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During 2016 an announcement was made that South Africans will be obliged to pay a 20% “sugar tax’’ that will soon be implemented in order to help curb the rising prevalence of cardio-metabolic diseases. This announcement was met with mixed responses, with strong support from some quarters while others questioned whether it would indeed lead to improved health and well-being of South Africans. As sugar-sweetened beverages (SSBs) constitute a significant portion of added sugars in modern-day diets, it is firmly in the cross-hairs of the new taxation. This perspective article reflects on the proposed sugar tax by exploring the nature of SSB consumption patterns, evaluating epidemiological evidence associating SSB intake to cardio-metabolic diseases risk and by considering examples where a similar tax had previously been introduced. Here data reveal that there is robust evidence supporting a detrimental link between high SSB consumption patterns and the onset of cardiometabolic diseases. It is therefore our strong opinion that the sugar tax option should be pursued in parallel with well-designed, long-term studies to evaluate whether it decreases SSB intake and lowers the prevalence of cardio-metabolic diseases within the South African context.

The authentic teaching and learning approach introduces real-world scenarios into the classroom to better engage Generation Z students. Considering this, we introduced an authentic learning practical exercise (breakfast meal and glycemic variation) to undergraduate biology students at the University of La Reunion (France). Here, students were initially briefed regarding the practical and subsequently determined their baseline glucose values (glucometer). They then consumed 200 mL of fruit juice together with a pain au chocolat (chocolate pastry) and subsequently recorded their glucose values at regular intervals. The last reading was done after 150 min, and they thereafter plotted such data to reveal temporal glycemic variations. During this time, the students also worked on a report to document information collected and began to supply responses to several listed questions. Three weeks after completion of the practical, we evaluated whether this intervention would lead to changes in their views regarding the nature and regularity of breakfast meal intake (employing survey questions). Our findings show that a reasonable proportion of the students indicated that the intervention did change their dietary habits, with 50% sometimes opting for an improved breakfast, whereas 10% also changed their habits albeit for only a small while. Of note, >60% of students indicated that they changed their breakfast intake habits by the end of the endocrinology module. These findings show that the beneficial effects of authentic teaching approaches may elicit relatively long-lasting changes in terms of breakfast behavioral patterns in young people and that such effects may also impact the broader society. New & Noteworthy: This study introduced an authentic learning exercise (endocrinology practical exercise) to undergraduate biology students and ascertained whether it changed their views regarding the nature and regularity of breakfast meals. Here, many altered their breakfast dietary habits, which persisted even after the completion of their module. Authentic teaching approaches can therefore trigger relatively long-lasting changes in terms of breakfast behavioral patterns in young people and may also impact the broader society.

Although there is increased uptake of active learning approaches in especially developed countries, this is still lagging within the African context. The current study therefore focused on the implementation of group learning at Stellenbosch University, with several modifications versus our earlier, pilot study. Students freely formed small groups at the start of a 5-wk cardiovascular physiology lecture series and were apportioned three separate assignments to complete over this period. This included three in-class group-learning sessions, while students also completed group work outside class times. The active learning element was embedded within a constructive alignment framework. Our data revealed that 75% of the students felt that the in-class sessions was a good use of their time and that they progressively improved their assignment scores, i.e., 67.5 ± 9.3%, 72.4 ± 9.8%, and 76.1 ± 9.5% for the first, second, and final ones, respectively (P < 0.0001). Moreover, the average class score for their final test (68 ± 15.1%) was higher when compared with the average class score (57.5 ± 19.4%) calculated for the previous 3 yr (P < 0.0001). This study revealed two major findings: i.e., 1) students displayed a strong positive response regarding the adoption of in-class collaborative group work, and 2) the introduction of such active learning elements correlated with improved student assignment and test scores. Based on these findings, we propose additional modifications (including a shift to more formative assessments) to ensure even greater success with the roll-out of such active learning elements within the African context.

