Male sex, increased comorbidity and age more than 85 years could be considered with lower functional recovery capacity potential after hip fracture, and thus should be individually assessed and continuously monitored. Functional status estimation by BBS could be taken as a sensitive predictive value for the evaluation of functional improvement in these patients.

Our study aimed to analyze the reliability, consistency, and temporal stability of the Alberta Infant Motor Scale (AIMS) in Serbian infants. Additionally, we aimed to present a percentile distribution of AIMS in the tested population. The prospective study included 60 infants that were divided into three age groups: 0–3 months, 4–7 months, and 8–14 months. The Serbian version of AIMS was tested by two raters on two different occasions (test/retest) with a five day period between tests. The observed inter-rater reliability (intraclass correlation coefficient (ICC)) was more than 0.75 for all AIMS scores, except for standing (ICC 0.655 = moderate) in the age group of 4–7 months on retest between raters. The observed intra-rater reliability (ICC) was more than 0.75 for all AIMS scores except standing (ICC 0.655 = moderate) in the age group 4–7 months in test–retest for Rater One, and for sitting (ICC 0.671 = moderate) and standing (ICC 0.725 = moderate) in the age group between 0–3 months on test–retest for Rater Two. The Serbian version of AIMS was shown to have high consistency and high reliability with good to high temporal stability. Thus, it can be used in the evaluation of infants’ motor development in Serbia.

Diabetic neuropathy (DN), the most common chronic and progressive complication of diabetes mellitus (DM), strongly affects patients’ quality of life. DN could be present as peripheral, autonomous or, clinically also relevant, uremic neuropathy. The etiopathogenesis of DN is multifactorial, and genetic components play a role both in its occurrence and clinical course. A number of gene polymorphisms in candidate genes have been assessed as susceptibility factors for DN, and most of them are linked to mechanisms such as reactive oxygen species production, neurovascular impairments and modified protein glycosylation, as well as immunomodulation and inflammation. Different epigenomic mechanisms such as DNA methylation, histone modifications and non-coding RNA action have been studied in DN, which also underline the importance of “metabolic memory” in DN appearance and progression. In this review, we summarize most of the relevant data in the field of genetics and epigenomics of DN, hoping they will become significant for diagnosis, therapy and prevention of DN.

IntroductionAssuming that spina bifida (SB) is a genetically controlled disease, the aim of our study was to evaluate the degree of genetic homozygosity and the distribution of AB0 blood types among patients with SB occulta and SB aperta by the homozygously recessive characteristics (HRC) test.Material and methodsOur study included an analysis of the presence, distribution and individual combination of 15 selected genetically controlled morpho-physiological traits in a sample of 100 patients with SB (SB occulta N = 50 and SB aperta N = 50) and a control group of individuals (N = 100).ResultsWe found a statistically significant difference between the mean values for genetic homozygosity (SB 4.5 ±0.3; control 3.0 ±0.2, p < 0.001) and also differences in the presence of certain individual combinations of such traits. In 12 (80.0%) of the 15 observed characteristics, recessive homozygosity was expressed to a greater degree among the group of SB patients, while for 9 (60.0%) of the traits this level of difference was statistically significant (Σχ 2 = 266.3, p < 0.001). There was no difference in average homozygosity of such genetic markers between groups of SB occulta and SB aperta patients, but the type of individual variation in the two studied groups significantly differed. In the group of patients with SB the frequency of 0 blood group was significantly increased while B blood group was significantly decreased.ConclusionsOur results clearly show that there is a populational genetic difference in the degree of genetic homozygosity and variability between the group of patients with SB and individuals without clinical manifestations, indicating a possible genetic component in the aetiopathogenesis of spina bifida.

