Ruthenium dithiophosphates: synthesis, X-ray crystal structure, spectroscopic and electrochemical properties

The reactions of ammonium salts of dialkyldithiophosphate ligands, (RO)2PS2−NH4+ (R=Me/Et), with RuIIICl3·3H2O in methanol solvent and under N2 atmosphere result in one-electron paramagnetic tris complexes {(RO)2PS2}3RuIII (1) in the solid state. The molecular structures of both complexes were determined by single-crystal X-ray diffraction. This shows the expected pseudo-octahedral geometry with reasonable strain due to the presence of a four-membered chelate ring. The reflectance spectra of the solid complexes display two bands in the range 596–476 nm and in the solid state the complexes exhibit one isotropic EPR signal at 77 K. Although the complexes 1 are stable in the solid state, in solution the complexes are transformed selectively into the diamagnetic and electrically non-conducting sulfur-bridged dimetallic species [{(RO)2PS2}2RuIV(μ-S)2RuIV{S2P(OR)2}2]. The formation of dimeric species in the solution state is authenticated by the electrospray mass spectrum of one representative complex where R=Et (1b). In dichloromethane solution the complexes show two moderately strong sulfur to ruthenium charge-transfer transitions in the range 514–419 nm, and two strong ligand based transitions in the UV region. The complexes exhibit two successive reversible reductions in the ranges 1.01→0.91 V and −0.44→−0.49 V versus SCE corresponding to RuIV–RuIV/RuIII–RuIII and RuIII–RuIII/RuII–RuII couples respectively. Electrochemically or chemically generated first step reduced complexes [{(RO)2PS2}2RuIII(μ-S)2RuIII{S2P(OR)2}2]2− display two ligand to metal charge-transfer transitions in the visible region and in the complexes the two one-electron paramagnetic metal centers (low-spin RuIII, t2g5, S=1/2) are antiferromagnetically coupled. The second step reduced species [{(RO)2PS2}2RuII(μ-S)2RuII{S2P(OR)2}2]4− are observed to be very unstable.© Elsevie

Unveiling HPV's hidden link: Cardiovascular diseases and the viral intrigue

Cardiovascular diseases (CVD) remain a major global health challenge, with an escalating impact on mortality despite advancements in managing conventional risk factors. This review investigates the intricate relationship between human papillomavirus (HPV) and CVD, shedding light on a novel aspect of cardiovascular health. Despite significant progress in understanding and managing traditional CVD risk factors, a substantial proportion of CVD cases lack these conventional markers. Recent research has unveiled HPV, a prevalent sexually transmitted infection, as a potential unconventional risk factor for CVD.This review delves into the underlying mechanisms linking HPV to CVD pathogenesis. HPV's influence on vascular endothelium and induction of systemic inflammation are key contributors. Additionally, HPV disrupts host lipid metabolism, further exacerbating the development of atherosclerosis. The link between HPV and CAD is not merely correlative; it encompasses a complex interplay of virological, immunological, and metabolic factors. Understanding the connection between HPV and CVD holds transformative potential. Insights from this review not only underscore the significance of considering HPV as a crucial risk factor but also advocate for targeted HPV screening and vaccination strategies to mitigate CVD risks. This multidisciplinary exploration bridges the gap between infectious diseases and cardiovascular health, emphasizing the need for a comprehensive approach to combating the global burden of cardiovascular disease. Further research and clinical guidelines in this realm are essential to harness the full scope of preventive and therapeutic interventions, ultimately shaping a healthier cardiovascular landscape

Value of CD16/CD66b/CD45 in comparison to CD55/CD59/CD45 in diagnosis of paroxysmal nocturnal haemoglobinuria: An Indian experience

Background & objectives: Diagnosis of paroxysmal nocturnal haemoglobinuria (PNH), a rare haematopoietic stem cell disorder, is challenging in patients with bone marrow failure (BMF) syndrome like aplastic anaemia (AA). This study was conducted with the aim to test the efficacy of the newly recommended markers viz. anti-CD16 and CD66b antibody over the existing anti-CD55 and CD59 antibody for PNH diagnosis in India. Methods: This study was conducted on 193 suspected cases of PNH by flow cytometry using lyse wash technique to stain the granulocytes with CD16/CD66b and CD55/CD59. Results: Of the 193 suspected cases, 62 patients showed the presence of PNH clone. Forty six patients were detected by CD55/CD59/CD45, whereas 61 were detected by CD16/CD66b/CD45. CD16/CD66b detected 16 (25.8%) additional patients over CD55/CD59 (P<0.05) and was more sensitive in detecting the PNH clone with higher negative predictive value. Most of the patients (11/16) who were picked up by CD16/CD66b were of AA who had small clone sizes. Further, the PNH clones were more discreetly identified in CD16/CD66b plots than by CD55/CD59. Clone size assessed by CD16/CD66b which reflects the clinical severity of classical PNH (thrombosis/haemolysis), was more representative of the underlying clinical condition than CD55/59. Interpretation & conclusions: In our experience of 62 patients of PNH, CD16/CD66b proved to be more efficacious in detecting PNH. The new panel was especially useful in monitoring PNH associated with BMF which had small clone sizes

Demographic and treatment outcome details of patients receiving DOT or SAT for tuberculosis in Andhra Pradesh/Chhattisgarh, India.

†<p>Patients with successful treatment outcomes (cured and completed).</p

Probability of adverse outcomes in patients receiving Category-1 ATT under intermittent DOT or daily SAT.

<p>Probability of adverse outcomes in patients receiving Category-1 ATT under intermittent DOT or daily SAT.</p