Chronic psychological stress is a recognized, yet understudied risk factor for heart disease, with potential sex-specific effects. We investigated whether chronic stress triggers sex-dependent cardiac dysfunction in isolated Wistar rat hearts subjected to ischemia-reperfusion injury. The experimental cohort underwent 1 h of daily restraint stress for 4 wk versus matched controls, followed by euthanasia (sodium pentobarbital) and heart excision for ex vivo perfusion. Blood analysis revealed sex-specific alterations in stress hormones and inflammatory markers. When compared with controls, chronic restraint stress (CRS) males displayed decreased plasma brain-derived neurotrophic factor (BDNF) levels (P < 0.05), whereas CRS females exhibited elevated plasma adrenocorticotropic hormone (ACTH) (P < 0.01) and reduced corticosterone (P < 0.001) alongside lower serum estradiol (P < 0.001) and estradiol/progesterone ratio (P < 0.01). Of note, CRS females showed increased serum cardiac troponin T (P < 0.05) and tumor necrosis factor-α (TNF-α) (P < 0.01) with suppressed interleukin (IL)-1α, IL-1β, IL-6, and IL-10 levels (P < 0.05) when compared with controls. Ex vivo Langendorff perfusions revealed that CRS female hearts displayed impaired postischemic functional recovery for baseline stroke volume (SV, P < 0.01), work performance (P < 0.05), aortic output (AO, P < 0.05), coronary flow (CF, P < 0.01), and overall cardiac output (CO, P < 0.01) when compared with matched controls and CRS males (P < 0.05). Our findings reveal intriguing sex-specific responses at both the systemic and functional levels in stressed hearts. Here, the dysregulation of stress hormones, proinflammatory state, and potential underlying cardiomyopathy in females following the stress protocol renders them more prone to damage following myocardial ischemia. This study emphasizes the importance of incorporating sex as a biological variable in cardiac research focusing on stress-related cardiomyopathy. NEW & NOTEWORTHY: Although chronic psychological stress is a risk factor for cardiovascular diseases, the underlying mechanisms remain poorly understood. This study revealed that chronic restraint stress resulted in systemic changes (dysregulated stress hormones, proinflammatory state) and potential cardiomyopathy in females versus controls and their male counterparts. The stressed female hearts also displayed reduced functional recovery following ex vivo ischemia-reperfusion. This highlights the importance of incorporating sex as a biological variable in cardiac research. [ABSTRACT FROM AUTHOR]

Teaching physiology can be challenging as students are initially required to understand basic and abstract concepts. Thus students typically view physiology as a "difficult" subject and place an emphasis on rote learning and memorization. Here, we attempted to address this knowledge gap by introducing a pedagogical intervention into the neurophysiology lesson plan of first-year medical and health physiology students at the University of La Réunion. This intervention aimed to better link abstract concepts (e.g., saltatory conduction) and a pathological disorder (multiple sclerosis), together with a discussion of a specific therapeutic intervention (fampridine). Students were required to complete readings (focused on neurophysiology aspects) and two online quizzes before two scheduled in-person lectures. They could also pose questions on a dedicated online forum. Thereafter, the in-person lectures discussed questions posted on the online forum, provided feedback on poorly answered questions (from the online quizzes), and dealt with questions posed by students attending classes. Student feedback regarding the pedagogic intervention was assessed by an anonymous online survey. This survey revealed that the pedagogical intervention was positively received. For example, 94% of respondents agreed the course was well developed, while 80% indicated that the pedagogical intervention was beneficial in terms of their understanding of basic and abstract neurophysiology concepts. Together, this pedagogical intervention was enthusiastically received by the students who better understood how basic nerve physiology concepts fit into the broader context and that such an understanding can result in the development and the roll-out of unique therapeutic interventions for multiple sclerosis. NEW & NOTEWORTHY: First-year physiology students can find the subject challenging, struggling to understand abstract concepts without any context. To address this, we introduced a pedagogical intervention for first-year medical and health physiology students that aimed to link abstract concepts and a pathological disorder, together with a discussion of a specific therapeutic intervention. This pedagogical intervention was well received by first-year physiology students who better understood how basic nerve physiology concepts can be applied within the clinical setting. Listen to this article's corresponding podcast at https://apspublicationspodcast.podbean.com/e/enhancing-the-understanding-of-abstract-neurophysiology-concepts-by-first-year-students/. [ABSTRACT FROM AUTHOR]

