Jordan weak amenability and orthogonal forms on JB*-algebras

We prove the existence of a linear isometric correspondence between the Banach space of all symmetric orthogonal forms on a JB$^*$-algebra $\mathcal{J}$ and the Banach space of all purely Jordan generalized derivations from $\mathcal{J}$ into $\mathcal{J}^*$. We also establish the existence of a similar linear isometric correspondence between the Banach spaces of all anti-symmetric orthogonal forms on $\mathcal{J}$, and of all Lie Jordan derivations from $\mathcal{J}$ into $\mathcal{J}^*$

On unitary convex decompositions of vectors in a JB∗JB^{*}-algebra

summary:By exploiting his recent results, the author further investigates the extent to which variation in the coefficients of a unitary convex decomposition of a vector in a unital $JB^{*}$-algebra permits the vector decomposable as convex combination of fewer unitaries; certain $C^{*}$-algebra results due to M. Rørdam have been extended to the general setting of $JB^{*}$-algebras

Lipid-Mediated Oxidative Stress and Inflammation in the Pathogenesis of Parkinson's Disease

Parkinson's disease (PD) is a neurodegenerative movement disorder of unknown etiology. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, depletion of dopamine in the striatum, abnormal mitochondrial and proteasomal functions, and accumulation of α-synuclein that may be closely associated with pathological and clinical abnormalities. Increasing evidence indicates that both oxidative stress and inflammation may play a fundamental role in the pathogenesis of PD. Oxidative stress is characterized by increase in reactive oxygen species (ROS) and depletion of glutathione. Lipid mediators for oxidative stress include 4-hydroxynonenal, isoprostanes, isofurans, isoketals, neuroprostanes, and neurofurans. Neuroinflammation is characterized by activated microglial cells that generate proinflammatory cytokines, such as TNF-α and IL-1β. Proinflammatory lipid mediators include prostaglandins and platelet activating factor, together with cytokines may play a prominent role in mediating the progressive neurodegeneration in PD

Neurological complications in patients with plasmodium vivax malaria from Karachi, Pakistan

Background: Malaria remains an endemic disease in Pakistan with an estimated healthcare burden of 1.6 million cases annually, with Plasmodium vivax accounting for 67% of reported cases. P. vivax is the most common species causing malaria outside of Africa, with approximately 13.8 million reported cases worldwide. Method: We report a series of P. vivax cases with cerebral involvement that presented at Aga Khan University Hospital, Karachi, Pakistan. Results: The majority of the patients presented with high-grade fever accompanied by projectile vomiting and abnormal behaviour, seizures, shock and unconsciousness. Seven of 801 patients with P. vivax monoinfection presented or developed cerebral complications. P. vivax infections were diagnosed based on peripheral smears and rapid diagnostic testing. Conclusion: P. vivax infection can lead to severe complications, although not with the frequency of Plasmodium falciparum infection. Current cases highlight an increasing trend of cerebral complications caused by P. vivax

Quasi-Jordan Banach Algebras

We initiate a study of quasi-Jordan normed algebras. It is demonstrated that any quasi-Jordan Banach algebra with a norm 1 unit can be given an equivalent norm making the algebra isometrically isomorphic to a closed right ideal of a unital split quasi-Jordan Banach algebra; the set of invertible elements may not be open; the spectrum of any element is nonempty, but it may be neither bounded nor closed and hence not compact. Some characterizations of the unbounded spectrum of an element in a split quasi-Jordan Banach algebra with certain examples are given in the end

Chemical models important in understanding the ways in which chromate can damage DNA.

Chromate is an established human carcinogen. There have been many studies of the reactivity of chromate aimed at improving understanding of chromate toxicity. In the present paper a number of conclusions of these studies are reviewed and considered in the light of new results obtained in our laboratories. A number of hypotheses are considered; it is concluded, however, that it is impossible to reconcile the generation of strand breaks by chromate during its reduction by glutathione with any simple mechanism involving the generation of DNA lesions by free hydroxyl radicals. Kinetic, spin-trapping, and competition kinetic studies, based on a strand-breaking assay, are reported in support of this conclusion