyte count 1.73 K/mm3. BNP, procalcitonin, lactate, autoimmune workup and Echocardiogram were normal. Inflammatory markers were elevated but decreased from last admission. Quantiferon Gold was positive with three negative AFB smears suggesting latent tuberculosis. PFTs showed a moderate restrictive pattern. He was treated with methylprednisolone and oxygen to prevent further fibrosis in areas of active inflammation and isoniazid for latent TB. After symptomatic improvement, he was discharged on home oxygen and steroid taper with outpatient follow up.

Lactic acidosis is the most common anion gap metabolic acidosis in critically ill patients. Type B lactic acidosis is most commonly seen with hematological malignancies, especially lymphomas. It is considered an oncological emergency and is associated with high mortality and poor outcomes if not treated promptly. Here, we present the case of a 48-year-old male who developed Type B lactic acidosis secondary to newly diagnosed diffuse large B-cell lymphoma. This case highlights the importance of including Type B lactic acidosis in the differential diagnosis in a patient with unexplained lactic acidosis and hypoglycemia with otherwise vague symptoms and the need for a thorough search for quick diagnosis and early management.