Physiology students grapple with large amounts of subject content and hence memorize facts to pass examinations. In parallel, students display limited critical-thinking and creative skills, integration abilities, and/or a deeper engagement with subject content. This study aimed to assess the feasibility of introducing active learning methods (cooperative learning) in a relatively large class to final-year undergraduate physiology students (Bachelor of Science stream) at Stellenbosch University in South Africa. An assignment designed to enhance active and engaged learning was made available to the students (n = 225) during the second week of a 5-wk cardiovascular physiology series of lectures. Students were instructed to freely form working groups (n = 3/group) and the assignment was due by the end of the module. Student groups were expected and encouraged to continuously work on the assignment (outside class time). Three cooperative learning slots were also created during class time, with the lecturer and postgraduate students acting as guides. After the module, students anonymously completed an electronic questionnaire. This study revealed three major findings in terms of implementing cooperative learning in large classes within a South African context, i.e., (1) relatively good reception by students with some indication of group work; (2) it is logistically feasible in relatively large classes, although adequate support is crucial; and (3) additional measures need to be adopted to ensure its success.

The COVID-19 pandemic has revealed a bidirectional relationship between SARS-CoV-2 infection and diabetes mellitus. Existing evidence strongly suggests hyperglycemia as an independent risk factor for severe COVID-19, resulting in increased morbidity and mortality. Conversely, recent studies have reported new-onset diabetes following SARS-CoV-2 infection, hinting at a potential direct viral attack on pancreatic beta cells. In this review, we explore how hyperglycemia, a hallmark of diabetes, might influence SARS-CoV-2 entry and accessory proteins in pancreatic β-cells. We examine how the virus may enter and manipulate such cells, focusing on the role of the spike protein and its interaction with host receptors. Additionally, we analyze potential effects on endosomal processing and accessory proteins involved in viral infection. Our analysis suggests a complex interplay between hyperglycemia and SARS-CoV-2 in pancreatic β-cells. Understanding these mechanisms may help unlock urgent therapeutic strategies to mitigate the detrimental effects of COVID-19 in diabetic patients and unveil if the virus itself can trigger diabetes onset. [ABSTRACT FROM AUTHOR]

This article reflects on the history and current activities of the African Association of Physiological Sciences (AAPS) and discusses recent progress. The AAPS was established in 1989 with the goal of training young physiologists, improving teaching and learning practices, and conducting relevant biomedical research in Africa. Despite initial challenges, there has been significant growth and development in recent years, with the number of affiliate societies increasing from four to 19. However, there are still challenges to overcome, such as limited grant funding, brain drain of African physiologists, and a need for more qualified instructors and research facilities. The article suggests establishing research centers of excellence, promoting collaborations, and lobbying governments for increased funding to address these challenges and further develop the field of Physiology in Africa. [Extracted from the article]

Chronic psychosocial stress is implicated in the onset and progression of noncommunicable diseases, and mechanisms underlying this relationship include alterations to the intracellular redox state. However, such changes are often investigated in isolation, with few studies adopting a system level approach. Here, male Wistar rats were exposed to 9.5 weeks of chronic unpredictable mild stress and redox status assays were subsequently performed on cardiac, hepatic, and brain tissues versus matched controls. The stressed rats displayed an anxious phenotype, with lowered plasma corticosterone levels (p = 0.04 vs. Controls) and higher plasma epinephrine concentrations (p = 0.03 vs. Controls). Our findings showed organ‐specific redox profiles, with stressed rats displaying increased myocardial lipid peroxidation (p = 0.04 vs. Controls) in the presence of elevated nonenzymatic antioxidant capacity (p = 0.04 vs. Controls). Conversely, hepatic tissues of stressed rats exhibited lowered nonenzymatic antioxidant capacity (p < 0.001 vs. Controls) together with increased superoxide dismutase (SOD) activity (p = 0.05 vs. Controls). The brain displayed region‐specific antioxidant perturbations, with increased SOD activity (p = 0.01 vs. Controls) in the prefrontal cortex of the stressed rats. These findings reveal distinct stress‐related organ‐specific vulnerability to redox perturbations and may provide novel insights into putative therapeutic targets. [ABSTRACT FROM AUTHOR]

