The modular product $G\diamond H$ of graphs $G$ and $H$ is a graph on vertex set $V(G)\times V(H)$. Two vertices $(g,h)$ and $(g^{\prime},h^{\prime})$ of $G\diamond H$ are adjacent if $g=g^{\prime}$ and $hh^{\prime}\in E(H)$, or $gg^{\prime}\in E(G)$ and $h=h^{\prime}$, or $gg^{\prime}\in E(G)$ and $hh^{\prime}\in E(H)$, or (for $g\neq g^{\prime}$ and $h\neq h^{\prime}$) $gg^{\prime}\notin E(G)$ and $hh^{\prime}\notin E(H)$. A set $D\subseteq V(G)$ is a dominating set of $G$ if every vertex outside of $D$ contains a neighbor in $D$. A set $D\subseteq V(G)$ is a total dominating set of $G$ if every vertex of $G$ contains a neighbor in $D$. The domination number $\gamma(G)$ (resp. total domination number $\gamma_{t}(G)$) of $G$ is the minimum cardinality of a dominating set (resp. total dominating set) of $G$. In this work we give several upper and lower bounds for $\gamma(G\diamond H)$ in terms of $\gamma(G),$ $\gamma(H)$, $\gamma_{t}(\overline{G})$ and $\gamma _{t}(\overline{H})$, where $\overline{G}$ is the complement graph of $G$. Further, we fully describe graphs where $\gamma(G\diamond H)=k$ for $k\in\{1,2,3\}$. Several conditions on $G$ and $H$ under which $\gamma (G\diamond H)$ is at most $4$ and $5$ are also given. A new type of simultaneous domination $\bar{\gamma}(G)$, defined as the smallest number of vertices that dominates $G$ and totally dominates the complement of $G,$ emerged as useful and we believe it could be of independent interest. We conclude the paper by proposing few directions for possible further research.

The auditory brainstem response (ABR) is a measure of subcortical activity in response to auditory stimuli. The wave V peak of the ABR depends on stimulus intensity level, and has been widely used for clinical hearing assessment. Conventional methods to estimate the ABR average electroencephalography (EEG) responses to short unnatural stimuli such as clicks. Recent work has moved towards more ecologically relevant continuous speech stimuli using linear deconvolution models called Temporal Response Functions (TRFs). Investigating whether the TRF waveform changes with stimulus intensity is a crucial step towards the use of natural speech stimuli for hearing assessments involving subcortical responses. Here, we develop methods to estimate level-dependent subcortical TRFs using EEG data collected from 21 participants listening to continuous speech presented at 4 different intensity levels. We find that level-dependent changes can be detected in the wave V peak of the subcortical TRF for almost all participants, and are consistent with level-dependent changes in click-ABR wave V. We also investigate the most suitable peripheral auditory model to generate predictors for level-dependent subcortical TRFs and find that simple gammatone filterbanks perform the best. Additionally, around 6 minutes of data may be sufficient for detecting level-dependent effects and wave V peaks above the noise floor for speech segments with higher intensity. Finally, we show a proof-of-concept that level dependent subcortical TRFs can be detected even for the inherent intensity fluctuations in natural continuous speech. Visual abstract Significance statement Subcortical EEG responses to sound depend on the stimulus intensity level and provide a window into the early human auditory pathway. However, current methods detect responses using unnatural transient stimuli such as clicks or chirps. We develop methods for detecting level-dependent responses to continuous speech stimuli, which is more ecologically relevant and may provide several advantages over transient stimuli. Critically, we find consistent patterns of level dependent subcortical responses to continuous speech at an individual level, that are directly comparable to those seen for conventional responses to click stimuli. Our work lays the foundation for the use of subcortical responses to natural speech stimuli in future applications such as clinical hearing assessment and hearing assistive technology.

In order to ensure the long-term sustainability of the conservation process of Norwegian plum germplasm, as well as to enhance the possibility of its utilization, a central plum heritage cultivar collection was established in 2020. In this study, 40 plum accessions maintained at the Ullensvang plum heritage cultivar collection were genetically characterized using a set of nine microsatellite markers recently approved by the ECPGR Prunus working group. The obtained molecular data were used to investigate the genetic identity, diversity, and structure among the analyzed accessions. No redundancies were detected among the plum accessions, which is in stark contrast to the previous molecular study on plum samples collected through an on-farm inventory of Southern Norway. Furthermore, the obtained data indicate that the Ullensvang collection contains a significant genetic diversity of Norwegian plum germplasm, previously held in decentralized sites. With that in mind, this collection can certainly be considered for the role of the National Clonal Plum Germplasm Repository. The nine microsatellite markers, recommended by ECPGR, revealed a genetic structure not entirely tied to previously proposed pomological groups, possibly indicating a history of hybridization among members of the various groups.

