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Malaria is one of the serious diseases threatening human health in Pakistan and contributes to a large proportion of the total malaria deaths in South Asia. However, little is known about the nature and extent of genetic diversity of the malarial parasites circulating in Pakistan. This study was designed to assess the infection status of Plasmodium and the genetic diversity of Plasmodium vivax and Plasmodium falciparum by analyzing msp-3α, msp-3β and msp-1, msp-2 genes respectively using allele specific nested PCR and RFLP assays. For this purpose, 130 field isolates were collected from the individuals who exhibited clinical symptoms associated with malaria in the Kohat region of Khyber Pakhtoonkhwa (KPK), Pakistan. Among 130 blood samples collected, P. vivax was detected in 105/130 (80.8%) and P. falciparum in 21/130 (16.2%). Mixed infections with both parasites were detected in 4/130 (3%) of the isolates. A large number of distinguishable alleles were found for msp genetic markers: 10 alleles for msp-3α and seven for msp-3β with one mixed infection in case of msp-3β. The genotyping of P. falciparum showed that K1+MAD20 mixed genotype was dominant in msp-1 and FC27 in msp-2. The results collectively suggest that P. vivax and P. falciparum populations in this region are highly polymorphic and mixed infections are prevalent.

Background. Valvular heart disease (VHD) is a major contributor to loss of physical function and longevity. Oxidative stress is one of the key causative factors involved in heart disease including VHD. Here, we aimed to illuminate the role and relation of oxidative stress to the VHD risk markers in the human population. Materials and Methods. 150 VHD patients and 103 healthy individuals as control were selected for the study and were divided into three groups: the aortic valve, mitral valve, and combined disease based on valvular calcification. Results. Our results demonstrated enhanced oxidative stress in the VHD condition, as we found elevated levels of reactive oxygen species (ROS) at the serum, supported by an increased level of thiobarbituric acid reactive substances (TBARs) in the cardiac valvular tissues of the VHD patients. In contrast, we experienced declined antioxidants including Super Oxide Dismutase (SOD), catalase (CAT), and peroxidase (POD) activities. Concurrently, increasing levels of C-reactive protein (CRP), high-sensitivity cardiac troponin I (hs-cTnI), and high-sensitivity cardiac troponin T (hs-cTnT) were detected in the aortic, mitral, and combined disease condition, suggesting a key association of oxidative stress to VHD conditions. Furthermore, regression analysis validated a key association between the impairment of the redox system (ROS and antioxidant enzyme activities) and VHD condition. Conclusion. Taken together, dysregulated oxidative stress contributes to the progression of VHD via positively correlating with CRP, hs-TnI, and hs-TnT level.

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