Growing evidence indicates that the pathophysiological link between the brain and heart underlies cardiovascular diseases, specifically acute myocardial infarction (AMI). Astrocytes are the most abundant glial cells in the central nervous system and provide support/protection for neurons. Astrocytes and peripheral glial cells are emerging as key modulators of the brain-heart axis in AMI, by affecting sympathetic nervous system activity (centrally and peripherally). This review, therefore, aimed to gain an improved understanding of glial cell activity and AMI risk. This includes discussions on the potential role of contributing factors in AMI risk, i.e., autonomic nervous system dysfunction, glial-neurotrophic and ischemic risk markers [glial cell line-derived neurotrophic factor (GDNF), astrocytic S100 calcium-binding protein B (S100B), silent myocardial ischemia, and cardiac troponin T (cTnT)]. Consideration of glial cell activity and related contributing factors in certain brain-heart disorders, namely, blood-brain barrier dysfunction, myocardial ischemia, and chronic psychological stress, may improve our understanding regarding the pathological role that glial dysfunction can play in the development/onset of AMI. Here, findings demonstrated perturbations in glial cell activity and contributing factors (especially sympathetic activity). Moreover, emerging AMI risk included sympathovagal imbalance, low GDNF levels reflecting prothrombic risk, hypertension, and increased ischemia due to perfusion deficits (indicated by S100B and cTnT levels). Such perturbations impacted blood-barrier function and perfusion that were exacerbated during psychological stress. Thus, greater insights and consideration regarding such biomarkers may help drive future studies investigating brain-heart axis pathologies to gain a deeper understanding of astrocytic glial cell contributions and unlock potential novel therapies for AMI. [ABSTRACT FROM AUTHOR]

The heart is a highly metabolic organ with extensive energy demands and hence relies on numerous fuel substrates including fatty acids and glucose. However, oxidative stress is a natural by-product of metabolism that, in excess, can contribute towards DNA damage and poly-ADP-ribose polymerase activation. This activation inhibits key glycolytic enzymes, subsequently shunting glycolytic intermediates into non-oxidative glucose pathways such as the hexosamine biosynthetic pathway (HBP). In this review we provide evidence supporting the dual role of the HBP, i.e. playing a unique role in cardiac physiology and pathophysiology where acute upregulation confers cardioprotection while chronic activation contributes to the onset and progression of cardio-metabolic diseases such as diabetes, hypertrophy, ischemic heart disease, and heart failure. Thus although the HBP has emerged as a novel therapeutic target for such conditions, proposed interventions need to be applied in a context- and pathology-specific manner to avoid any potential drawbacks of relatively low cardiac HBP activity. [ABSTRACT FROM AUTHOR]

Although the underlying mechanisms driving human immunodeficiency virus (HIV)-mediated cardiovascular diseases (CVD) onset and progression remain unclear, the role of chronic immune activation as a significant mediator is increasingly being highlighted. Chronic inflammation is a characteristic feature of CVD and considered a contributor to diastolic dysfunction, heart failure, and sudden cardiac death. This can trigger downstream effects that result in the increased release of pro-coagulant, pro-fibrotic, and pro-inflammatory cytokines. Subsequently, this can lead to an enhanced thrombotic state (by platelet activation), endothelial dysfunction, and myocardial fibrosis. Of note, recent studies have revealed that myocardial fibrosis is emerging as a mediator of HIV-related CVD. Together, such factors can eventually result in systolic and diastolic dysfunction, and an increased risk for CVD. In light of this, the current review article will focus on (a) the contributions of a chronic inflammatory state and persistent immune activation, and (b) the role of immune cells (mainly platelets) and cardiac fibrosis in terms of HIV-related CVD onset/progression. It is our opinion that such a focus may lead to the development of promising therapeutic targets for the treatment and management of CVD in HIV-positive patients. [ABSTRACT FROM AUTHOR]