Biomonitoring of human populations exposed to chemical substances that can act as potential mutagens or carcinogens, may enable the detection of damage and early disease prevention. In recent years, the comet assay has become an important tool for assessing DNA damage, both in environmental and occupational exposure contexts. To evidence the role of the comet assay in human biomonitoring, we have analysed original research studies of environmental or occupational exposure that used the comet assay in their assessments, following the PRISMA-ScR method (preferred reporting items for systematic reviews and meta-analyses extension for scoping reviews). Groups of chemicals were designated according to a broad classification, and the results obtained from over 300 original studies (n = 123 on air pollutants, n = 14 on anaesthetics, n = 18 on antineoplastic drugs, n = 57 on heavy metals, n = 59 on pesticides, and n = 49 on solvents) showed overall higher values of DNA strand breaks in the exposed subjects in comparison with the unexposed. In summary, our systematic scoping review strengthens the relevance of the use of the comet assay in assessing DNA damage in human biomonitoring studies.

Aim This study aimed to assess the impact of forced repeated swimming stress on serum adiponectin and endothelin-1 levels in Wistar rats, comparing the effects between those fed a standard diet and those on a high-fat diet. Methods Twenty adult male Wistar rats were divided into two dietary groups: a standard food diet group (NFD, n=10) and a high-fat diet group (HFD, n=10). Both groups underwent daily forced swimming stress for six days, with durations increasing from 5 to 30 minutes. The protocol finished in an acute bout of swimming exercise on the seventh day with a duration of 40 minutes. Adherence to ethical guidelines was strictly maintained, and serum adiponectin and endothelin-1 levels were measured pre- and post-exercise using the ELISA method. Results Before swimming, the mean adiponectin levels were 4.30±1.50 ng/mL in the NFD group and 3.53±0.70 ng/mL in the HFD group. Post-exercise, these levels significantly decreased to 2.4±0.84 ng/mL (p=0.003) and 1.58±0.23 ng/mL (p=0.001), respectively. Endothelin-1 levels also showed significant decreases from 0.86 pg/mL (0.74-0.87) to 0.49 pg/mL (0.43-0.62) (p=0.003) in the NFD group, and from 0.89 pg/mL (0.86-0.93) to 0.69 pg/mL (0.60-0.75) (p=0.027) in the HFD group after swimming. Conclusion The study highlighted the significant effects of forced swimming stress on lowering serum adiponectin and endothelin-1 levels in Wistar rats, with more pronounced decreases observed in rats on a high-fat diet. The results of the study suggest the potential of exercise as a crucial component of strategies aimed at managing obesity and improving cardiovascular health, emphasizing the interaction between physical stress and dietary factors on metabolic and cardiovascular biomarkers.

Summary Background Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. Methods The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model—a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates—with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality—which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. Findings The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2–100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1–290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1–211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4–48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3–37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7–9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. Interpretation Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. Funding Bill & Melinda Gates Foundation.

The aim of this paper is focused on reducing sodium chloride content by partial replacement with potassium chloride and magnesium chloride in cooked cheese samples. For the production of cheese, standardized cow's milk from a domestic market producer was used, and the cheese was produced by heating the milk to a temperature of 95°C and coagulation with acetic acid. The one salted only with NaCl was designated as the standard sample, and the other samples were salted with combinations of salts in which NaCl reduction was performed: sample A1 had a ratio of 15% KCl:85% NaCl, sample A2 30% KCl:70% NaCl, sample B1 15% MgCl2:85% NaCl and sample B2 30% MgCl2:70% NaCl. The cheese samples were stored at + 4°C and color parameters and sensory properties were analyzed on the 1st, 3rdand 5thdays of storage. Based on the performed analyses, it was concluded that it is completely acceptable to replace sodium chloride with potassium chloride in the ratio of 15% KCl:85% NaCl. It is acceptable to replace sodium chloride with potassium chloride inthe ratio of 30% KCl:70% NaCl, with the note that on the 5thday of storage there is a gradual deterioration of the sensory properties compared to the samples analyzed on the 1stday of storage. Replacement of sodium chloride with magnesium chloride in the ratios 15% MgCl2:85% NaCl and 30% MgCl2:70% NaCl is not acceptable.As such, it is not recommended in the production of cooked cheeses due to the appearance of a metallic and bitter taste that is present in cheese samples from the 1st to the 5th day of storage. KEYWORDS:cooked cheese, sodium chloride, potassium chloride, magnesium chloride

