Elucidating arsenic-bound proteins in the protein data bank: data mining and amino acid cross-validation through Raman spectroscopy.

The International Agency for Research on Cancer has unequivocally classified inorganic arsenic as a Group 1 carcinogen, definitively establishing its potential to induce cancer in humans. Paradoxically, despite its well-documented toxicity, arsenic finds utility as a chemotherapeutic agent. Notable examples include melarsoprol and arsenic trioxide, both employed in the treatment of acute promyelocytic leukemia. In both therapeutic and hazardous contexts, arsenic can accumulate within cellular environments, where it engages in intricate interactions with protein molecules. Gaining a comprehensive understanding of how arsenic compounds interact with proteins holds immense promise for the development of innovative inhibitors and pharmaceutical agents. These advancements could prove invaluable in addressing a spectrum of arsenic-related diseases. In pursuit of this knowledge, we undertook a systematic exploration of the Protein Data Bank, with a focus on 902 proteins intricately associated with 26 arsenic compounds. Our comprehensive investigation reveals insights into the interactions between these arsenical compounds and amino acids located within a 4.0 Å molecular distance from arsenic-binding sites. Our findings identify that cysteine, glutamic acid, aspartic acid, serine, and arginine frequently engage with arsenic. In complement to our computational analyses, we conducted rigorous Raman spectroscopy studies on the top five amino acids displaying robust interactions with arsenic. The results derived from experimental Raman spectroscopy were meticulously compared with our computational assessments, thereby enhancing the reliability and depth of our investigations. The current study presents a multidimensional exploration into the elaborate interplay between arsenic compounds and proteins. By elucidating the specific amino acids that preferentially interact with arsenic, this study not only contributes to the fundamental understanding of these molecular associations but also lays the foundation for future endeavors in drug design and therapeutic interventions targeting arsenic-related illnesses. Our work at the convergence of toxicology, medicine, and molecular biology carries profound implications for advancing our knowledge of arsenic's dual nature as both a poison and a potential cure.

Late onset ST-elevation myocardial infarction (STEMI) in patient with COVID-19: A case report from Nepal.

Introduction: Although pulmonary consequences are less common in COVID-19 than cardiac issues, it is critical to understand the cause of probable cardiac complications and put the patient on constant watch, especially if they have risk factors such as diabetes mellitus. Case presentation: Here, we report a case of 82-years old male with ST-segment elevated myocardial infarction (STEMI) that was developed as a complication of COVID-19. Discussion: COVID-19 is now known to cause cardiovascular issues such as myocardial damage, heart failure, arrhythmia, and venous thromboembolism. With the involvement of COVID-19, the prevalence of cardiovascular manifestation has increased. The precise processes of extrapulmonary and systemic manifestations following COVID-19 are unknown. There is an elevated risk of cardiovascular harm, notably myocardial infraction followed by acute infection. Conclusion: It is essential to understand the mechanism of potential cardiac complications and to keep the patient on close watch, especially if the patient has risk factors such as diabetes mellitus.

Impact of COVID­19 infection in patients with neurodegenerative diseases with particular focus on Alzheimer's and Parkinson's disease.

Neurodegenerative disorders (NDD) are chronic neurological diseases characterized by loss and/or damage to neurons along with the myelin sheath, and patients are at higher risk of severe infection with the SARS­CoV­2. A comprehensive literature search was performed using relevant terms and inclusion­exclusion criteria. Recent articles, subjects older than 50 years, and articles written in the English language were included, whereas letters to the editor and articles related to pregnant women were excluded from the review study. COVID­19 appears to damage angiotensin­II receptors which cause natural killer cells to lose the ability to clear virus­infected cells, owing to worse outcomes in patients with NDD. COVID­19 can worsen the symptoms of Alzheimer's disease. In addition, COVID­19 worsens drug­responsive motor symptoms in Parkinson's disease (PD) and other symptoms like fatigue and urinary complaints. Vitamin D is essential in decreasing pro­inflammatory and increasing anti­inflammatory cytokines in ongoing COVID­19 infections and reducing angiotensin receptors and, hence, decreasing COVID­19 infection severity. Telemedicine shows promise for patients with NDD but is yet to overcome legal issues and personal barriers. COVID­19 has a significant effect on neurodegenerative conditions, which appears partly to the nature of the NDD and the neuro­invasive capabilities of the SARS­CoV­2. The protective role of vitamin D in patients with NDD further supports this hypothesis. Modifications in current health care, like the telemedicine platform, are required to address the increased risk of serious infection in this population. Further studies will be required to clarify conflicting reports in many fields.

Conformational analysis of two new organotin(IV) structures completed with a CSD survey.

The conformational flexibilities are studied in two new organotin(IV) complexes, namely, trans-dichloridodimethylbis[N,N',N''-tris(2-chlorobenzyl)phosphoric triamide]tin(IV), [Sn(CH3)2(C21H21Cl3N3OP)2Cl2] or Sn(CH3)2Cl2{OP[NHCH2C6H4(2-Cl)]3}2, (I), and bis(dipropylammonium) tetrachloridodimethylstannate(IV), [(CH3CH2CH2)2NH2]2[Sn(CH3)2Cl4], (II), and their analogous structures from the Cambridge Structural Database (CSD). The conformations are considered based on the N-P=O-Sn torsion angles for (I) and the C-C-C-N, C-C-N-C, C-N-C-C and N-C-C-C torsion angles for the two symmetry-independent [CH3CH2CH2NH2CH2CH2CH3]+ cations in (II), and the ±ac±sp±ac (ac = anticlinal and sp = synperiplanar) and ±ap±ap±ap±ap (ap = antiperiplanar) conformations are observed, respectively. In both structures, the four atoms in the corners of the square-planar segment of the octahedral shape around the Sn atom participate in normal hydrogen-bonding interactions as acceptors, which include two O and two Cl atoms for (I), and four Cl atoms for (II). However, the phosphoric triamide ligands block the environment around the Sn atom and limit the hydrogen-bond pattern to form a supramolecular ribbon assembly, while in the presence of small organic cations in (II), a two-dimensional hydrogen-bonded architecture is achieved. The weak interactions π-π, C-H...π and C-Cl...π in (I), and C-H...Cl in (II) do not change the dimensionality of the hydrogen-bond pattern. The 62 CSD structures analogous to (I), i.e. with an SnOPN3 segment (including 83 entries) fall into four categories of conformations based on the N-P=O-Sn torsion angles. The 132 [(CH3CH2CH2)2NH2]+ cations from 85 CSD structures are classified into seven groups based on the torsion angles noted for (II). Most of the CSD structures adopt the same associated conformations noted for (I) and (II). 15 [Sn(CH3)2Cl4]2- anions extracted from the CSD are compared with the structure of (II).