The mechanisms mediating hyperglycemia-mediated myocardial cell death are poorly defined. Since elevated flux through the hexosamine biosynthetic pathway (HBP) is closely linked with the diabetic phenotype, we hypothesized that hyperglycemia-mediated oxidative stress results in greater O-GlcNAcylation (HBP end product) of the proapoptotic peptide BAD, thereby increasing myocardial apoptosis. H9c2 cardiomyoblasts were exposed to high glucose (33 raM) [+ or -] HBP modulators [+ or -] antioxidant treatment for 5 days vs. matched controls (5.5 mM), and we subsequently evaluated apoptosis by immunoblotting, immunofluorescence staining, and caspase activity measurements. In vitro reactive oxygen species (ROS) levels were quantified by 2',7'-dichlorodihydrofluorescein diacetate staining (fluorescence microscopy and flow cytometry). We determined total and BAD O-GlcNAcylation, respectively, by immunoblotting and immunofluorescence microscopy. The current study shows that high glucose treatment of cells significantly increased the degree of apoptosis. In parallel, overall O-GlcNAcylation, BAD O-GlcNAcylation, and ROS levels were increased. HBP inhibition and antioxidant treatment attenuated these effects, while increased end product levels exacerbated it. As BAD-Bcl-2 dimer formation enhances apoptosis, we performed immunoprecipitation analysis and colocalization and found increased dimerization in cells exposed to hyperglycemia. Our study identified a novel pathway whereby hyperglycemia results in greater oxidative stress and increased HBP activation and BAD O-GlcNAcylation in H9c2 cardiomyoblasts. Since greater BAD-Bc1-2 dimerization increases myocardial apoptosis, this pathway may play a crucial role in diabetes-related onset of heart diseases. oxidative stress; heart; cell death; O-GlcNAc doi: 10.1152/ajpcell.00020.2010.

With the successful roll-out of combination antiretroviral treatment, HIV is currently managed as a chronic illness. Of note, immune activation and chronic inflammation are hallmarks of HIV-1 infection that persists even though patients are receiving treatments. Despite strong evidence linking immune activation and low-grade inflammation to HIV-1 pathogenesis, the underlying mechanisms remain less well-understood. As intracellular metabolism is emerging as a crucial factor determining the fate and activity of immune cells, this review article focuses on how links between early immune responses and metabolic reprograming may contribute to HIV pathogenicity. Here, the collective data reveal that immunometabolism plays a key role in HIV-1 pathogenesis. For example, the shift from quiescent immune cells to its activation leads to perturbed metabolic circuits that are major drivers of immune cell dysfunction and an altered phenotype. These findings suggest that immunometabolic perturbations play a key role in the onset of non-AIDS-associated comorbidities and that they represent an attractive target to develop improved diagnostic tools and novel therapeutic strategies to help blunt HIV-1 pathogenesis. [ABSTRACT FROM AUTHOR]

The cardiac-enriched isoform of acetyl-CoA carboxylase (ACC2) is a key regulator of mitochondrial fatty acid (FA) uptake via carnitine palmitoyl-transferase 1 (CPT1). To test the hypothesis that oxidative metabolism is upregulated in hearts from animals lacking ACC2 (employing a transgenic Acc2-mutant mouse), we assessed cardiac function in vivo and determined rates of myocardial substrate oxidation ex vivo. When examined by echocardiography, there was no difference in systolic function, but left ventricular mass of the Acc2-mutant (MUT) mouse was significantly reduced (~25%) compared with wild-types (WT). Reduced activation of the mammalian target of rapamycin (roTOR) and its downstream target p70S6K was found in MUT hearts. Exogenous oxidation rates of oleate were increased ~22%, and, unexpectedly, exogenous glucose oxidation rates were also increased in MUT hearts. Using a hyperinsulinemic-euglycemic clamp, we found that glucose uptake in MUT hearts was increased by ~83%. Myocardial triglyceride levels were significantly reduced in MUT vs. WT while glycogen content was the same. In parallel, transcript levels of PPAR[alpha] and its target genes, pyruvate dehydrogenase kinase-4 (PDK-4), malonyl-CoA decarboxylase (MCD), and mCPT1, were downregulated in MUT mice. In summary, we report that 1) Acc2-mutant hearts exhibit a marked preference for the oxidation of both glucose and FAs coupled with greater utilization of endogenous fuel substrates (triglycerides), 2) attenuated mTOR signaling may result in reduced heart sizes observed in Acc2-mutant mice, and 3) Acc2-mutant hearts displayed normal functional parameters despite a significant decrease in size. acetyl-CoA carboxylase; fatty acid [beta]-oxidation; glucose oxidation; PPAR[alpha]

