Schizophrenia and psychosis in general, are health problems for a lot of patients around the world. The causes of developing those mental illnesses are still unknown. Several hypotheses have been introduced to justify these malfunctions. Our article focuses on the glutaminergic hypothesis and how it might lead to the onset of the disorders. The NMDA receptor controls the release of acetylcholine, GABA, and dopamine, while at the same time, it downregulates the 5HT1A receptor and upregulates the 5HT2A. While NMDA antagonists can produce psychosis, NMDA agonists might have the opposite effect. To that end, we found a ligand called 2-Phenylcyclohexane-1-carboxamide and studied its pharmacological properties through the use of the program mcule. What we found was an affinity for the NMDA receptor, the GABA transporter, and acetylcholinesterase. We urge researchers to study further this particular molecule in hopes of identifying all possible in silico interactions and measuring their respective Kds.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes the disease covid-19, is characterized by high mortality among the elderly. The main manifestation that separates this virus from other beta-coronaviruses, is associated with the increased risk of pneumonia, that leads to acute respiratory distress syndrome (ARDS). Any tissue damage in the periphery, is triggered by the excess of cytokines, that are released in the bloodstream, after the initiation of ARDS. Moreover, the virus appears to have the RNAemia trait, a condition that is also witnessed in the case of the human immunodeficiency virus (HIV), but the difference lies in the inability of the former to be transmitted through blood. The angiotensin-converting enzyme 2 receptor (ACE2R) downregulation leads to increased renin-angiotensin system (RAS) activation, and also decreased activity of the Mas receptor, a well-known GPCR, which is the substrate for the ligand angiotensin 1-7, which is produced by the conversion of angiotensin II, by the ACE2R. Last but not least, since pneumonia is one of the main causes of acute lung injury (ALI), the latter, present due to severe damage to the main pulmonary artery, we hence claim that medication used for the treatment of pulmonary hypertension could decrease the fatality risk of pneumonia, and in combination with the standard approach of corticosteroids, antiviral agents, and NO administration, could alleviate, or even eradicate pneumonia symptoms.

Flavocillin, a newly discovered beta-lactam antibiotic, shows promise in its ability to be a TrxR inhibitor. Through our docking experiments, we identified key residues in the docking process, namely ALA295, GLN294, GLY41, GLY12, GLY36, GLY38, SER13, PRO15, ALA16, SER298 that prove the idea that this molecule can increase the susceptibility of various bacteria to beta-lactams, combined with this TrxR inhibitor. Moreover, HIV is known to thrive with the help of reduced oxidative stress. The opposite effect could minimize the viral copies, without the intervention of antiviral drugs.

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The purpose of this article is to emphasize the role of the dopamine D5 receptor in the pathophysiology of schizophrenia, through its actions on the hippocampus, the prefrontal cortex, the striatum, and the basal ganglia. We believe that this receptor, along with other key receptor systems, mainly the 5HT2A/C, the GABA(A), the NMDA, and some nAchRs are vital for long-term potentiation(LTP) and long-term depression(LTD) effects, that control the plasticity of the brain. We assume that the anatomical and physiological traits that have been found, show us a loss of plasticity, which may be intertwined with a degree of atrophy in the brain, noted in a percentage of schizophrenia patients, as a loss of grey matter. Of course, the plasticity is mediated by different receptors in each brain region, and the tissues associated with the dopamine D5 receptor, show us a multi-parameter function, through the LTP and LTD. The effect that the dysfunction of the LTP and LTD has on the brain, is related to the dysconnectivity between parts of the CNS, a trait associated with many neurodevelopmental disorders, especially schizophrenia.