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IntroductionPatients with spina bifida in the lumbosacral region usually have various degrees of motor and sensory dysfunctions of the lower extremities and anal sphincter. The aim of our study was to evaluate the distribution and differences in frequencies of affected muscles, number of affected muscles and degree of neurogenic lesion between patients with spina bifida occulta (SBO) and spina bifida aperta (SBA).Material and methodsIn 100 patients with SB, 6 muscles in the lower limbs were separately analysed. Due to the number of affected muscles, we evaluated 5 groups of patients: with 1 affected muscle, 2 affected muscles, 3 affected muscles, 4 affected muscles and 5 affected muscles. Three degrees of neurogenic lesions were assessed: mild, moderate and severe.ResultsThe tibialis anterior muscle was most frequently affected in SB patients. The outer anal sphincter was frequently affected in the group of SBA patients. Single muscle affection is frequent in the group of patients with SBO, while in the group of patients with SBA, 4 muscles were significantly frequently affected. The great majority of patients (45.46%) with affected outer anal sphincter (OAS) in the group of SBO were without affection of other muscles, while for the SBA group it was for every third patient. Mild neurogenic lesion was significantly frequent in SBO patients, while severe form was significantly frequent in SBA patients.ConclusionsPatients with SBO usually present with mild to moderate clinical presentation, while multiple root involvement and severe degree of neurogenic lesion is associated more frequently with SBA.

We aimed to evaluate the prevalence of sociodemographic factors with the presence and different degrees of walking difficulties in elderly above 65 years, and to analyze association between evaluated variables and the presence and degree of waking difficulties. In the population based study, 3540 individuals age above 65 years from Serbia were recruited. Further predictors were analyzed: gender, age, level of education, marital status, body mass index (BMI), index of well-being and place of residence. We assessed difficulty in walking half a km on level ground without the use of any aid (Group-1); and difficulty in walking up or down 12 steps (Group-2). Walking difficulties were categorized as no difficulty, some difficulty, a lot of difficulty and cannot do at all. For present difficulty significant predictors were: age (Group-1 (OR-3.022)/Group-2 (OR-3.825)), gender (Group-1 (OR-0.337)/Group-2 (OR-0.311)), educational level (Group-1 (OR-0.689)/Group-2 (OR-0.556)) and place of residence (Group-2 (OR-1.523)) while for non-performing the task, significant predictors were: age (Group-1 (OR-1.998)/Group-2 (OR-2.096)), gender (Group-1 (OR-0.629)/Group-2 (OR-0.495)), BMI (Group-1 (OR-1.219)/Group-2 (OR-1.305)), marital status (Group-1 (OR 0.764)/Group-2 (OR-0.769)), educational level (Group-1 (OR-0.679)/Group-2 (OR-0.719)) and index of well-being (Group-2 (OR-0.764)). Understanding of predictors, and their role on functional decline in elderly is of great importance for the development of specific population-based health programs to prevent further functional loss and preserve achieved functional gains.

IntroductionObesity is a complex condition with multifactorial origin. Assuming that such a state is genetically controlled, the aim of our study was to evaluate the degree of genetic homozygosity among overweight and obese individuals by the homozygously recessive characteristics (HRC) test.Material and methodsWe analysed the presence, distribution and individual combination of 15 selected genetically controlled recessive phenotype traits in a sample of 140 individuals with increased body mass index (overweight individuals n = 100 and obese individuals n = 40) and a control group of normal weight individuals (n = 300).ResultsObese individuals have significantly higher mean values for genetic homozygosity than those with normal weight (normal weight: 3.61 ±1.48; obese: 4.13 ±1.47, p < 0.05) and difference in the presence of certain individual combinations of evaluated phenotype traits (Σχ2 = 76.9; p < 0.01). There was no difference in average homozygosity of such genetic markers between groups of normal weight and overweight individuals (normal weight: 3.61 ±1.48; overweight: 3.93 ±1.51, p > 0.05) and between groups of overweight and obese individuals (overweight: 3.93 ±1.51; obese: 4.13 ±1.47, p > 0.05). There is no difference in the presence of certain individual combinations of evaluated phenotype traits between overweight and obese individuals (Σχ2 = 20.6; p > 0.05).ConclusionsThere is a populational genetic difference in the degree of genetic homozygosity and variability between the group of normal weight and group of obese individuals, indicating a possible genetic component. Overweight and obese individuals have a genetic predisposition, but different expression of genetic loads could be one of the possible explanations for different susceptibility to increase of fat mass and body mass index.