We hypothesized the coordinate induction of mitochondrial regulatory genes in the hypertrophied right ventricle to sustain mitochondrial respiratory capacity and contractile function in response to increased load. Wistar rats were exposed to hypobaric hypoxia (11% [O.sub.2]) or normoxia for 2 wk. Cardiac contractile and mitochondrial respiratory function were separately assessed for the right and left ventricles. Transcript levels of several mitochondrial regulators were measured. A robust hypertrophic response was observed in the right (but not left) ventricle in response to hypobaric hypoxia. Mitochondrial [O.sub.2] consumption was increased in the right ventricle, while proton leak was reduced vs. normoxic controls. Citrate synthase activity and mitochondrial DNA content were significantly increased in the hypertrophied right ventricle, suggesting higher mitochondrial number. Transcript levels of nuclear respiratory factor-i, peroxisome proliferator-activated receptor-[gamma]-coactivator-1[alpha], cytochrome oxidase (COX) subunit II, and uncoupling protein-2 (UCP2) were coordinately induced in the hypertrophied right ventricle following hypoxia. UCP3 transcript levels were significantly reduced in the hypertrophied right ventricle vs. normoxic controls. Exposure to chronic hypobaric hypoxia had no significant effects on left ventricular mitochondrial respiration or contractile function. However, COXIV and UCP2 gene expression were increased in the left ventricle in response to chronic hypobaric hypoxia. In summary, we found coordinate induction of several genes regulating mitochondfial function and higher mitochondrial number in a model of physiological right ventricular hypertrophy, linking the efficiency of mitochondrial oxidative phosphorylation and respiratory function to sustained contractile function in response to the increased load. gene expression; mitochondria; hypertrophy; hypobaric hypoxia

Evidence for mitochondrial thioesterase 1 as a peroxisome proliferator-activated receptor-[alpha]-regulated gene in cardiac and skeletal muscle. Am J Physiol Endocrinol Metab 287: E888-E895, 2004. First published August 3, 2004; doi:10.1152/ajpendo.00190.2004.--The physiological role of mitochondrial thioesterase 1 (MTE1) is unknown. It was proposed that MTE1 promotes fatty acid (FA) oxidation (FAO) by acting in concert with uncoupling protein (UCP)3. We previously showed that ucp3 is a peroxisome proliferator-activated receptor-[alpha] (PPAR[alpha])-regulated gene, allowing induction when FA availability increases. On the assumption that UCP3 and MTE1 act in partnership to increase FAO, we hypothesized that mte1 is also a PPAR[alpha]-regulated gene in cardiac and skeletal muscle. Using real-time RT-PCR, we characterized mte1 gene expression in rat heart and soleus muscles. Messenger RNA encoding for mte1 was 3.2-fold higher in heart than in soleus muscle. Cardiac mte1 mRNA exhibited modest diurnal variation, with 1.4-fold higher levels during dark phase. In contrast, skeletal muscle mte1 mRNA remained relatively constant over the course of the day. High-fat feeding, fasting, and streptozotocin-induced diabetes, interventions that increase FA availability, muscle PPAR[alpha] activity, and muscle FAO rates, increased mte1 mRNA in heart and soleus muscle. Conversely, pressure overload and hypoxia, interventions that decrease cardiac PPAR[alpha] activity and FAO rates, repressed cardiac mte1 expression. Specific activation of PPAR[alpha] in vivo through WY-14643 administration rapidly induced mte1 mRNA in cardiac and skeletal muscle. WY-14643 also induced mte1 mRNA in isolated adult rat cardiomyocytes dose dependently. Expression of mte1 was markedly lower in hearts and soleus muscles isolated from PPAR[alpha]-null mice. Alterations in cardiac and skeletal muscle ucp3 expression mirrored that of mte1 in all models investigated. In conclusion, mte1, like ucp3, is a PPAR[alpha]-regulated gene in cardiac and skeletal muscle. nonesterified fatty acids; uncoupling protein 3; diurnal variations; diabetes; fasting

