Introduction: Appropriate care and treatment of a wound is the need of the hour whether it is an infected or a non-infected wound. If wound healing is delayed for some reason, it leads to serious complications and further increases the hospital stay and cost of treatment. Herein, we describe a novel antimicrobial wound dressing formulation (VG111), with an objective to generate the preliminary data showing the distinct advantages in various types of wounds.

Method: This case series involved the treatment of acute cases of wounds or chronic wounds that did not respond well to conventional wound healing treatments with VG111 in patients with different etiologies. Thirteen cases of patients that included patients with diabetes, pressure ulcers, burns, trauma, and others treated with VG111 showed rapid wound healing in all the cases, even obviating the need for a graft when complete skin regeneration occurred.

Result: This was illustrated by clearing of the wound infections, reduction/disappearance of the exudate, appearance of intense granulation, epithelialization, and anti-biofilm activity followed by complete wound closure. This VG111 precludes the need for systemic antimicrobial agents in localized infections and therefore, this single agent is an attempt to address the limitations and the drawbacks of the available products.

Conclusion: Despite patients belonging to the old age group and having comorbidities like diabetes, still VG111 showed effective rapid wound healing, and that too without any scar formation in hardto- heal, infected, and non-infected wounds.

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When the production of reactive oxygen species (ROS) is overloaded surpassing the capacity of the reductive rheostat, mammalian cells undergo a series of oxidative damage termed oxidative stress (OS). This phenomenon is ubiquitously detected in many human pathological conditions. Wound healing program implicates continuous neovascularization, cell proliferation, and wound remodeling. Increasing evidence indicates that reactive oxygen species (ROS) have profound impacts on the wound healing process through regulating a series of the physiological and pathological program including inflammatory response, cell proliferation, angiogenesis, granulation as well as extracellular matrix formation. In most pathological wound healing processes, excessive ROS exerts a negative role on the wound healing process. Interestingly, the moderate increase of ROS levels is beneficial in killing bacteria at the wound site, which creates a sterile niche for revascularization. In this review, we discussed the physiological rhythms of wound healing and the role of ROS in this progress, aim to explore the potential manipulation of OS as a promising therapeutic avenue.

OBJECTIVE: Chimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment of various B-cell malignancies. However, it can cause serious adverse effects like immune effector cell-associated neurotoxicity syndrome (ICANS). ICANS is attributed to disruption of the blood-brain barrier due to inflammatory cytokines and increased levels of immune effector cells (IECs) in the cerebrospinal fluid (CSF). Corticosteroids and supportive management are the mainstays of ICANS treatment. However, no guidelines exist for the treatment of steroid-refractory ICANS. Some reports have shown favorable outcomes with no long-term complications in patients with steroid-refractory ICANS treated with intrathecal (IT) chemotherapy.
METHODS: We describe the outcomes of two patients with steroid-refractory ICANS treated with IT chemotherapy. Both patients had refractory large B-cell lymphoma and were not candidates for autologous transplant. They developed steroid-refractory ICANS after CAR T-cell infusion. IT chemotherapy with 12 mg methotrexate and 50 mg hydrocortisone resulted in prompt neurological improvement in both patients. One of them passed away due to multiple other comorbidities, and the other patient continues to do well without any complications.
CONCLUSIONS: IT chemotherapy could be considered as a potential approach for the management of steroid-refractory ICANS based on our experience. Prospective studies are needed to validate this approach.

In the light of thousands of infections and deaths, the World Health Organization (WHO) has declared the outbreak of coronavirus disease (COVID-19) a worldwide pandemic. It has spread to about 22 million people worldwide, with a total of 0.45 million expiries, limiting the movement of most people worldwide in the last 6 months. However, COVID-19 became the foremost health, economic, and humanitarian challenge of the twenty-first century. Measures intended to curb the pandemic of COVID-19 included travel bans, lockdowns, and social distances through shelter orders, which will further stop human activities suddenly and eventually impact the world and the national economy. The viral disease is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). After SARS-CoV-2 virus and Middle East respiratory syndrome (MERS)-related CoV, COVID-19 is the third most significant lethal disease to humans. According to WHO, COVID-19 mortality exceeded that of SARS and MERS since COVID-19 was declared an international public health emergency. Genetic sequencing has recently established that COVID-19 is close to SARS-CoV and bat coronavirus which has not yet been recognized as the key cause of this pandemic outbreak, its transmission, and human pathogen mechanism. This review focuses on a brief introduction of novel coronavirus pathogens, including coronavirus in humans and animals, its taxonomic classification, symptoms, pathogenicity, social impact, economic impact, and potential treatment therapy for COVID-19.

Stroke is a major cause of death and adult disability. However, therapeutic options remain limited. Numerous pathways underlie acute responses of brain tissue to stroke. Early events following ischemic damage include reactive oxygen species (ROS)-mediated oxidative stress and glutamate-induced excitotoxicity, both of which contribute to rapid cell death within the infarct core. A subsequent cascade of inflammatory events escalates damage progression. This review explores potential neuroprotective strategies for targeting key steps in the cascade of ischemia-reperfusion (I/R) injury. NADPH oxidase (NOX) inhibitors and several drugs currently approved by the U.S. Food and Drug Administration including glucose-lowering agents, antibiotics, and immunomodulators, have shown promise in the treatment of stroke in both animal experiments and clinical trials. Ischemic conditioning, a phenomenon by which one or more cycles of a short period of sublethal ischemia to an organ or tissue protects against subsequent ischemic events in another organ, may be another potential neuroprotective strategy for the treatment of stroke by targeting key steps in the I/R injury cascade.

A novel potential treatment technique applied to a glucose biosensor that is based on pyrroloquinoline quinone (PQQ)-dependent glucose dehydrogenase (GDH) and chromium hexacyanoferrate (CrHCF) incorporated into a platinum (Pt) electrode was demonstrated. CrHCF, serving as a mediator, was electrochemically deposited on the Pt electrode as ascertained by CV, SEM, FTIR and XPS measurements. The potential treatment of CrHCF, which converts Fe(II) to Fe(III), enables the glucose detection. The amperometric measurement linearity of the biosensor was up to 20 mM (R = 0.9923), and the detection sensitivity was 199.94 nA/mM per cm(2). More importantly, this biosensor remained stable for >270 days.