Toxicity caused by carbon tetrachloride (CCl4) can lead to serious liver injury. The aim of the study is to investigate the protective effects of oregano oil (Origanum minutiflorum extract oil) against CCl4‐induced liver injury. Two doses of oregano oil were used in the experiment: a low dose (LD; 20 mg/kg) and a high dose (HD; 60 mg/kg) during 2 weeks. CCl4 caused severe liver damage, nucleolus destruction in hepatocytes and cytogenetic changes in the nucleus. Indirectly, CCl4 causes decreased protein synthesis and significantly high creatinine and urea values. Hematological disorders have been recorded, such as decreased RBC and hemoglobin concentration, increased WBC and deformability of the erythrocyte membrane. Both doses of oregano oil had protective effects. Improved protein synthesis and high globulins level, creatinine and urea were found in both groups. Cytogenetic changes in the nucleus of hepatocytes were reduced. A high dose of oregano oil had maximal protective effects for RBC, but a very weak effect on hemoglobin synthesis. Also, WBC and lymphocyte values were low. Origanum stimulates protein synthesis and recovery of hepatocytes after liver injury, reduces the deformability of the erythrocyte membrane. High doses of oregano oil decreased WBC and lymphocytes which may lead to a weakening of the immune response. However, high doses are more effective against severe platelet aggregation than low doses, suggesting an effective treatment against thrombocytosis.

In addition to their undeniable importance for industry, natural plant products are widely used in the production of functional food, which, in addition to satisfying nutritional properties, also exhibits certain pharmacological and physiological effects on human health. Chokeberryfruit and products are considered to be excellent sources of polyphenoliccompounds. A large part of polyphenolic compounds from aronia berriesis found in the juice, but the flesh of the berry that remains behind in the juice production process is also richin these bioactive compounds. The aim of the conducted research was to examine the antioxidant potentialof thechokeberry juices from Bosnia and Herzegovina.The antioxidant potentialof chokeberryjuicesin this study wastestedbythe ferric reducing antioxidant power(FRAP)andtotal phenol content (FC). Tests were carried out in other juices for the same parameters in order to compare the obtained values.The research results show that the values of FRAP and total phenols in chokeberry juices vary (20-63 mmol Fe II/L; 850-4930 mgGAE/L), but are significantly higher than in other analyzed juices (7-25 mmol FeII/L; 220–1265 mgGAE/L). By comparing the content of total phenols and FRAP values in pasteurized and unpasteurized chokeberry juice samples, it can be concluded that they are higher in the sample prepared by the pasteurization process. Statistical parameters showthat thelinearcorrelation between thetotal phenols and the FRAP valuesof chokeberry juices (r=0,964; p ˂0,001) and other analysedjuices (r=0,960;p ˂0,001 ) isstatisticallysignificant. KEYWORDS:chokeberry(Aronia melanocarpaL.)juice,antioxidant potential, FC, FRAP

Objectives: The aim of this study was to determine the short-term consequences of coronavirus disease 2019 (COVID-19) infection on pulmonary diffusion in patients with severe (but not critical) and moderately severe COVID-19 pneumonia during three months after COVID-19 infection. Methods: A prospective study included 81 patients with an RT-PCR-test confirmed diagnosis of COVID-19 infection treated in the COVID Department of Lung Diseases of University Clinical Hospital Mostar. Inclusion criteria were ≥18-year-old patients, COVID-19 infection confirmed using real-time RT-PCR, radiologically confirmed bilateral COVID-19 pneumonia, and diffusion capacity of the lungs for carbon monoxide (DLCO) one and three months after COVID-19 infection. The pulmonary function was tested using the MasterScreen Body Jaeger (Jaeger Corporation, Omaha, USA) and MasterScreen PFT Jaeger (Jaeger Corporation, Omaha, USA) according to American Thoracic Society guidelines one and three months after COVID-19 infection. Results: Forced vital capacity significantly increased three months after COVID-19 infection compared to the first-month control (p<0.0005). Also, a statistically significant increase in the FEV1 value (p<0.0005), FEV1%FVC ratio (p<0.005), DLCO/SB (p<0.0005), DLCO/VA value (p<0.0005), and total lung capacity (TLC) (p<0.0005) was observed in all patients. Conclusion: Our study showed that recovery of DLCO/VA and spirometry parameters was complete after three months, while DLCO/SB was below normal values even after three months. Therefore, one month after the COVID-19 infection patients had partial recovery of lung function, while a significant recovery of lung function was observed three months after the COVID-19 infection.