Morphogenetic Variability and Hypertension in Ischemic Stroke Patients—Preliminary Study

Abstract

In this study, we evaluated and compared the morphogenetic variability and the degree of recessive homozygosity in patients with manifested ischemic stroke compared to healthy controls. We have evaluated 120 patients with manifested ischemic stroke, of which 64 did not have hypertension and 56 have hypertension. For comparison, we additionally tested 194 healthy individuals without manifested ischemic stroke (controls). For the estimation of the degree of recessive homozygosity, we have performed the homozygously recessive characteristics (HRC) test and tested 19 HRCs. There was a significant difference in the individual variations of 19 HRCs between the controls and patients with manifested ischemic stroke (∑χ2 = 60.162, p < 0.01). The mean values of the tested HRCs significantly differed between the controls and group with manifested ischemic stroke (Controls − 5.71 ± 1.61, Ischemic stroke group − 6.25 ± 1.54, p = 0.012). For the tested individuals with hypertension, the mean values of HRCs did not significantly differ between the controls and those that had manifested ischemic stroke (Controls − 5.28 ± 1.75, Ischemic stroke group − 5.64 ± 1.48, p = 0.435). We found a significant difference in the frequencies of HRCs between those with and without hypertension for controls (p < 0.003) and for those with manifested ischemic stroke (p < 0.001). There are increased degrees of recessive homozygosity along with decreased variability in patients with manifested ischemic stroke compared to controls.

Morphogenetic Variability as Potential Biomarker of Functional Outcome After Ischemic Stroke

“…Numerous studies we performed show that a higher degree of genetic homozygosity leads to a decrease in genetic variability in what may change, together with an increase of genetic loads and genetic physiological homeostasis [12,13,17,24,25,26]. We may presume that all this influence decreases the number of possible body responses to action in numerous environmental factors.…”

“…A higher degree of genetic homozygosity, followed by a decrease in functional improvement and increase in variability of functional outcome, particularly three months post-discharge for both FIM and BI, might bring these patients into a specific state of genetic-physiological homeostasis where certain mechanisms will influence the potential for functional recovery, along with medicamentous and rehabilitation treatment. Furthermore, it is worth mentioning that an increase in genetic (recessive) homozygosity could enlarge the genetic load degree, potentially causing a decrease in body immunity [24], with the potential effects on the ability of the organism to respond in a less wide variation to the treatment methods, thus reducing the potential for functional improvement.…”

Genetic homozygosity as a marker of smoking dependency

“…The HRC-test that has been developed by authors of Belgrade population genetics school is used to investigate the proportion of homozygously-recessive clearly-expressed traits in tested respondents as markers of chromosomal homozygosities, pointing to the degree of genetic homozygosity in humans (MARINKOVIC et al, 2008;NIKOLIC et al, 2012a;MARINKOVIC et al, 1994;MARINKOVIC and CVJETICANIN, 2013). Such test could be considered as a method for estimating the individual homozygosity and is done by the direct observation of defined phenotype traits (MARINKOVIC et al, 2008;NIKOLIC et al, 2012a;MARINKOVIC et al, 1994;MARINKOVIC and CVJETICANIN, 2013;NIKOLIC et al, 2010;MILAŠINOVIĆ et al, 2017;NIKOLIC et al, 2012b;KARAN et al, 2018;SAVIC et al, 2018;PETRICEVIC and CVJETICANIN, 2011;CVJETICANIN and MARINKOVIC, 2009;CVJETIĆANIN, 2009). To preserve the same objectivity and equal criteria for estimation of HRCs presence, one person performed the testing on both studied population samples.…”

“…Presence of a higher degree of recessive homozygosity might bring tested sample of individuals with a pattern of smoking dependence into a characteristic state of genetic-physiological homeostasis where certain processes could have the influence in the maintenance of smoking dependence. Moreover, an increase in recessive homozygosity might enlarge the degree of genetic loads, thus potentially causing a decrease in body immunity (MARINKOVIC and CVJETICANIN, 2013;SAVIC et al, 2018) when the organism could respond in a less wider variation to the mechanisms involved in the maintenance of smoking dependence. Further, significant difference in the individual variations of tested HRCs between these two groups of individuals (ΣX 2 C/S=61.400; p<0.001; Table 1), % of Individuals could suggest possible population-genetic difference with possible certain preferential phenotypes for greater potential for smoking dependence .…”

Morphogenetic dispositions for variability in acute kidney injury after cardiac surgery: Pilot study

“…Despite the numerous morphophysiological and genetic studies that were previously conducted (6)(7)(8)(9), it is still a challenging task to establish expected phenotype variations in not only healthy human individuals but also in diseased groups as well.…”