Hypobaric hypoxia induces right ventricular hypertrophy. The relative contribution of pulmonary hypertension, decreased arterial oxygen, and neuroendocrine stimulation to the transcriptional profile of hypoxia-induced right ventricular hypertrophy is unknown. Whereas both ventricles are exposed to hypoxia and neuroendocrine stimulation, only the right ventricle is exposed to increased load. We postulated that right ventricular hypertrophy would reactivate the fetal gene transcriptional profile in response to increased load. We measured the expression of candidate genes in the right ventricle of rats exposed to hypobaric hypoxia (11% [O.sub.2]) and compared the results with the left ventricle. Hypoxia induced right ventricular hypertrophy without fibrosis. In the right ventricle only, atrial natriuretic factor transcript levels progressively increased starting at day 7. Metabolic genes were differentially regulated, suggesting a substrate switch from fatty acids to glucose during early hypoxia and a switch back to fatty acids by day 14. There was also a switch in myosin isogene expression and a downregulation of sarcoplasmic/ endoplasmic ATPase 2a during early hypoxia, whereas later, both myosin isoforms and SERCA2a were upregulated. When the right and left ventricle were compared, the transcript levels of all genes, except for myosin isoforms and pyruvate dehydrogenase kinase-4, differed dramatically suggesting that all these genes are regulated by load. Our findings demonstrate that hypoxia-induced right ventricular hypertrophy transiently reactivates the fetal gene program. Furthermore, myosin iso-gene and pyruvate dehydrogenase kinase-4 expression is not affected by load, suggesting that either hypoxia itself or neuroendocrine stimulation is the primary regulator of these genes. transcriptional profile; quantitative reverse transcriptase-polymerase chain reaction; metabolism

Background Little is known about how human immunodeficiency virus (HIV) affects walking biomechanics, or about associations between HIV-related gait deviations, functional performance, and self-reported outcomes. This paper reports on (1) gait biomechanics and variability in people with HIV (PWH) and (2) associations with clinical tests, self-reported function, and falls. Methods A cross-sectional study tested consecutively sampled PWH (n = 50) and HIV-seronegative participants ([SNP] n = 50). Participants underwent 3-dimensional gait analysis, performed clinical tests (short walk and single leg stance tests with and without dual tasking, chair-rise tests, and a physical performance battery), and completed questionnaires about function and falls. Between-group comparisons were done using analysis of covariance. Linear correlations between gait variability, clinical tests, and patient-reported outcomes were established. Results People with HIV and SNP had comparable median ages (PWH = 36.6, interquartile range [IQR] = 32.0–45.6]; SNP = 31.1, IQR = 23.2–45.1). Compared with SNP, PWH walked slower (adjusted mean difference [MD] = −0.2 meters per second [m/s], 95% confidence interval [CI] = −0.3 to −0.1) with greater variability (adjusted MD = 14.7 variability score points, 95% CI = 9.9–19.5). Moreover, PWH were slower in five-times sit-to-stand (5STS) performance (adjusted MD = 1.9 seconds, 95% CI = 1.00–2.9). Significant deviations in hip kinematics (increased flexion; adjusted MDs = 2.4°–2.8°, P  = .012–.016) and knee kinematics (reduced flexion; adjusted MDs = 2.3°–3.7°, P  = .007–.027) were found in PWH during dual-task (DT) walking. The PWH's 5STS moderately correlated with larger gait variability (usual pace r  = −0.5; dual task r  = −0.6), poorer self-reported mobility (r  = 0.4) and self-care function (r  = 0.5), and fear of falling (P  = .003). Conclusions People with HIV presented with biomechanical deviations suggestive of a slowed and variable gait, especially under cognitive challenges. Five-times STS may be useful to screen for gait deviations in PWH. [ABSTRACT FROM AUTHOR]

Summary: This narrative review summarizes current knowledge on the effects of physical activity (PA) on adipokine levels in individuals with overweight and obesity. Approximately 90 investigations including randomized control, cross‐sectional and longitudinal studies that reported on the effects of a single session of PA (acute) or long‐term PA (chronic) on adipokine levels in individuals with overweight/obesity were reviewed. The findings support the notion that there is consensus on the benefits of chronic exercise training—regardless of the mode (resistance vs. aerobic), intensity and cohort (healthy vs. diabetes)—on adipokine levels (such as tumour necrosis factor‐alpha, interleukin‐6, adiponectin, visfatin, omentin‐1 and leptin). However, several confounding factors (frequency, intensity, time and type of exercise) can alter the magnitude of the effects of an acute exercise session. Available evidence suggests that PA, as a part of routine lifestyle behaviour, improves obesity complications by modulating adipokine levels. However, additional research is needed to help identify the most effective interventions to elicit the most beneficial changes in adipokine levels in individuals with overweight/obesity. [ABSTRACT FROM AUTHOR]